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Point/Counterpoint: Dual antiplatelet therapy for vascular patients: Yes, no, or sometimes?
Introduction
As evidenced by this month’s Point/Counterpoint article by Dr. William Jordan and Dr. Joseph Mills, there is still debate as to the benefit of antiplatelet agents in patients with peripheral artery disease. Currently, dual antiplatelet agents refer to aspirin and clopidogrel, but over the last year or two, ticagrelor and vorapaxar are also being prescribed for patients with peripheral atherosclerosis. The addition of these medications will probably only add to our confusion! Why don’t you weigh in on this discussion by voting on our online poll at www.vascularspecialistonline.com?
Dr. Russell Samson is the medical editor of Vascular Specialist.
Definitely, maybe.
William D. Jordan, M.D.
First, primary prevention must be considered, as few patients with no prior intervention require dual antiplatelet therapy. It seems that we only have some scant data on the prevention of first-time events in at-risk patients when they are treated with aspirin alone.
While lipid management seems to be the most recent focus for primary prevention, single antiplatelet therapy seems appropriate for many patients who have higher risk due to atherosclerotic disease. A recent study from the University of Alabama at Birmingham found that asymptomatic carotid artery stenosis patients treated with dual antiplatelet therapy actually had higher bleed rates, higher mortality, and lower neurologic event rates, compared with those treated with aspirin alone.
While this study examined only a select group of patients treated for carotid artery disease, these vascular patients had worse outcomes when treated with aspirin and clopidogrel. Thus, caution should be considered before adding too many medical therapies.
Now, consider the short-term outlook for patients – specifically those who undergo some type of vascular intervention. The very nature of vascular intervention is disruptive to the arterial endothelium. Of course, most of the arteries that we enter have some underlying pathology; thus the intimal layer is not normal. The pathologic process is already, at least, partly underway. The concept of antiplatelet therapy is focused on limiting the platelet adhesions that might exaggerate the response to injury that creates a hyperplastic reaction within the vessels. We abhor the excessive response to injury due to the potential failure of the arterial reconstruction. Paradoxically, the same platelet inhibition can also cause excessive bleeding that may complicate the vascular repair. In the current medical climate, most of us tolerate the aggravation of diminished platelet function during open reconstruction in order to protect the target repair site and to avoid the dreaded “troponin leak” that may get classified as a myocardial infarction.
Some of our nonvascular colleagues avoid intervention (e.g., axial anesthesia, endoscopic biopsy) if stronger antiplatelet medication is present.
Now, to borrow some insight from other specialties, we should consider the extensive cardiology literature that shows the value of dual platelet inhibition after percutaneous coronary intervention or a recent cardiac event. While this strategy has shown improvement in PCI results, probably due to the great risk of thrombosis when disrupting the endothelial layer of a 2- to 3-mm coronary artery, the bleeding complications, including access-site hematomas, pseudoaneurysms, or retroperitoneal bleeding, are not analyzed as extensively. The preponderance of literature supports aggressive inhibition, but the long term needs to be considered – both expense and bleeding risk.
Currently, we use short-term dual treatment when the arterial endothelium is intentionally disrupted such as after an endarterectomy, angioplasty, with or without a stent, or atherectomy. Specifically, we add short-term IV dextran to oral agents for patients undergoing a carotid endarterectomy, but most are discharged on a single oral agent unless there is another indication for dual therapy.
Patients undergoing lower-extremity, catheter-based interventions are given dual therapy for the first 30 days, which is then adjusted according to the clinical response, duplex findings and other medical conditions. Bypass graft patients (yes, we still do some) are usually given a single agent unless the graft or patient has exhibited some concern for early failure.
In summary, I suspect that dual therapy is overused in our “pill-driven” population, but there still seem to be areas for its application. On each encounter with patients, I would encourage all vascular specialists to review the indications for antiplatelet therapy to consider removing a medication, improving compliance, and limiting bleeding risk.
Dr. Jordan is the director of the division of vascular surgery at the University of Alabama Birmingham School of Medicine. He has no relevant conflicts.
Dueling over dual antiplatelet therapy
Joseph L. Mills Sr., M.D.
Amidst a background of constant clamoring for data-driven and evidence-based medical decision-making, the practice of vascular medicine and surgery remains mired in the anecdotal. If a little is good, more must be better, seems the rationale for dual antiplatelet therapy. There may be small, as yet unclearly defined subsets of patients for whom dual therapy is actually beneficial, but an unbiased review of the current literature leads to the inescapable conclusion that more patients would be harmed by injudicious application of the more-is-better principle as concerns antiplatelet therapy for patients with carotid artery and peripheral artery disease (PAD).
The best evidence for antiplatelet therapy in patients with carotid disease suggests that aspirin as a single agent in doses ranging from 75 to 150 mg daily is preferred, and at least two meta-analyses and systematic reviews were unable to support the use of dual antiplatelet therapy.1 At least in symptomatic patients, combination or dual antiplatelet therapy may increase the short-term risk of hemorrhagic complications in patients with acute ischemic stroke caused by large-artery disease.2 Long-term dual therapy for secondary stroke prevention with aspirin and clopidogrel has been associated with four times the bleeding risk of monotherapy.3 These bleeds are often intracranial or gastrointestinal and are serious.
With respect to asymptomatic patients, while the CHARISMA trial did demonstrate a modest reduction in subsequent thrombotic events in a subset analysis of patients with stable, preexisting vascular disease, the bottom line was that dual antiplatelet therapy was associated with a 4% risk of moderate to severe bleeding and that there were strong correlations between moderate bleeding and all cause mortality (hazard ratio, 2.55), myocardial infarction (HR, 2.92) and stroke (HR, 4.2).4 The bleeding risk of dual antiplatelet therapy thus seems to outweigh the benefits.
Other data muddy the situation, but only a little. While at least two small studies (one a randomized controlled trial – CARESS [Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis])5 have suggested that the combination of aspirin and clopidogrel may reduce the frequency of perioperative microembolic signals detected early after carotid endarterectomy compared with monotherapy, it is not established that this surrogate measure would translate into long-term clinical benefit and would outweigh the established bleeding risk of dual therapy.
At present, the vascular surgeon should urge his patients to stop smoking, prescribe a statin, control blood pressure (but not necessarily with a beta-blocker), control diabetes, and prescribe a single antiplatelet agent, most often baby aspirin, for most of his or her patients. More good than harm will result.
References
Dr. Mills is professor of surgery and chief, division of vascular and endovascular surgery, University of Arizona Health Sciences Center, Tucson, and an associate medical editor for Vascular Specialist. He has no relevant conflicts.
Introduction
As evidenced by this month’s Point/Counterpoint article by Dr. William Jordan and Dr. Joseph Mills, there is still debate as to the benefit of antiplatelet agents in patients with peripheral artery disease. Currently, dual antiplatelet agents refer to aspirin and clopidogrel, but over the last year or two, ticagrelor and vorapaxar are also being prescribed for patients with peripheral atherosclerosis. The addition of these medications will probably only add to our confusion! Why don’t you weigh in on this discussion by voting on our online poll at www.vascularspecialistonline.com?
Dr. Russell Samson is the medical editor of Vascular Specialist.
Definitely, maybe.
William D. Jordan, M.D.
First, primary prevention must be considered, as few patients with no prior intervention require dual antiplatelet therapy. It seems that we only have some scant data on the prevention of first-time events in at-risk patients when they are treated with aspirin alone.
While lipid management seems to be the most recent focus for primary prevention, single antiplatelet therapy seems appropriate for many patients who have higher risk due to atherosclerotic disease. A recent study from the University of Alabama at Birmingham found that asymptomatic carotid artery stenosis patients treated with dual antiplatelet therapy actually had higher bleed rates, higher mortality, and lower neurologic event rates, compared with those treated with aspirin alone.
While this study examined only a select group of patients treated for carotid artery disease, these vascular patients had worse outcomes when treated with aspirin and clopidogrel. Thus, caution should be considered before adding too many medical therapies.
Now, consider the short-term outlook for patients – specifically those who undergo some type of vascular intervention. The very nature of vascular intervention is disruptive to the arterial endothelium. Of course, most of the arteries that we enter have some underlying pathology; thus the intimal layer is not normal. The pathologic process is already, at least, partly underway. The concept of antiplatelet therapy is focused on limiting the platelet adhesions that might exaggerate the response to injury that creates a hyperplastic reaction within the vessels. We abhor the excessive response to injury due to the potential failure of the arterial reconstruction. Paradoxically, the same platelet inhibition can also cause excessive bleeding that may complicate the vascular repair. In the current medical climate, most of us tolerate the aggravation of diminished platelet function during open reconstruction in order to protect the target repair site and to avoid the dreaded “troponin leak” that may get classified as a myocardial infarction.
Some of our nonvascular colleagues avoid intervention (e.g., axial anesthesia, endoscopic biopsy) if stronger antiplatelet medication is present.
Now, to borrow some insight from other specialties, we should consider the extensive cardiology literature that shows the value of dual platelet inhibition after percutaneous coronary intervention or a recent cardiac event. While this strategy has shown improvement in PCI results, probably due to the great risk of thrombosis when disrupting the endothelial layer of a 2- to 3-mm coronary artery, the bleeding complications, including access-site hematomas, pseudoaneurysms, or retroperitoneal bleeding, are not analyzed as extensively. The preponderance of literature supports aggressive inhibition, but the long term needs to be considered – both expense and bleeding risk.
Currently, we use short-term dual treatment when the arterial endothelium is intentionally disrupted such as after an endarterectomy, angioplasty, with or without a stent, or atherectomy. Specifically, we add short-term IV dextran to oral agents for patients undergoing a carotid endarterectomy, but most are discharged on a single oral agent unless there is another indication for dual therapy.
Patients undergoing lower-extremity, catheter-based interventions are given dual therapy for the first 30 days, which is then adjusted according to the clinical response, duplex findings and other medical conditions. Bypass graft patients (yes, we still do some) are usually given a single agent unless the graft or patient has exhibited some concern for early failure.
In summary, I suspect that dual therapy is overused in our “pill-driven” population, but there still seem to be areas for its application. On each encounter with patients, I would encourage all vascular specialists to review the indications for antiplatelet therapy to consider removing a medication, improving compliance, and limiting bleeding risk.
Dr. Jordan is the director of the division of vascular surgery at the University of Alabama Birmingham School of Medicine. He has no relevant conflicts.
Dueling over dual antiplatelet therapy
Joseph L. Mills Sr., M.D.
Amidst a background of constant clamoring for data-driven and evidence-based medical decision-making, the practice of vascular medicine and surgery remains mired in the anecdotal. If a little is good, more must be better, seems the rationale for dual antiplatelet therapy. There may be small, as yet unclearly defined subsets of patients for whom dual therapy is actually beneficial, but an unbiased review of the current literature leads to the inescapable conclusion that more patients would be harmed by injudicious application of the more-is-better principle as concerns antiplatelet therapy for patients with carotid artery and peripheral artery disease (PAD).
The best evidence for antiplatelet therapy in patients with carotid disease suggests that aspirin as a single agent in doses ranging from 75 to 150 mg daily is preferred, and at least two meta-analyses and systematic reviews were unable to support the use of dual antiplatelet therapy.1 At least in symptomatic patients, combination or dual antiplatelet therapy may increase the short-term risk of hemorrhagic complications in patients with acute ischemic stroke caused by large-artery disease.2 Long-term dual therapy for secondary stroke prevention with aspirin and clopidogrel has been associated with four times the bleeding risk of monotherapy.3 These bleeds are often intracranial or gastrointestinal and are serious.
With respect to asymptomatic patients, while the CHARISMA trial did demonstrate a modest reduction in subsequent thrombotic events in a subset analysis of patients with stable, preexisting vascular disease, the bottom line was that dual antiplatelet therapy was associated with a 4% risk of moderate to severe bleeding and that there were strong correlations between moderate bleeding and all cause mortality (hazard ratio, 2.55), myocardial infarction (HR, 2.92) and stroke (HR, 4.2).4 The bleeding risk of dual antiplatelet therapy thus seems to outweigh the benefits.
Other data muddy the situation, but only a little. While at least two small studies (one a randomized controlled trial – CARESS [Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis])5 have suggested that the combination of aspirin and clopidogrel may reduce the frequency of perioperative microembolic signals detected early after carotid endarterectomy compared with monotherapy, it is not established that this surrogate measure would translate into long-term clinical benefit and would outweigh the established bleeding risk of dual therapy.
At present, the vascular surgeon should urge his patients to stop smoking, prescribe a statin, control blood pressure (but not necessarily with a beta-blocker), control diabetes, and prescribe a single antiplatelet agent, most often baby aspirin, for most of his or her patients. More good than harm will result.
References
Dr. Mills is professor of surgery and chief, division of vascular and endovascular surgery, University of Arizona Health Sciences Center, Tucson, and an associate medical editor for Vascular Specialist. He has no relevant conflicts.
Introduction
As evidenced by this month’s Point/Counterpoint article by Dr. William Jordan and Dr. Joseph Mills, there is still debate as to the benefit of antiplatelet agents in patients with peripheral artery disease. Currently, dual antiplatelet agents refer to aspirin and clopidogrel, but over the last year or two, ticagrelor and vorapaxar are also being prescribed for patients with peripheral atherosclerosis. The addition of these medications will probably only add to our confusion! Why don’t you weigh in on this discussion by voting on our online poll at www.vascularspecialistonline.com?
Dr. Russell Samson is the medical editor of Vascular Specialist.
Definitely, maybe.
William D. Jordan, M.D.
First, primary prevention must be considered, as few patients with no prior intervention require dual antiplatelet therapy. It seems that we only have some scant data on the prevention of first-time events in at-risk patients when they are treated with aspirin alone.
While lipid management seems to be the most recent focus for primary prevention, single antiplatelet therapy seems appropriate for many patients who have higher risk due to atherosclerotic disease. A recent study from the University of Alabama at Birmingham found that asymptomatic carotid artery stenosis patients treated with dual antiplatelet therapy actually had higher bleed rates, higher mortality, and lower neurologic event rates, compared with those treated with aspirin alone.
While this study examined only a select group of patients treated for carotid artery disease, these vascular patients had worse outcomes when treated with aspirin and clopidogrel. Thus, caution should be considered before adding too many medical therapies.
Now, consider the short-term outlook for patients – specifically those who undergo some type of vascular intervention. The very nature of vascular intervention is disruptive to the arterial endothelium. Of course, most of the arteries that we enter have some underlying pathology; thus the intimal layer is not normal. The pathologic process is already, at least, partly underway. The concept of antiplatelet therapy is focused on limiting the platelet adhesions that might exaggerate the response to injury that creates a hyperplastic reaction within the vessels. We abhor the excessive response to injury due to the potential failure of the arterial reconstruction. Paradoxically, the same platelet inhibition can also cause excessive bleeding that may complicate the vascular repair. In the current medical climate, most of us tolerate the aggravation of diminished platelet function during open reconstruction in order to protect the target repair site and to avoid the dreaded “troponin leak” that may get classified as a myocardial infarction.
Some of our nonvascular colleagues avoid intervention (e.g., axial anesthesia, endoscopic biopsy) if stronger antiplatelet medication is present.
Now, to borrow some insight from other specialties, we should consider the extensive cardiology literature that shows the value of dual platelet inhibition after percutaneous coronary intervention or a recent cardiac event. While this strategy has shown improvement in PCI results, probably due to the great risk of thrombosis when disrupting the endothelial layer of a 2- to 3-mm coronary artery, the bleeding complications, including access-site hematomas, pseudoaneurysms, or retroperitoneal bleeding, are not analyzed as extensively. The preponderance of literature supports aggressive inhibition, but the long term needs to be considered – both expense and bleeding risk.
Currently, we use short-term dual treatment when the arterial endothelium is intentionally disrupted such as after an endarterectomy, angioplasty, with or without a stent, or atherectomy. Specifically, we add short-term IV dextran to oral agents for patients undergoing a carotid endarterectomy, but most are discharged on a single oral agent unless there is another indication for dual therapy.
Patients undergoing lower-extremity, catheter-based interventions are given dual therapy for the first 30 days, which is then adjusted according to the clinical response, duplex findings and other medical conditions. Bypass graft patients (yes, we still do some) are usually given a single agent unless the graft or patient has exhibited some concern for early failure.
In summary, I suspect that dual therapy is overused in our “pill-driven” population, but there still seem to be areas for its application. On each encounter with patients, I would encourage all vascular specialists to review the indications for antiplatelet therapy to consider removing a medication, improving compliance, and limiting bleeding risk.
Dr. Jordan is the director of the division of vascular surgery at the University of Alabama Birmingham School of Medicine. He has no relevant conflicts.
Dueling over dual antiplatelet therapy
Joseph L. Mills Sr., M.D.
Amidst a background of constant clamoring for data-driven and evidence-based medical decision-making, the practice of vascular medicine and surgery remains mired in the anecdotal. If a little is good, more must be better, seems the rationale for dual antiplatelet therapy. There may be small, as yet unclearly defined subsets of patients for whom dual therapy is actually beneficial, but an unbiased review of the current literature leads to the inescapable conclusion that more patients would be harmed by injudicious application of the more-is-better principle as concerns antiplatelet therapy for patients with carotid artery and peripheral artery disease (PAD).
The best evidence for antiplatelet therapy in patients with carotid disease suggests that aspirin as a single agent in doses ranging from 75 to 150 mg daily is preferred, and at least two meta-analyses and systematic reviews were unable to support the use of dual antiplatelet therapy.1 At least in symptomatic patients, combination or dual antiplatelet therapy may increase the short-term risk of hemorrhagic complications in patients with acute ischemic stroke caused by large-artery disease.2 Long-term dual therapy for secondary stroke prevention with aspirin and clopidogrel has been associated with four times the bleeding risk of monotherapy.3 These bleeds are often intracranial or gastrointestinal and are serious.
With respect to asymptomatic patients, while the CHARISMA trial did demonstrate a modest reduction in subsequent thrombotic events in a subset analysis of patients with stable, preexisting vascular disease, the bottom line was that dual antiplatelet therapy was associated with a 4% risk of moderate to severe bleeding and that there were strong correlations between moderate bleeding and all cause mortality (hazard ratio, 2.55), myocardial infarction (HR, 2.92) and stroke (HR, 4.2).4 The bleeding risk of dual antiplatelet therapy thus seems to outweigh the benefits.
Other data muddy the situation, but only a little. While at least two small studies (one a randomized controlled trial – CARESS [Clopidogrel and Aspirin for Reduction of Emboli in Symptomatic Carotid Stenosis])5 have suggested that the combination of aspirin and clopidogrel may reduce the frequency of perioperative microembolic signals detected early after carotid endarterectomy compared with monotherapy, it is not established that this surrogate measure would translate into long-term clinical benefit and would outweigh the established bleeding risk of dual therapy.
At present, the vascular surgeon should urge his patients to stop smoking, prescribe a statin, control blood pressure (but not necessarily with a beta-blocker), control diabetes, and prescribe a single antiplatelet agent, most often baby aspirin, for most of his or her patients. More good than harm will result.
References
Dr. Mills is professor of surgery and chief, division of vascular and endovascular surgery, University of Arizona Health Sciences Center, Tucson, and an associate medical editor for Vascular Specialist. He has no relevant conflicts.
Point/Counterpoint: Endo first for the treatment of infrainguinal PAD?
The BASIL study originally published in the Lancet in 2005 (366:1925-34) and subsequently reiterated in multiple publications proposes that an endovascular approach should be utilized as the first invasive treatment modality in patients with infrainguinal peripheral arterial disease whose life expectancy is less than 2 years. By contrast, those patients expected to live beyond 2 years usually should be offered bypass surgery first, especially where a vein is available as a conduit. However, as can be seen from this month’s Point/Counterpoint by Dr. George Meier III and Dr. Michael S. Conte, the debate still rages as to the benefit of open vs. endovascular procedures for these patients. We encourage readers to voice their opinions in our “Letters to the Editor” section, as well as by participating in our web-based Quick Poll to the right of this story. - Dr. Russell Samson, Medical Editor, Vascular Specialist
POINT/COUNTERPOINT
Yes, endo is generally the way to go.
By Dr. George Meier III
Endovascular treatment of lower-extremity arterial disease has rapidly expanded, now approaching the standard for treatment of patients with lower-extremity disease. While open bypass remains a gold standard for the clinical treatment of limb-threatening ischemia, there are many limitations to the use of open surgery.
First and foremost, open surgical intervention represents pain and suffering for the patient as well as a delayed recovery, compared with endovascular treatment. All other factors being equal, most patients would prefer a less-invasive approach to minimize these factors and to maximize the speed of recovery. Open surgical interventions typically require 6 weeks or longer to get back to a functional status even remotely close to the patient’s initial level of function. With more severe tissue loss or with greater pain preoperatively, the difficulty of getting the patient back to full functional status remains problematic. In John Porter’s classic paper published in the Journal of Vascular Surgery in 1998,1 wound complications occurred in 24% of the patients with a 5-year survival rate of only 49% in this relatively young population, average age 66 years. Repeat operations to maintain graft patency, treat wound complications, or treat recurrent or contralateral ischemia were required in 54% of the patients and 23% ultimately required major limb amputation.
Of the 112 patients in this study, only 14.3% achieved the ideal surgical result of an uncomplicated operation: long-term symptom relief, maintenance of functional status, and no recurrence or repeat operations. These are sobering statistics for anyone facing open revascularization for critical limb ischemia.
The BASIL trial is often put forward as an example of the best data available currently to define patient treatments in patients with critical limb ischemia.2 Despite this, BASIL was a flawed trial from the beginning because of the difficulties of truly randomizing patients with vascular disease to open surgical treatment vs. percutaneous treatment. First, all patients had to be appropriate candidates for both open and endovascular treatment. In the real world, we readily recognize that the luxury of this choice is not available to many of our patients. A lack of conduit or increased surgical risk results in endovascular treatment being the only management option for many. Additionally, patient preference increasingly plays a role in treatment selection, obviously increasing the likelihood of less invasive percutaneous treatment. Yes, the mortality of open bypass in BASIL is reported to be in the 1%-3% range, but this population has been carefully selected based on screening and treatment of underlying cardiac disease. The true incidence of cardiovascular disease is impossible to determine since significant cardiac disease negated randomization.
Unfortunately, even with all of the advances in endovascular treatments the results of percutaneous treatment have never reached the results of open bypass. Nonetheless, while the success may not be as great the risks are not as high either. The main challenge to endovascular treatment is the durability of the intervention. While we can usually treat pre-existing disease in the lower-extremity arterial tree, maintaining patency and durability is the challenge. As my esteemed colleague has noted, failure of endovascular treatment in the BASIL trial resulted in significantly worse outcomes for open bypass in those patients. While much was made about this fact when the BASIL trial was published, endovascular treatment after open failure has even a worse outcome than did open treatment after endovascular failure. The truth of the matter is that, for obvious reasons, failure begets failure.
Generally, there are two imaging approaches to defining the extent of vascular disease: first, contrast angiography via percutaneous access; and second, CT angiography using intravenous contrast. If contrast angiography is undertaken to diagnose the extent of disease, then it is a relatively limited extrapolation to treat the patient’s disease percutaneously at the time of the diagnostic angiogram. For this reason, I discuss with all patients coming for diagnostic angiography the issue of endovascular treatment. It is rare that we make patients worse with an attempt at endovascular treatment by an experienced interventionalist. Similarly, it is rare that we alter a bypass level based on an attempt at endovascular treatment. If, in my opinion, the risk of an attempted endovascular treatment is acceptable, then this is done at the time of the diagnostic angiogram. Patients appreciate this discussion prior to proceeding with diagnostic angiography.
What about inadequate autogenous conduit? Even my counterpoint opponent has published a documented 20% risk of absent or inadequate ipsilateral greater saphenous vein.3 While he and his colleagues have documented excellent results using contralateral greater saphenous vein, there is still an inevitable morbidity and, yes, even a mortality risk associated with contralateral leg vein harvest. While in a good cardiac risk patient this may be negligible, we are again facing an ever more complex and medically ill patient population to subject to vascular treatment. It is in this setting that many vascular surgeons move to prosthetic conduits for the treatment of the patient’s vascular disease. While this may provide a short-term fix for the conduit problem, in the long term the risk of sudden, uncompensated failure of limb perfusion by prosthetic graft failure may often result in a higher risk procedure at a time when the patient may be older and more severely limited. Endovascular treatment is clearly a reasonable alternative in patients where autogenous conduit is not readily available.
While this debate will inevitably continue as long as practitioners have bias toward either open or endovascular management of vascular disease, one thing is for certain: We will continue to extend the limits of treatment to ever more ill and complex patients. While we have been very successful at performing fewer and fewer morbid interventions for limb-threatening vascular disease, these patients continue to be increasingly challenging to manage.
As the overall population continues to age, the need for less invasive treatment of limb-threatening vascular disease will continue to grow. And, yes, I agree that vascular surgeons in the role of interventionalist or surgeon are the leadership for the management of CLI in the future.
Dr. Meier is professor and chief of vascular surgery at the University of Cincinnati.
References
1. J. Vasc. Surg. 1998;27:256-63; discussion 264-6
3. J. Vasc. Surg. 2002:35:1085-92
No: A selective approach remains the key.
By Dr. MICHAEL S. CONTE
Recently the term “pandemic” has been applied to the growing global impact of peripheral artery disease (PAD), currently estimated to afflict more than 200 million individuals.1 The term “critical limb ischemia” (CLI), connoting the most advanced stage of PAD with imminent limb threat, is inadequately defined2 but likely encompasses 1%-3% of PAD. Aging of the global population and the increasing prevalence of diabetes are fueling increases in CLI and its impact on public health. While traditionally treated largely by vascular surgeons plying the open bypass trade, the ongoing development and market dispersion of catheter-based technologies for CLI has led to major secular changes.
Recent estimates suggest that upward of 5 billion dollars are spent annually on CLI in the Medicare population.3, 4 Increasing volumes and costs associated with revascularizations for CLI are a major driver, yet recent data suggest that regional spending in the United States is widely disparate and not directly associated with amputation rates.5 Thus defining effectiveness and value in CLI care has become a major challenge to the vascular community.
In current everyday practice, clinicians are faced with making treatment choices for CLI patients based on limited data and lots of anecdote. While the “open vs. endo” debate goes on, in many ways it has become less broadly relevant as the sophisticated clinician recognizes the real challenge lies in defining which approach to apply first in the right patient, at the right time. The only randomized, controlled trial (RCT) done in the field, the BASIL trial,6 is more than a decade old. However its findings remain important. For patients with “severe limb ischemia” likely to survive for at least 2 years, open bypass surgery offered better outcomes over angioplasty as an initial strategy.7 Moreover, the finding in BASIL that patients undergoing bypass after prior failed angioplasty did poorly,8 suggesting “no free lunch” for endovascular failures, has since been confirmed in other large registry studies.9
Simply stated, failure matters in CLI. And although endovascular techniques have continued to improve, the growing epidemic of restenosis shows no signs of abating.10 As in the case of percutaneous coronary intervention (PCI), we will know when endo results are meaningfully improved in PAD when the procedure volume curves actually flatten, not continue to grow geometrically.
So, in selecting the optimal strategy for CLI today, let’s focus on what we seem to know and try to apply an evidence-based mentality. We know that open bypass surgery is an effective and versatile treatment, but one that carries real morbidity (10%-20%) and some mortality (1%-3%). Among many large studies, the PREVENT III multicenter trial provides benchmark data on perioperative and 1-year outcomes.11
We know that the quality of the vein is the critical technical determinant of success, and arterial anatomy is less influential as long as there is outflow to the foot.12 We know that poor quality veins, prosthetics, and other alternatives are much inferior in CLI. And we know that there is a subset of CLI patients who are at high risk for adverse surgical outcomes.13, 14 However one defines them, up to 10% of patients in the large surgical series are in a high-risk group and may not experience meaningful benefit. For endovascular treatments, the data are less clear but certain trends have been consistent. Multilevel disease, long-segment occlusions, heavily calcified lesions, and more advanced tissue loss are negative predictors of clinical success.
Thus at first glance the weaknesses of the two strategies are largely complementary.15 When I encounter an average-risk CLI patient, with an adequate saphenous vein and more than one unfavorable endo factor, I am inclined towards bypass first.
Conversely, endo-favorable anatomy in higher risk patients is a no-brainer. Lots of people fall in the middle, and a significant minority should be considered for primary amputation. Currently my practice is roughly 50% bypass surgery-first in CLI.
Endovascular innovations have made a huge impact on vascular practice, and the leadership of many vascular surgeons (e.g., my esteemed counterpoint author) has been central to advancing the field. Better wires and catheters, retrograde approaches, and drug-eluting technologies continue to be developed at a dizzying pace.
We are all continually learning. Unfortunately, we lack good objective evidence to support most of the expanding armamentarium for CLI. However it is abundantly clear that technical (angiographic) success and clinical success are far apart, which is no surprise. What is surprising is an unsettlingly common lack of honesty about such an obvious fact. Are we all guilty of looking through rose-colored glasses?
Is it really such big news that patency actually matters for most patients with CLI? Technologies will not improve quickly enough if there is no market imperative to make them better. If we continue to buy and use things that are frequently ineffective, or don’t measure it carefully, where is the motivation?
No matter the lens through which one looks at the CLI field, it is desperate for improvement. We need much better technologies that provide longer lasting solutions for patients. We need better diagnostics to predict disease progression and responses to treatment.
We need some new medical or biological therapies that truly alleviate suffering. And we largely lack data on comparative effectiveness, and value, to support thoughtful application of our current treatment arsenal.
Most importantly what we need now is less dogma, and a lot more science. Over more than two decades, multiple RCTs comparing medical, interventional and surgical therapies for coronary artery disease have formed the basis for practice guidelines.
By comparison, our field is nearly incoherent both to vascular specialists and referring physicians. It will not be easy, but this can be done in PAD as well, and the vascular community must embrace it. Moreover it is imperative that vascular surgeons help to lead these multidisciplinary efforts, and develop evidence-based global guidelines to guide best practice in CLI.16 The recent funding of the BEST-CLI trial in the United States and the BASIL-2 trial in the United Kingdom demonstrate the importance to public health and offer great opportunities.
Until better evidence is available, a rational approach to limb salvage requires flexibility, understanding of the factors predicting success/failure for each modality, and the continued use of open bypass surgery as the initial treatment option for a significant number of patients.
And for the sake of our most vulnerable patients, we better keep training vascular surgeons to do all of it well.
Dr. Conte is professor and chief, division of vascular & endovascular surgery and the Edwin J. Wylie, M.D. Chair in Vascular Surgery at the University of California, San Francisco.
References
2. J. Vasc. Surg. 2014;59:220-34
7. J. Vasc. Surg. 2010;51:5S-17S
8. J. Vasc. Surg. 2010;51:18S-31S
9. J. Vasc. Surg. 2011;54:730-6
10. J. Amer. Heart Assoc. 2013;2:e000345
11. J. Vasc. Surg. 2006;43:742-51
12. J. Vasc. Surg. 2007;46:1180-90
13. J. Vasc. Surg. 2009;50:769-75
14. J. Vasc. Surg. 2010;52:1218-25
15. J. Vasc. Surg. 2013;57:8S-13S16. J. Vasc. Surg. 2014;59:510
The BASIL study originally published in the Lancet in 2005 (366:1925-34) and subsequently reiterated in multiple publications proposes that an endovascular approach should be utilized as the first invasive treatment modality in patients with infrainguinal peripheral arterial disease whose life expectancy is less than 2 years. By contrast, those patients expected to live beyond 2 years usually should be offered bypass surgery first, especially where a vein is available as a conduit. However, as can be seen from this month’s Point/Counterpoint by Dr. George Meier III and Dr. Michael S. Conte, the debate still rages as to the benefit of open vs. endovascular procedures for these patients. We encourage readers to voice their opinions in our “Letters to the Editor” section, as well as by participating in our web-based Quick Poll to the right of this story. - Dr. Russell Samson, Medical Editor, Vascular Specialist
POINT/COUNTERPOINT
Yes, endo is generally the way to go.
By Dr. George Meier III
Endovascular treatment of lower-extremity arterial disease has rapidly expanded, now approaching the standard for treatment of patients with lower-extremity disease. While open bypass remains a gold standard for the clinical treatment of limb-threatening ischemia, there are many limitations to the use of open surgery.
First and foremost, open surgical intervention represents pain and suffering for the patient as well as a delayed recovery, compared with endovascular treatment. All other factors being equal, most patients would prefer a less-invasive approach to minimize these factors and to maximize the speed of recovery. Open surgical interventions typically require 6 weeks or longer to get back to a functional status even remotely close to the patient’s initial level of function. With more severe tissue loss or with greater pain preoperatively, the difficulty of getting the patient back to full functional status remains problematic. In John Porter’s classic paper published in the Journal of Vascular Surgery in 1998,1 wound complications occurred in 24% of the patients with a 5-year survival rate of only 49% in this relatively young population, average age 66 years. Repeat operations to maintain graft patency, treat wound complications, or treat recurrent or contralateral ischemia were required in 54% of the patients and 23% ultimately required major limb amputation.
Of the 112 patients in this study, only 14.3% achieved the ideal surgical result of an uncomplicated operation: long-term symptom relief, maintenance of functional status, and no recurrence or repeat operations. These are sobering statistics for anyone facing open revascularization for critical limb ischemia.
The BASIL trial is often put forward as an example of the best data available currently to define patient treatments in patients with critical limb ischemia.2 Despite this, BASIL was a flawed trial from the beginning because of the difficulties of truly randomizing patients with vascular disease to open surgical treatment vs. percutaneous treatment. First, all patients had to be appropriate candidates for both open and endovascular treatment. In the real world, we readily recognize that the luxury of this choice is not available to many of our patients. A lack of conduit or increased surgical risk results in endovascular treatment being the only management option for many. Additionally, patient preference increasingly plays a role in treatment selection, obviously increasing the likelihood of less invasive percutaneous treatment. Yes, the mortality of open bypass in BASIL is reported to be in the 1%-3% range, but this population has been carefully selected based on screening and treatment of underlying cardiac disease. The true incidence of cardiovascular disease is impossible to determine since significant cardiac disease negated randomization.
Unfortunately, even with all of the advances in endovascular treatments the results of percutaneous treatment have never reached the results of open bypass. Nonetheless, while the success may not be as great the risks are not as high either. The main challenge to endovascular treatment is the durability of the intervention. While we can usually treat pre-existing disease in the lower-extremity arterial tree, maintaining patency and durability is the challenge. As my esteemed colleague has noted, failure of endovascular treatment in the BASIL trial resulted in significantly worse outcomes for open bypass in those patients. While much was made about this fact when the BASIL trial was published, endovascular treatment after open failure has even a worse outcome than did open treatment after endovascular failure. The truth of the matter is that, for obvious reasons, failure begets failure.
Generally, there are two imaging approaches to defining the extent of vascular disease: first, contrast angiography via percutaneous access; and second, CT angiography using intravenous contrast. If contrast angiography is undertaken to diagnose the extent of disease, then it is a relatively limited extrapolation to treat the patient’s disease percutaneously at the time of the diagnostic angiogram. For this reason, I discuss with all patients coming for diagnostic angiography the issue of endovascular treatment. It is rare that we make patients worse with an attempt at endovascular treatment by an experienced interventionalist. Similarly, it is rare that we alter a bypass level based on an attempt at endovascular treatment. If, in my opinion, the risk of an attempted endovascular treatment is acceptable, then this is done at the time of the diagnostic angiogram. Patients appreciate this discussion prior to proceeding with diagnostic angiography.
What about inadequate autogenous conduit? Even my counterpoint opponent has published a documented 20% risk of absent or inadequate ipsilateral greater saphenous vein.3 While he and his colleagues have documented excellent results using contralateral greater saphenous vein, there is still an inevitable morbidity and, yes, even a mortality risk associated with contralateral leg vein harvest. While in a good cardiac risk patient this may be negligible, we are again facing an ever more complex and medically ill patient population to subject to vascular treatment. It is in this setting that many vascular surgeons move to prosthetic conduits for the treatment of the patient’s vascular disease. While this may provide a short-term fix for the conduit problem, in the long term the risk of sudden, uncompensated failure of limb perfusion by prosthetic graft failure may often result in a higher risk procedure at a time when the patient may be older and more severely limited. Endovascular treatment is clearly a reasonable alternative in patients where autogenous conduit is not readily available.
While this debate will inevitably continue as long as practitioners have bias toward either open or endovascular management of vascular disease, one thing is for certain: We will continue to extend the limits of treatment to ever more ill and complex patients. While we have been very successful at performing fewer and fewer morbid interventions for limb-threatening vascular disease, these patients continue to be increasingly challenging to manage.
As the overall population continues to age, the need for less invasive treatment of limb-threatening vascular disease will continue to grow. And, yes, I agree that vascular surgeons in the role of interventionalist or surgeon are the leadership for the management of CLI in the future.
Dr. Meier is professor and chief of vascular surgery at the University of Cincinnati.
References
1. J. Vasc. Surg. 1998;27:256-63; discussion 264-6
3. J. Vasc. Surg. 2002:35:1085-92
No: A selective approach remains the key.
By Dr. MICHAEL S. CONTE
Recently the term “pandemic” has been applied to the growing global impact of peripheral artery disease (PAD), currently estimated to afflict more than 200 million individuals.1 The term “critical limb ischemia” (CLI), connoting the most advanced stage of PAD with imminent limb threat, is inadequately defined2 but likely encompasses 1%-3% of PAD. Aging of the global population and the increasing prevalence of diabetes are fueling increases in CLI and its impact on public health. While traditionally treated largely by vascular surgeons plying the open bypass trade, the ongoing development and market dispersion of catheter-based technologies for CLI has led to major secular changes.
Recent estimates suggest that upward of 5 billion dollars are spent annually on CLI in the Medicare population.3, 4 Increasing volumes and costs associated with revascularizations for CLI are a major driver, yet recent data suggest that regional spending in the United States is widely disparate and not directly associated with amputation rates.5 Thus defining effectiveness and value in CLI care has become a major challenge to the vascular community.
In current everyday practice, clinicians are faced with making treatment choices for CLI patients based on limited data and lots of anecdote. While the “open vs. endo” debate goes on, in many ways it has become less broadly relevant as the sophisticated clinician recognizes the real challenge lies in defining which approach to apply first in the right patient, at the right time. The only randomized, controlled trial (RCT) done in the field, the BASIL trial,6 is more than a decade old. However its findings remain important. For patients with “severe limb ischemia” likely to survive for at least 2 years, open bypass surgery offered better outcomes over angioplasty as an initial strategy.7 Moreover, the finding in BASIL that patients undergoing bypass after prior failed angioplasty did poorly,8 suggesting “no free lunch” for endovascular failures, has since been confirmed in other large registry studies.9
Simply stated, failure matters in CLI. And although endovascular techniques have continued to improve, the growing epidemic of restenosis shows no signs of abating.10 As in the case of percutaneous coronary intervention (PCI), we will know when endo results are meaningfully improved in PAD when the procedure volume curves actually flatten, not continue to grow geometrically.
So, in selecting the optimal strategy for CLI today, let’s focus on what we seem to know and try to apply an evidence-based mentality. We know that open bypass surgery is an effective and versatile treatment, but one that carries real morbidity (10%-20%) and some mortality (1%-3%). Among many large studies, the PREVENT III multicenter trial provides benchmark data on perioperative and 1-year outcomes.11
We know that the quality of the vein is the critical technical determinant of success, and arterial anatomy is less influential as long as there is outflow to the foot.12 We know that poor quality veins, prosthetics, and other alternatives are much inferior in CLI. And we know that there is a subset of CLI patients who are at high risk for adverse surgical outcomes.13, 14 However one defines them, up to 10% of patients in the large surgical series are in a high-risk group and may not experience meaningful benefit. For endovascular treatments, the data are less clear but certain trends have been consistent. Multilevel disease, long-segment occlusions, heavily calcified lesions, and more advanced tissue loss are negative predictors of clinical success.
Thus at first glance the weaknesses of the two strategies are largely complementary.15 When I encounter an average-risk CLI patient, with an adequate saphenous vein and more than one unfavorable endo factor, I am inclined towards bypass first.
Conversely, endo-favorable anatomy in higher risk patients is a no-brainer. Lots of people fall in the middle, and a significant minority should be considered for primary amputation. Currently my practice is roughly 50% bypass surgery-first in CLI.
Endovascular innovations have made a huge impact on vascular practice, and the leadership of many vascular surgeons (e.g., my esteemed counterpoint author) has been central to advancing the field. Better wires and catheters, retrograde approaches, and drug-eluting technologies continue to be developed at a dizzying pace.
We are all continually learning. Unfortunately, we lack good objective evidence to support most of the expanding armamentarium for CLI. However it is abundantly clear that technical (angiographic) success and clinical success are far apart, which is no surprise. What is surprising is an unsettlingly common lack of honesty about such an obvious fact. Are we all guilty of looking through rose-colored glasses?
Is it really such big news that patency actually matters for most patients with CLI? Technologies will not improve quickly enough if there is no market imperative to make them better. If we continue to buy and use things that are frequently ineffective, or don’t measure it carefully, where is the motivation?
No matter the lens through which one looks at the CLI field, it is desperate for improvement. We need much better technologies that provide longer lasting solutions for patients. We need better diagnostics to predict disease progression and responses to treatment.
We need some new medical or biological therapies that truly alleviate suffering. And we largely lack data on comparative effectiveness, and value, to support thoughtful application of our current treatment arsenal.
Most importantly what we need now is less dogma, and a lot more science. Over more than two decades, multiple RCTs comparing medical, interventional and surgical therapies for coronary artery disease have formed the basis for practice guidelines.
By comparison, our field is nearly incoherent both to vascular specialists and referring physicians. It will not be easy, but this can be done in PAD as well, and the vascular community must embrace it. Moreover it is imperative that vascular surgeons help to lead these multidisciplinary efforts, and develop evidence-based global guidelines to guide best practice in CLI.16 The recent funding of the BEST-CLI trial in the United States and the BASIL-2 trial in the United Kingdom demonstrate the importance to public health and offer great opportunities.
Until better evidence is available, a rational approach to limb salvage requires flexibility, understanding of the factors predicting success/failure for each modality, and the continued use of open bypass surgery as the initial treatment option for a significant number of patients.
And for the sake of our most vulnerable patients, we better keep training vascular surgeons to do all of it well.
Dr. Conte is professor and chief, division of vascular & endovascular surgery and the Edwin J. Wylie, M.D. Chair in Vascular Surgery at the University of California, San Francisco.
References
2. J. Vasc. Surg. 2014;59:220-34
7. J. Vasc. Surg. 2010;51:5S-17S
8. J. Vasc. Surg. 2010;51:18S-31S
9. J. Vasc. Surg. 2011;54:730-6
10. J. Amer. Heart Assoc. 2013;2:e000345
11. J. Vasc. Surg. 2006;43:742-51
12. J. Vasc. Surg. 2007;46:1180-90
13. J. Vasc. Surg. 2009;50:769-75
14. J. Vasc. Surg. 2010;52:1218-25
15. J. Vasc. Surg. 2013;57:8S-13S16. J. Vasc. Surg. 2014;59:510
The BASIL study originally published in the Lancet in 2005 (366:1925-34) and subsequently reiterated in multiple publications proposes that an endovascular approach should be utilized as the first invasive treatment modality in patients with infrainguinal peripheral arterial disease whose life expectancy is less than 2 years. By contrast, those patients expected to live beyond 2 years usually should be offered bypass surgery first, especially where a vein is available as a conduit. However, as can be seen from this month’s Point/Counterpoint by Dr. George Meier III and Dr. Michael S. Conte, the debate still rages as to the benefit of open vs. endovascular procedures for these patients. We encourage readers to voice their opinions in our “Letters to the Editor” section, as well as by participating in our web-based Quick Poll to the right of this story. - Dr. Russell Samson, Medical Editor, Vascular Specialist
POINT/COUNTERPOINT
Yes, endo is generally the way to go.
By Dr. George Meier III
Endovascular treatment of lower-extremity arterial disease has rapidly expanded, now approaching the standard for treatment of patients with lower-extremity disease. While open bypass remains a gold standard for the clinical treatment of limb-threatening ischemia, there are many limitations to the use of open surgery.
First and foremost, open surgical intervention represents pain and suffering for the patient as well as a delayed recovery, compared with endovascular treatment. All other factors being equal, most patients would prefer a less-invasive approach to minimize these factors and to maximize the speed of recovery. Open surgical interventions typically require 6 weeks or longer to get back to a functional status even remotely close to the patient’s initial level of function. With more severe tissue loss or with greater pain preoperatively, the difficulty of getting the patient back to full functional status remains problematic. In John Porter’s classic paper published in the Journal of Vascular Surgery in 1998,1 wound complications occurred in 24% of the patients with a 5-year survival rate of only 49% in this relatively young population, average age 66 years. Repeat operations to maintain graft patency, treat wound complications, or treat recurrent or contralateral ischemia were required in 54% of the patients and 23% ultimately required major limb amputation.
Of the 112 patients in this study, only 14.3% achieved the ideal surgical result of an uncomplicated operation: long-term symptom relief, maintenance of functional status, and no recurrence or repeat operations. These are sobering statistics for anyone facing open revascularization for critical limb ischemia.
The BASIL trial is often put forward as an example of the best data available currently to define patient treatments in patients with critical limb ischemia.2 Despite this, BASIL was a flawed trial from the beginning because of the difficulties of truly randomizing patients with vascular disease to open surgical treatment vs. percutaneous treatment. First, all patients had to be appropriate candidates for both open and endovascular treatment. In the real world, we readily recognize that the luxury of this choice is not available to many of our patients. A lack of conduit or increased surgical risk results in endovascular treatment being the only management option for many. Additionally, patient preference increasingly plays a role in treatment selection, obviously increasing the likelihood of less invasive percutaneous treatment. Yes, the mortality of open bypass in BASIL is reported to be in the 1%-3% range, but this population has been carefully selected based on screening and treatment of underlying cardiac disease. The true incidence of cardiovascular disease is impossible to determine since significant cardiac disease negated randomization.
Unfortunately, even with all of the advances in endovascular treatments the results of percutaneous treatment have never reached the results of open bypass. Nonetheless, while the success may not be as great the risks are not as high either. The main challenge to endovascular treatment is the durability of the intervention. While we can usually treat pre-existing disease in the lower-extremity arterial tree, maintaining patency and durability is the challenge. As my esteemed colleague has noted, failure of endovascular treatment in the BASIL trial resulted in significantly worse outcomes for open bypass in those patients. While much was made about this fact when the BASIL trial was published, endovascular treatment after open failure has even a worse outcome than did open treatment after endovascular failure. The truth of the matter is that, for obvious reasons, failure begets failure.
Generally, there are two imaging approaches to defining the extent of vascular disease: first, contrast angiography via percutaneous access; and second, CT angiography using intravenous contrast. If contrast angiography is undertaken to diagnose the extent of disease, then it is a relatively limited extrapolation to treat the patient’s disease percutaneously at the time of the diagnostic angiogram. For this reason, I discuss with all patients coming for diagnostic angiography the issue of endovascular treatment. It is rare that we make patients worse with an attempt at endovascular treatment by an experienced interventionalist. Similarly, it is rare that we alter a bypass level based on an attempt at endovascular treatment. If, in my opinion, the risk of an attempted endovascular treatment is acceptable, then this is done at the time of the diagnostic angiogram. Patients appreciate this discussion prior to proceeding with diagnostic angiography.
What about inadequate autogenous conduit? Even my counterpoint opponent has published a documented 20% risk of absent or inadequate ipsilateral greater saphenous vein.3 While he and his colleagues have documented excellent results using contralateral greater saphenous vein, there is still an inevitable morbidity and, yes, even a mortality risk associated with contralateral leg vein harvest. While in a good cardiac risk patient this may be negligible, we are again facing an ever more complex and medically ill patient population to subject to vascular treatment. It is in this setting that many vascular surgeons move to prosthetic conduits for the treatment of the patient’s vascular disease. While this may provide a short-term fix for the conduit problem, in the long term the risk of sudden, uncompensated failure of limb perfusion by prosthetic graft failure may often result in a higher risk procedure at a time when the patient may be older and more severely limited. Endovascular treatment is clearly a reasonable alternative in patients where autogenous conduit is not readily available.
While this debate will inevitably continue as long as practitioners have bias toward either open or endovascular management of vascular disease, one thing is for certain: We will continue to extend the limits of treatment to ever more ill and complex patients. While we have been very successful at performing fewer and fewer morbid interventions for limb-threatening vascular disease, these patients continue to be increasingly challenging to manage.
As the overall population continues to age, the need for less invasive treatment of limb-threatening vascular disease will continue to grow. And, yes, I agree that vascular surgeons in the role of interventionalist or surgeon are the leadership for the management of CLI in the future.
Dr. Meier is professor and chief of vascular surgery at the University of Cincinnati.
References
1. J. Vasc. Surg. 1998;27:256-63; discussion 264-6
3. J. Vasc. Surg. 2002:35:1085-92
No: A selective approach remains the key.
By Dr. MICHAEL S. CONTE
Recently the term “pandemic” has been applied to the growing global impact of peripheral artery disease (PAD), currently estimated to afflict more than 200 million individuals.1 The term “critical limb ischemia” (CLI), connoting the most advanced stage of PAD with imminent limb threat, is inadequately defined2 but likely encompasses 1%-3% of PAD. Aging of the global population and the increasing prevalence of diabetes are fueling increases in CLI and its impact on public health. While traditionally treated largely by vascular surgeons plying the open bypass trade, the ongoing development and market dispersion of catheter-based technologies for CLI has led to major secular changes.
Recent estimates suggest that upward of 5 billion dollars are spent annually on CLI in the Medicare population.3, 4 Increasing volumes and costs associated with revascularizations for CLI are a major driver, yet recent data suggest that regional spending in the United States is widely disparate and not directly associated with amputation rates.5 Thus defining effectiveness and value in CLI care has become a major challenge to the vascular community.
In current everyday practice, clinicians are faced with making treatment choices for CLI patients based on limited data and lots of anecdote. While the “open vs. endo” debate goes on, in many ways it has become less broadly relevant as the sophisticated clinician recognizes the real challenge lies in defining which approach to apply first in the right patient, at the right time. The only randomized, controlled trial (RCT) done in the field, the BASIL trial,6 is more than a decade old. However its findings remain important. For patients with “severe limb ischemia” likely to survive for at least 2 years, open bypass surgery offered better outcomes over angioplasty as an initial strategy.7 Moreover, the finding in BASIL that patients undergoing bypass after prior failed angioplasty did poorly,8 suggesting “no free lunch” for endovascular failures, has since been confirmed in other large registry studies.9
Simply stated, failure matters in CLI. And although endovascular techniques have continued to improve, the growing epidemic of restenosis shows no signs of abating.10 As in the case of percutaneous coronary intervention (PCI), we will know when endo results are meaningfully improved in PAD when the procedure volume curves actually flatten, not continue to grow geometrically.
So, in selecting the optimal strategy for CLI today, let’s focus on what we seem to know and try to apply an evidence-based mentality. We know that open bypass surgery is an effective and versatile treatment, but one that carries real morbidity (10%-20%) and some mortality (1%-3%). Among many large studies, the PREVENT III multicenter trial provides benchmark data on perioperative and 1-year outcomes.11
We know that the quality of the vein is the critical technical determinant of success, and arterial anatomy is less influential as long as there is outflow to the foot.12 We know that poor quality veins, prosthetics, and other alternatives are much inferior in CLI. And we know that there is a subset of CLI patients who are at high risk for adverse surgical outcomes.13, 14 However one defines them, up to 10% of patients in the large surgical series are in a high-risk group and may not experience meaningful benefit. For endovascular treatments, the data are less clear but certain trends have been consistent. Multilevel disease, long-segment occlusions, heavily calcified lesions, and more advanced tissue loss are negative predictors of clinical success.
Thus at first glance the weaknesses of the two strategies are largely complementary.15 When I encounter an average-risk CLI patient, with an adequate saphenous vein and more than one unfavorable endo factor, I am inclined towards bypass first.
Conversely, endo-favorable anatomy in higher risk patients is a no-brainer. Lots of people fall in the middle, and a significant minority should be considered for primary amputation. Currently my practice is roughly 50% bypass surgery-first in CLI.
Endovascular innovations have made a huge impact on vascular practice, and the leadership of many vascular surgeons (e.g., my esteemed counterpoint author) has been central to advancing the field. Better wires and catheters, retrograde approaches, and drug-eluting technologies continue to be developed at a dizzying pace.
We are all continually learning. Unfortunately, we lack good objective evidence to support most of the expanding armamentarium for CLI. However it is abundantly clear that technical (angiographic) success and clinical success are far apart, which is no surprise. What is surprising is an unsettlingly common lack of honesty about such an obvious fact. Are we all guilty of looking through rose-colored glasses?
Is it really such big news that patency actually matters for most patients with CLI? Technologies will not improve quickly enough if there is no market imperative to make them better. If we continue to buy and use things that are frequently ineffective, or don’t measure it carefully, where is the motivation?
No matter the lens through which one looks at the CLI field, it is desperate for improvement. We need much better technologies that provide longer lasting solutions for patients. We need better diagnostics to predict disease progression and responses to treatment.
We need some new medical or biological therapies that truly alleviate suffering. And we largely lack data on comparative effectiveness, and value, to support thoughtful application of our current treatment arsenal.
Most importantly what we need now is less dogma, and a lot more science. Over more than two decades, multiple RCTs comparing medical, interventional and surgical therapies for coronary artery disease have formed the basis for practice guidelines.
By comparison, our field is nearly incoherent both to vascular specialists and referring physicians. It will not be easy, but this can be done in PAD as well, and the vascular community must embrace it. Moreover it is imperative that vascular surgeons help to lead these multidisciplinary efforts, and develop evidence-based global guidelines to guide best practice in CLI.16 The recent funding of the BEST-CLI trial in the United States and the BASIL-2 trial in the United Kingdom demonstrate the importance to public health and offer great opportunities.
Until better evidence is available, a rational approach to limb salvage requires flexibility, understanding of the factors predicting success/failure for each modality, and the continued use of open bypass surgery as the initial treatment option for a significant number of patients.
And for the sake of our most vulnerable patients, we better keep training vascular surgeons to do all of it well.
Dr. Conte is professor and chief, division of vascular & endovascular surgery and the Edwin J. Wylie, M.D. Chair in Vascular Surgery at the University of California, San Francisco.
References
2. J. Vasc. Surg. 2014;59:220-34
7. J. Vasc. Surg. 2010;51:5S-17S
8. J. Vasc. Surg. 2010;51:18S-31S
9. J. Vasc. Surg. 2011;54:730-6
10. J. Amer. Heart Assoc. 2013;2:e000345
11. J. Vasc. Surg. 2006;43:742-51
12. J. Vasc. Surg. 2007;46:1180-90
13. J. Vasc. Surg. 2009;50:769-75
14. J. Vasc. Surg. 2010;52:1218-25
15. J. Vasc. Surg. 2013;57:8S-13S16. J. Vasc. Surg. 2014;59:510
Point/Counterpoint: Is TEVAR required for all Type B aortic dissections?
Yes, TEVAR is clearly indicated.
Aortic dissection is a devastating condition afflicting an estimated two to eight per 100,000 people annually and comprises a large portion of the clinical entity known as the acute aortic syndromes. Patients presenting with an uncomplicated type B acute aortic dissection (TBAD) generally have low in-hospital mortality rates (2.4%-9%) when managed appropriately with anti-impulse therapy. However, survival continues to decrease with follow-up, with survival ranging between 80% and more than 95% at 1 year, progressing to approximately 75% at 3-4 years, and 48%-65% at 10 years. In late follow-up, the development of a new dissection with complications is estimated to occur in 20%-50% of patients. Complicated aortic dissections affect between 22% and 47%, and when present, mortality reaches more than 50% within the first week. TEVAR in these patients has been shown to be clearly indicated in a variety of studies with marked improvements in early mortality and late survival. Thus, one can see that aortic dissection is a disease that needs to be managed lifelong, and is associated with a high risk of mortality for the next 10 years after the initial presentation.1,2,3
The long-term effects of a patent false lumen have been well documented. Several studies following patients with chronic TBAD have documented progressive enlargement in aortic diameter with a patent false lumen. The mean increase in maximum aortic diameter ranges from 3.8 to 7.1 mm annually with any flow in the false lumen (FL) versus 1-2 mm per year with a thrombosed FL. Patients with a patent FL had 7.5 times increased risk of a dissection-related death or need for surgery as compared to patients with thrombosis of the FL. Dissection-related death or need for surgery occurred at a significantly earlier follow-up period in the patients with a patent FL.1,2,3
The aortic diameter may also influence the patency of the FL at presentation. In a review of 110 patients presenting with acute uncomplicated TBAD, 44% were identified to have a patent FL on initial imaging. Thirty-one percent of these patients had a maximum aortic diameter of 45 mm or more versus 14% of patients with a thrombosed FL (P = .053). Incidentally, patients with FL patency were on average 4 years younger than their thrombosed counterparts (62 vs. 66 years, P = .009).
Moreover, it appears that the long-term risks associated with a patent FL are further augmented by aortic dilatation at presentation. When combining both risk factors (FL patency and aortic diameter of 40 mm or more), only 22% of patients are dissection-related event–free at 5-year follow-up.Onitsuka et al.4 substantiated this finding on multivariate analysis. Interestingly, 10 of the 76 patients included in that study met both conditions, and seven of those patients (70%) experienced a dissection-related death or surgical conversion. Certainly patients meeting both criteria merit close follow-up for the development of aortic enlargement or symptoms of impending rupture.
The natural history of TBAD lends itself to at least some thrombus formation within the FL and is a common finding as the dissection becomes chronic. But in fact, partial thrombosis of the FL is associated with higher mortality in patients discharged from the hospital with stable TBAD at 1- and 3-year follow-up (15.4% and 31.6%, respectively). Matched patients with a patent FL had a 5.4% and 13.7% rate of mortality at 1 and 3 years, and patients with complete FL thrombosis were found to have mortality rates of 0% and 22.6% at the same follow-up.
Aortic remodeling after TEVAR
Placement of a thoracic endograft under these acute circumstances can often significantly alter the preoperative morphology of the true and false lumen. Schoder and colleagues5 followed changes in the TL and FL diameter in 20 patients after TEVAR for acute complicated dissection. Ninety percent of patients were found to have complete FL thrombosis of the thoracic aorta at 1 year, with a mean decrease in FL diameter of 11.6 mm. Two patients with a patent FL showed a mean increase in the maximal aortic diameter of 4.5 mm. In a similar study, Conrad et al.6 documented aortic remodeling of 21 patients in the year following TEVAR, 88% of whom had thrombosis of the FL. Most often the mobile septum is easily displaced by the radial force of the stent graft, with minimal limitation of expansion to the design diameter. Thus, endograft selection should be directed by the diameter of the normal unaffected aorta with minimal oversizing commonly limited to 5%-10%. Balloon profiling is not typically necessary.
The INSTEAD trial7 evaluated the management of uncomplicated type B aortic dissection and compared optimum medical therapy (OMT) to OMT with TEVAR. A total of 140 subjects were enrolled at seven European sites with 68 patients enrolled in OMT and 72 in OMT with TEVAR. In patients treated with TEVAR there was 90.6% complete FL thrombosis with a maximum true lumen diameter of 32.6 mm as compared to 22% and 18.7 mm in those treated with medical therapy alone. Furthermore, there was a 12.4% absolute risk reduction in aortic specific mortality and a 19.1% absolute risk reduction in disease progression in patients treated with TEVAR.
It is clear that patients that present with complicated type B aortic dissections mandate intervention with TEVAR and potentially other interventions to alleviate the complications at presentation. INSTEAD demonstrates that elective TEVAR results in favorable aortic remodeling and long-term survival, reinterventions were low, and it prevents late expansion and malperfusion. TEVAR was also associated with improved 5-year aortic-specific survival. TEVAR appears to be beneficial in those patients who present initially with a false lumen diameter of greater than 22 mm and an aortic diameter of greater than 40 mm with a patent false lumen.
References
1. Circ. Cardiovasc. Interv. 2013;4:407-16.
2. J. Vasc. Surg. 2012;55:641-51.
3. J. Vasc. Surg. 2011;54:985-92
4. Ann. Thorac. Surg. 2004;78:1268-73.
5. Ann. Thorac. Surg. 2007;83:1059-66.
6. J. Vasc. Surg. 2009;50:510-17.
7. Circulation 2009;120:2519-28.
Dr. Arko is with the Aortic Institute, Sanger Heart & Vascular Institute, Charlotte, N.C. He reported no relevant conflicts.
No, evidence supports careful choice of patients.
While the role of TEVAR has been proven to treat complications of acute type B dissections,1 its value as a prophylactic treatment in uncomplicated cases remains controversial. Optimal medical treatment (OMT) with strict blood pressure (SBP less than 120 mm Hg) and heart rate control is associated with a low morbidity and mortality, despite the risk of progressive aortic dilation. On the other hand TEVAR can result in early death and significant neurologic complications; other devastating complications of TEVAR include retrograde aortic dissection and access vessel rupture with a high associated mortality.
A meta-analysis of the published literature reported a high technical success of TEVAR for uncomplicated type B dissection and a relatively high conversion rate (20%) for patient treated with OMT, however the results did not identify an advantage for TEVAR with respect to 30-day and 2-year mortality.2
An expert panel review of the world literature also did not find significant data to support use of TEVAR for uncomplicated type B dissection.3 In the only randomized prospective trial to examine the role of TEVAR for uncomplicated type B dissection, the INSTEAD trial randomized 140 patients to OMT vs. OMT and TEVAR.4 The study results also did not support the use of TEVAR for the treatment of uncomplicated type B dissection, there was no survival advantage at 2 years, while TEVAR was associated with a 11.1% overall mortality and 4.3% neurologic complication rate, compared with 4.4% and 1.4% in the OMT group. The initial study did however report improved aortic remodeling at 2 years with TEVAR. The results of INSTEAD have been challenged because critical analysis of the INSTEAD trial has determined that the results were underpowered and that there was a 21% crossover in the OMT group and four patients received TEVAR that should have been excluded.5
Subsequent long-term analysis of the INSTEAD XL data do demonstrate a significant survival benefit and freedom from aortic adverse events in the TEVAR group after the initial 2-year analysis.6 At the 5-year follow up only 27 patients remained without a TEVAR. Fortunately there were no adverse events in the patients that crossed over to TEVAR from the OMT group demonstrating the safety of delayed TEVAR in this group. The high rate of aortic associated adverse events may favor early TEVAR. The INSTEAD XL study did identify a large primary tear (more than 10 mm) and an initial aortic diameter of 40 mm as risk factors to crossover suggesting a more aggressive approach in this subset of patients.
So while the INSTEAD XL trial now supports the use of TEVAR for uncomplicated type B dissections this was a relatively small trial that was underpowered in its initial analysis. Expert review of the world literature still supports medical management in the initial phase of treatment. Obviously in cases of failure of medical management TEVAR provides an effective treatment to restore the true lumen and visceral perfusion with possible sustained remodeling of the false lumen.
Given the not insignificant morbidity associated with TEVAR placement, routine treatment of all acute, uncomplicated type B dissections cannot be supported with the current evidence. However, a strategy of selective treatment based on size of the entry tear, extent of dissection, false lumen diameter and extent of thrombosis, effectiveness of antihypertension medications, ability to comply with medical therapy, and surveillance may be implemented. Furthermore treatment at centers of excellence with extensive TEVAR experience based on established protocols favor improved patient outcomes.
References
1. N. Engl. J. Med. 199;340:1546-52
2. Vasc. Endovascular. Surg. 2013 Oct 12;47(7):497-501. Epub 2013 Jul 12.
3. J. Am. Coll. Cardiol. 2013;61(16):1661-78.
4. Circulation 2009;120:2519-28.
5. Circulation 2009;120:2513-14.
6. Circ. Cardiovasc. Interv. 2013;6:407-16.
Dr. Shames is professor of surgery and radiology and program director of vascular surgery at the University of South Florida, Tampa. He reported no relevant conflicts.
Yes, TEVAR is clearly indicated.
Aortic dissection is a devastating condition afflicting an estimated two to eight per 100,000 people annually and comprises a large portion of the clinical entity known as the acute aortic syndromes. Patients presenting with an uncomplicated type B acute aortic dissection (TBAD) generally have low in-hospital mortality rates (2.4%-9%) when managed appropriately with anti-impulse therapy. However, survival continues to decrease with follow-up, with survival ranging between 80% and more than 95% at 1 year, progressing to approximately 75% at 3-4 years, and 48%-65% at 10 years. In late follow-up, the development of a new dissection with complications is estimated to occur in 20%-50% of patients. Complicated aortic dissections affect between 22% and 47%, and when present, mortality reaches more than 50% within the first week. TEVAR in these patients has been shown to be clearly indicated in a variety of studies with marked improvements in early mortality and late survival. Thus, one can see that aortic dissection is a disease that needs to be managed lifelong, and is associated with a high risk of mortality for the next 10 years after the initial presentation.1,2,3
The long-term effects of a patent false lumen have been well documented. Several studies following patients with chronic TBAD have documented progressive enlargement in aortic diameter with a patent false lumen. The mean increase in maximum aortic diameter ranges from 3.8 to 7.1 mm annually with any flow in the false lumen (FL) versus 1-2 mm per year with a thrombosed FL. Patients with a patent FL had 7.5 times increased risk of a dissection-related death or need for surgery as compared to patients with thrombosis of the FL. Dissection-related death or need for surgery occurred at a significantly earlier follow-up period in the patients with a patent FL.1,2,3
The aortic diameter may also influence the patency of the FL at presentation. In a review of 110 patients presenting with acute uncomplicated TBAD, 44% were identified to have a patent FL on initial imaging. Thirty-one percent of these patients had a maximum aortic diameter of 45 mm or more versus 14% of patients with a thrombosed FL (P = .053). Incidentally, patients with FL patency were on average 4 years younger than their thrombosed counterparts (62 vs. 66 years, P = .009).
Moreover, it appears that the long-term risks associated with a patent FL are further augmented by aortic dilatation at presentation. When combining both risk factors (FL patency and aortic diameter of 40 mm or more), only 22% of patients are dissection-related event–free at 5-year follow-up.Onitsuka et al.4 substantiated this finding on multivariate analysis. Interestingly, 10 of the 76 patients included in that study met both conditions, and seven of those patients (70%) experienced a dissection-related death or surgical conversion. Certainly patients meeting both criteria merit close follow-up for the development of aortic enlargement or symptoms of impending rupture.
The natural history of TBAD lends itself to at least some thrombus formation within the FL and is a common finding as the dissection becomes chronic. But in fact, partial thrombosis of the FL is associated with higher mortality in patients discharged from the hospital with stable TBAD at 1- and 3-year follow-up (15.4% and 31.6%, respectively). Matched patients with a patent FL had a 5.4% and 13.7% rate of mortality at 1 and 3 years, and patients with complete FL thrombosis were found to have mortality rates of 0% and 22.6% at the same follow-up.
Aortic remodeling after TEVAR
Placement of a thoracic endograft under these acute circumstances can often significantly alter the preoperative morphology of the true and false lumen. Schoder and colleagues5 followed changes in the TL and FL diameter in 20 patients after TEVAR for acute complicated dissection. Ninety percent of patients were found to have complete FL thrombosis of the thoracic aorta at 1 year, with a mean decrease in FL diameter of 11.6 mm. Two patients with a patent FL showed a mean increase in the maximal aortic diameter of 4.5 mm. In a similar study, Conrad et al.6 documented aortic remodeling of 21 patients in the year following TEVAR, 88% of whom had thrombosis of the FL. Most often the mobile septum is easily displaced by the radial force of the stent graft, with minimal limitation of expansion to the design diameter. Thus, endograft selection should be directed by the diameter of the normal unaffected aorta with minimal oversizing commonly limited to 5%-10%. Balloon profiling is not typically necessary.
The INSTEAD trial7 evaluated the management of uncomplicated type B aortic dissection and compared optimum medical therapy (OMT) to OMT with TEVAR. A total of 140 subjects were enrolled at seven European sites with 68 patients enrolled in OMT and 72 in OMT with TEVAR. In patients treated with TEVAR there was 90.6% complete FL thrombosis with a maximum true lumen diameter of 32.6 mm as compared to 22% and 18.7 mm in those treated with medical therapy alone. Furthermore, there was a 12.4% absolute risk reduction in aortic specific mortality and a 19.1% absolute risk reduction in disease progression in patients treated with TEVAR.
It is clear that patients that present with complicated type B aortic dissections mandate intervention with TEVAR and potentially other interventions to alleviate the complications at presentation. INSTEAD demonstrates that elective TEVAR results in favorable aortic remodeling and long-term survival, reinterventions were low, and it prevents late expansion and malperfusion. TEVAR was also associated with improved 5-year aortic-specific survival. TEVAR appears to be beneficial in those patients who present initially with a false lumen diameter of greater than 22 mm and an aortic diameter of greater than 40 mm with a patent false lumen.
References
1. Circ. Cardiovasc. Interv. 2013;4:407-16.
2. J. Vasc. Surg. 2012;55:641-51.
3. J. Vasc. Surg. 2011;54:985-92
4. Ann. Thorac. Surg. 2004;78:1268-73.
5. Ann. Thorac. Surg. 2007;83:1059-66.
6. J. Vasc. Surg. 2009;50:510-17.
7. Circulation 2009;120:2519-28.
Dr. Arko is with the Aortic Institute, Sanger Heart & Vascular Institute, Charlotte, N.C. He reported no relevant conflicts.
No, evidence supports careful choice of patients.
While the role of TEVAR has been proven to treat complications of acute type B dissections,1 its value as a prophylactic treatment in uncomplicated cases remains controversial. Optimal medical treatment (OMT) with strict blood pressure (SBP less than 120 mm Hg) and heart rate control is associated with a low morbidity and mortality, despite the risk of progressive aortic dilation. On the other hand TEVAR can result in early death and significant neurologic complications; other devastating complications of TEVAR include retrograde aortic dissection and access vessel rupture with a high associated mortality.
A meta-analysis of the published literature reported a high technical success of TEVAR for uncomplicated type B dissection and a relatively high conversion rate (20%) for patient treated with OMT, however the results did not identify an advantage for TEVAR with respect to 30-day and 2-year mortality.2
An expert panel review of the world literature also did not find significant data to support use of TEVAR for uncomplicated type B dissection.3 In the only randomized prospective trial to examine the role of TEVAR for uncomplicated type B dissection, the INSTEAD trial randomized 140 patients to OMT vs. OMT and TEVAR.4 The study results also did not support the use of TEVAR for the treatment of uncomplicated type B dissection, there was no survival advantage at 2 years, while TEVAR was associated with a 11.1% overall mortality and 4.3% neurologic complication rate, compared with 4.4% and 1.4% in the OMT group. The initial study did however report improved aortic remodeling at 2 years with TEVAR. The results of INSTEAD have been challenged because critical analysis of the INSTEAD trial has determined that the results were underpowered and that there was a 21% crossover in the OMT group and four patients received TEVAR that should have been excluded.5
Subsequent long-term analysis of the INSTEAD XL data do demonstrate a significant survival benefit and freedom from aortic adverse events in the TEVAR group after the initial 2-year analysis.6 At the 5-year follow up only 27 patients remained without a TEVAR. Fortunately there were no adverse events in the patients that crossed over to TEVAR from the OMT group demonstrating the safety of delayed TEVAR in this group. The high rate of aortic associated adverse events may favor early TEVAR. The INSTEAD XL study did identify a large primary tear (more than 10 mm) and an initial aortic diameter of 40 mm as risk factors to crossover suggesting a more aggressive approach in this subset of patients.
So while the INSTEAD XL trial now supports the use of TEVAR for uncomplicated type B dissections this was a relatively small trial that was underpowered in its initial analysis. Expert review of the world literature still supports medical management in the initial phase of treatment. Obviously in cases of failure of medical management TEVAR provides an effective treatment to restore the true lumen and visceral perfusion with possible sustained remodeling of the false lumen.
Given the not insignificant morbidity associated with TEVAR placement, routine treatment of all acute, uncomplicated type B dissections cannot be supported with the current evidence. However, a strategy of selective treatment based on size of the entry tear, extent of dissection, false lumen diameter and extent of thrombosis, effectiveness of antihypertension medications, ability to comply with medical therapy, and surveillance may be implemented. Furthermore treatment at centers of excellence with extensive TEVAR experience based on established protocols favor improved patient outcomes.
References
1. N. Engl. J. Med. 199;340:1546-52
2. Vasc. Endovascular. Surg. 2013 Oct 12;47(7):497-501. Epub 2013 Jul 12.
3. J. Am. Coll. Cardiol. 2013;61(16):1661-78.
4. Circulation 2009;120:2519-28.
5. Circulation 2009;120:2513-14.
6. Circ. Cardiovasc. Interv. 2013;6:407-16.
Dr. Shames is professor of surgery and radiology and program director of vascular surgery at the University of South Florida, Tampa. He reported no relevant conflicts.
Yes, TEVAR is clearly indicated.
Aortic dissection is a devastating condition afflicting an estimated two to eight per 100,000 people annually and comprises a large portion of the clinical entity known as the acute aortic syndromes. Patients presenting with an uncomplicated type B acute aortic dissection (TBAD) generally have low in-hospital mortality rates (2.4%-9%) when managed appropriately with anti-impulse therapy. However, survival continues to decrease with follow-up, with survival ranging between 80% and more than 95% at 1 year, progressing to approximately 75% at 3-4 years, and 48%-65% at 10 years. In late follow-up, the development of a new dissection with complications is estimated to occur in 20%-50% of patients. Complicated aortic dissections affect between 22% and 47%, and when present, mortality reaches more than 50% within the first week. TEVAR in these patients has been shown to be clearly indicated in a variety of studies with marked improvements in early mortality and late survival. Thus, one can see that aortic dissection is a disease that needs to be managed lifelong, and is associated with a high risk of mortality for the next 10 years after the initial presentation.1,2,3
The long-term effects of a patent false lumen have been well documented. Several studies following patients with chronic TBAD have documented progressive enlargement in aortic diameter with a patent false lumen. The mean increase in maximum aortic diameter ranges from 3.8 to 7.1 mm annually with any flow in the false lumen (FL) versus 1-2 mm per year with a thrombosed FL. Patients with a patent FL had 7.5 times increased risk of a dissection-related death or need for surgery as compared to patients with thrombosis of the FL. Dissection-related death or need for surgery occurred at a significantly earlier follow-up period in the patients with a patent FL.1,2,3
The aortic diameter may also influence the patency of the FL at presentation. In a review of 110 patients presenting with acute uncomplicated TBAD, 44% were identified to have a patent FL on initial imaging. Thirty-one percent of these patients had a maximum aortic diameter of 45 mm or more versus 14% of patients with a thrombosed FL (P = .053). Incidentally, patients with FL patency were on average 4 years younger than their thrombosed counterparts (62 vs. 66 years, P = .009).
Moreover, it appears that the long-term risks associated with a patent FL are further augmented by aortic dilatation at presentation. When combining both risk factors (FL patency and aortic diameter of 40 mm or more), only 22% of patients are dissection-related event–free at 5-year follow-up.Onitsuka et al.4 substantiated this finding on multivariate analysis. Interestingly, 10 of the 76 patients included in that study met both conditions, and seven of those patients (70%) experienced a dissection-related death or surgical conversion. Certainly patients meeting both criteria merit close follow-up for the development of aortic enlargement or symptoms of impending rupture.
The natural history of TBAD lends itself to at least some thrombus formation within the FL and is a common finding as the dissection becomes chronic. But in fact, partial thrombosis of the FL is associated with higher mortality in patients discharged from the hospital with stable TBAD at 1- and 3-year follow-up (15.4% and 31.6%, respectively). Matched patients with a patent FL had a 5.4% and 13.7% rate of mortality at 1 and 3 years, and patients with complete FL thrombosis were found to have mortality rates of 0% and 22.6% at the same follow-up.
Aortic remodeling after TEVAR
Placement of a thoracic endograft under these acute circumstances can often significantly alter the preoperative morphology of the true and false lumen. Schoder and colleagues5 followed changes in the TL and FL diameter in 20 patients after TEVAR for acute complicated dissection. Ninety percent of patients were found to have complete FL thrombosis of the thoracic aorta at 1 year, with a mean decrease in FL diameter of 11.6 mm. Two patients with a patent FL showed a mean increase in the maximal aortic diameter of 4.5 mm. In a similar study, Conrad et al.6 documented aortic remodeling of 21 patients in the year following TEVAR, 88% of whom had thrombosis of the FL. Most often the mobile septum is easily displaced by the radial force of the stent graft, with minimal limitation of expansion to the design diameter. Thus, endograft selection should be directed by the diameter of the normal unaffected aorta with minimal oversizing commonly limited to 5%-10%. Balloon profiling is not typically necessary.
The INSTEAD trial7 evaluated the management of uncomplicated type B aortic dissection and compared optimum medical therapy (OMT) to OMT with TEVAR. A total of 140 subjects were enrolled at seven European sites with 68 patients enrolled in OMT and 72 in OMT with TEVAR. In patients treated with TEVAR there was 90.6% complete FL thrombosis with a maximum true lumen diameter of 32.6 mm as compared to 22% and 18.7 mm in those treated with medical therapy alone. Furthermore, there was a 12.4% absolute risk reduction in aortic specific mortality and a 19.1% absolute risk reduction in disease progression in patients treated with TEVAR.
It is clear that patients that present with complicated type B aortic dissections mandate intervention with TEVAR and potentially other interventions to alleviate the complications at presentation. INSTEAD demonstrates that elective TEVAR results in favorable aortic remodeling and long-term survival, reinterventions were low, and it prevents late expansion and malperfusion. TEVAR was also associated with improved 5-year aortic-specific survival. TEVAR appears to be beneficial in those patients who present initially with a false lumen diameter of greater than 22 mm and an aortic diameter of greater than 40 mm with a patent false lumen.
References
1. Circ. Cardiovasc. Interv. 2013;4:407-16.
2. J. Vasc. Surg. 2012;55:641-51.
3. J. Vasc. Surg. 2011;54:985-92
4. Ann. Thorac. Surg. 2004;78:1268-73.
5. Ann. Thorac. Surg. 2007;83:1059-66.
6. J. Vasc. Surg. 2009;50:510-17.
7. Circulation 2009;120:2519-28.
Dr. Arko is with the Aortic Institute, Sanger Heart & Vascular Institute, Charlotte, N.C. He reported no relevant conflicts.
No, evidence supports careful choice of patients.
While the role of TEVAR has been proven to treat complications of acute type B dissections,1 its value as a prophylactic treatment in uncomplicated cases remains controversial. Optimal medical treatment (OMT) with strict blood pressure (SBP less than 120 mm Hg) and heart rate control is associated with a low morbidity and mortality, despite the risk of progressive aortic dilation. On the other hand TEVAR can result in early death and significant neurologic complications; other devastating complications of TEVAR include retrograde aortic dissection and access vessel rupture with a high associated mortality.
A meta-analysis of the published literature reported a high technical success of TEVAR for uncomplicated type B dissection and a relatively high conversion rate (20%) for patient treated with OMT, however the results did not identify an advantage for TEVAR with respect to 30-day and 2-year mortality.2
An expert panel review of the world literature also did not find significant data to support use of TEVAR for uncomplicated type B dissection.3 In the only randomized prospective trial to examine the role of TEVAR for uncomplicated type B dissection, the INSTEAD trial randomized 140 patients to OMT vs. OMT and TEVAR.4 The study results also did not support the use of TEVAR for the treatment of uncomplicated type B dissection, there was no survival advantage at 2 years, while TEVAR was associated with a 11.1% overall mortality and 4.3% neurologic complication rate, compared with 4.4% and 1.4% in the OMT group. The initial study did however report improved aortic remodeling at 2 years with TEVAR. The results of INSTEAD have been challenged because critical analysis of the INSTEAD trial has determined that the results were underpowered and that there was a 21% crossover in the OMT group and four patients received TEVAR that should have been excluded.5
Subsequent long-term analysis of the INSTEAD XL data do demonstrate a significant survival benefit and freedom from aortic adverse events in the TEVAR group after the initial 2-year analysis.6 At the 5-year follow up only 27 patients remained without a TEVAR. Fortunately there were no adverse events in the patients that crossed over to TEVAR from the OMT group demonstrating the safety of delayed TEVAR in this group. The high rate of aortic associated adverse events may favor early TEVAR. The INSTEAD XL study did identify a large primary tear (more than 10 mm) and an initial aortic diameter of 40 mm as risk factors to crossover suggesting a more aggressive approach in this subset of patients.
So while the INSTEAD XL trial now supports the use of TEVAR for uncomplicated type B dissections this was a relatively small trial that was underpowered in its initial analysis. Expert review of the world literature still supports medical management in the initial phase of treatment. Obviously in cases of failure of medical management TEVAR provides an effective treatment to restore the true lumen and visceral perfusion with possible sustained remodeling of the false lumen.
Given the not insignificant morbidity associated with TEVAR placement, routine treatment of all acute, uncomplicated type B dissections cannot be supported with the current evidence. However, a strategy of selective treatment based on size of the entry tear, extent of dissection, false lumen diameter and extent of thrombosis, effectiveness of antihypertension medications, ability to comply with medical therapy, and surveillance may be implemented. Furthermore treatment at centers of excellence with extensive TEVAR experience based on established protocols favor improved patient outcomes.
References
1. N. Engl. J. Med. 199;340:1546-52
2. Vasc. Endovascular. Surg. 2013 Oct 12;47(7):497-501. Epub 2013 Jul 12.
3. J. Am. Coll. Cardiol. 2013;61(16):1661-78.
4. Circulation 2009;120:2519-28.
5. Circulation 2009;120:2513-14.
6. Circ. Cardiovasc. Interv. 2013;6:407-16.
Dr. Shames is professor of surgery and radiology and program director of vascular surgery at the University of South Florida, Tampa. He reported no relevant conflicts.
Point/Counterpoint: Is screening for asymptomatic carotid artery stenosis justified?
Introduction
The U.S. Preventive Services Task Force has just published its latest guidance on carotid screening for asymptomatic disease, basically stating that it should not be done (see story page 1). In this Point-Counterpoint Dr. Zierler and Dr. Berland provide their views on this controversial issue. From my perspective the debate must revolve around the following questions: The gist of the USPSTF statement seems to be that screening is being performed only to detect patients with critical carotid stenosis so that an intervention (CEA or CAS) can be performed. However, shouldn’t screening also be used to identify atherosclerotic burden in order to prevent cardiovascular morbidity? Whatever the reasons for screening, should national health systems pay for screening? If not, what about individual physicians charging for screenings on selected/nonselected patients? What about free screenings? And as Dr. Zierler and Dr. Berland suggest, is screening getting a bad rap just because screening and subsequent CEA or CAS are being poorly performed? Finally, I wouldn\'t be surprised if some of the task force members have had their own carotids screened despite their negative recommendation. We would be interested in your viewpoint, so please take our online, interactive poll on our home page (bottom right) to weigh in on this important issue.
Dr. Russell Samson is the Medical Editor of Vascular Specialist.
YES: Screen, but screen well.
By Todd Berland, M.D.
Every patient with symptomatic carotid artery stenosis was asymptomatic the day before. The impact of stroke can be devastating, with a 20% mortality from the acute event and 40%-50% survival over the next 5 years. Of those surviving the initial event, a significant percentage of patients are unable to return to work, and up to 25% over the age of 65 require long-term institutional care.1 There is no doubt that the emotional, financial, and societal burden of caring for stroke patients is significant. The Asymptomatic Carotid Atherosclerosis Study and the Asymptomatic Carotid Surgery Trial demonstrated a significant reduction in stroke in asymptomatic, high-grade carotid artery stenosis patients treated with carotid endarterectomy compared to medical management alone.2,3 So wouldn’t it seem as if carotid artery screening would be beneficial?
The U.S. Preventive Services Task Force recommended against routine carotid screening because of its "high risk" and low reward. I believe that when a certified lab screens the appropriate population such as individuals over 55 with cardiovascular risk factors that include hypertension, diabetes, smoking, and hypercholesterolemia, and combines this with an intervention that has a low stroke and morbidity rate, then the balance is tipped and carotid screening becomes both low risk and high reward.
One of the problems with carotid ultrasound is that too many entrepreneurs have made a business of it. Suboptimal equipment is being used by uncertified technicians in medical offices and church parking lots all across this country. It’s no surprise that the false positives are going to be high in these situations. Also, when one combines all of the above with the screening of those who aren’t at risk, where the general prevalence of disease is low, it can be a recipe for disaster. This is going to lead to additional studies such as CT angiograms or possibly even cerebral angiograms, both of which have inherent risks.
Even though it’s possible to understand why the USPSTF may have concluded against routine screening, I believe that at-risk patients should be screened by a certified lab, and that physicians performing the interventions should be able to do so with low morbidity and mortality. Vascular surgeons have been marginalized over recent years as many others have become interested in finding and treating carotid disease. Most of us are either registered vascular technologists or registered physicians in vascular interpretation, and our labs are certified by the Intersocietal Accreditation Commission. We go through hours of continuing medical education in regard to vascular ultrasound, and our labs’ results are tested and certified for accuracy.
We need to convince insurance companies and the Centers for Medicare & Medicaid Services that these studies should be permitted only in certified labs and the results interpreted by certified physicians such as vascular surgeons.
Moreover, when indicated, the interventions should be carried out by vascular surgeons who are trained to perform both carotid endarter- ectomy and carotid artery stenting to be able to offer the patient the best individualized treatment.
Dr. Berland is director of outpatient vascular interventions at NYU Langone Medical Center.
References
1. Circulation 2012;125:188.
2. JAMA 1995:273:1421-8.
3. Lancet 2004;363:1491-502.
NO: General screening is not appropriate.
By R. Eugene Zierler, M.D.
To most vascular specialists, the concept of detecting asymptomatic carotid stenosis and intervening to prevent stroke makes intuitive sense, but is it consistent with the evidence? In 2007, the USPSTF concluded that the general asymptomatic adult population should not be screened for carotid stenosis, and this recommendation has been reiterated in a 2014 draft recommendation statement.1,2 Other groups, including our own Society for Vascular Surgery, have published similar recommendations.3,4
Arguments in favor of screening for asymptomatic carotid stenosis are often based on the results of randomized controlled trials such as the Asymptomatic Carotid Atherosclerosis Study, which was reported in 1995.5 However, while these trials are historically important, they are no longer clinically relevant. Surgical and catheter-based interventions for carotid atherosclerosis have evolved significantly in the last 2 decades, but the outcomes associated with modern intensive medical therapy have also improved dramatically.6,7 It is not clear that carotid endarterectomy or stenting is superior to current medical management for asymptomatic carotid stenosis, and new trials such as the recently announced CREST-2 are designed to answer these important questions.
The relatively poor reliability and accuracy of duplex ultrasound as a screening test for carotid stenosis is a major theme in the USPSTF draft recommendations, but in spite of this criticism, carotid duplex scanning has served as a clinically valuable method for classifying the severity of carotid stenosis for more than 30 years.8 As pointed out by others, the best way to ensure quality in the vascular laboratory is to recognize the importance of certified vascular sonographers, accredited vascular laboratories, and qualified medical staff. But despite high-quality ultrasound testing, relying on carotid stenosis as a marker of stroke risk has significant limitations. While there is an association between the degree of carotid stenosis and risk of stroke, many patients with severe carotid stenosis do not have strokes and some with moderate stenosis do have strokes. For example, it was reported that 61% of the symptomatic patients in the North American Symptomatic Carotid Endarterectomy Trial had less than 50% carotid stenosis.9 This suggests that stenosis severity alone does not identify those patients who are at the highest risk for stroke. Fortunately, the concept of the "vulnerable plaque" is promising as a means for more accurate risk stratification, and features such as intraplaque hemorrhage and thin or ruptured fibrous caps do correlate with a high risk for stroke.10 Experience has shown that these features can be characterized by ultrasound.11
So although screening of the general population for asymptomatic carotid stenosis is not justified, there still may be subgroups of patients with specific risk factors and plaque features that could benefit from early intervention, and future clinical trials will establish whether or not this hypothesis has merit. Until more data are available the issue of screening for asymptomatic carotid stenosis will continue to provoke debate on multiple levels. Carotid disease screening is not covered by insurance, so cost and ability to pay are key factors to consider. In these discussions, the health of the patient and the population must always be the first priority, and clinical decision-making should be evidence based.
Dr. Zierler is professor of surgery at the University of Washington and medical director of the D.E. Strandness Jr. Vascular Laboratory at the university’s medical center and Harborview Medical Center, Seattle. He is also an associate medical editor of Vascular Specialist.
References
1. Ann. Intern. Med. 2007;147:860-70.
2. uspreventiveservicestaskforce.org/.htm.
3. JACC 2011;57:e16-94.
4. J. Vasc. Surg. 2011;54:e1-31.
5. JAMA 1995:273:1421-8.
6. Circulation 2013;127:739-42.
7. Stroke 2009;40:e573-83.
8. Vasc. Endovascular Surg. 2012;46:466-74.
9. N. Engl. J. Med. 1998;339:1415-25.
10. Imaging Med. 2010;2:63-75.
11. J. Vasc. Surg. 2010;52:1486-96.
Introduction
The U.S. Preventive Services Task Force has just published its latest guidance on carotid screening for asymptomatic disease, basically stating that it should not be done (see story page 1). In this Point-Counterpoint Dr. Zierler and Dr. Berland provide their views on this controversial issue. From my perspective the debate must revolve around the following questions: The gist of the USPSTF statement seems to be that screening is being performed only to detect patients with critical carotid stenosis so that an intervention (CEA or CAS) can be performed. However, shouldn’t screening also be used to identify atherosclerotic burden in order to prevent cardiovascular morbidity? Whatever the reasons for screening, should national health systems pay for screening? If not, what about individual physicians charging for screenings on selected/nonselected patients? What about free screenings? And as Dr. Zierler and Dr. Berland suggest, is screening getting a bad rap just because screening and subsequent CEA or CAS are being poorly performed? Finally, I wouldn\'t be surprised if some of the task force members have had their own carotids screened despite their negative recommendation. We would be interested in your viewpoint, so please take our online, interactive poll on our home page (bottom right) to weigh in on this important issue.
Dr. Russell Samson is the Medical Editor of Vascular Specialist.
YES: Screen, but screen well.
By Todd Berland, M.D.
Every patient with symptomatic carotid artery stenosis was asymptomatic the day before. The impact of stroke can be devastating, with a 20% mortality from the acute event and 40%-50% survival over the next 5 years. Of those surviving the initial event, a significant percentage of patients are unable to return to work, and up to 25% over the age of 65 require long-term institutional care.1 There is no doubt that the emotional, financial, and societal burden of caring for stroke patients is significant. The Asymptomatic Carotid Atherosclerosis Study and the Asymptomatic Carotid Surgery Trial demonstrated a significant reduction in stroke in asymptomatic, high-grade carotid artery stenosis patients treated with carotid endarterectomy compared to medical management alone.2,3 So wouldn’t it seem as if carotid artery screening would be beneficial?
The U.S. Preventive Services Task Force recommended against routine carotid screening because of its "high risk" and low reward. I believe that when a certified lab screens the appropriate population such as individuals over 55 with cardiovascular risk factors that include hypertension, diabetes, smoking, and hypercholesterolemia, and combines this with an intervention that has a low stroke and morbidity rate, then the balance is tipped and carotid screening becomes both low risk and high reward.
One of the problems with carotid ultrasound is that too many entrepreneurs have made a business of it. Suboptimal equipment is being used by uncertified technicians in medical offices and church parking lots all across this country. It’s no surprise that the false positives are going to be high in these situations. Also, when one combines all of the above with the screening of those who aren’t at risk, where the general prevalence of disease is low, it can be a recipe for disaster. This is going to lead to additional studies such as CT angiograms or possibly even cerebral angiograms, both of which have inherent risks.
Even though it’s possible to understand why the USPSTF may have concluded against routine screening, I believe that at-risk patients should be screened by a certified lab, and that physicians performing the interventions should be able to do so with low morbidity and mortality. Vascular surgeons have been marginalized over recent years as many others have become interested in finding and treating carotid disease. Most of us are either registered vascular technologists or registered physicians in vascular interpretation, and our labs are certified by the Intersocietal Accreditation Commission. We go through hours of continuing medical education in regard to vascular ultrasound, and our labs’ results are tested and certified for accuracy.
We need to convince insurance companies and the Centers for Medicare & Medicaid Services that these studies should be permitted only in certified labs and the results interpreted by certified physicians such as vascular surgeons.
Moreover, when indicated, the interventions should be carried out by vascular surgeons who are trained to perform both carotid endarter- ectomy and carotid artery stenting to be able to offer the patient the best individualized treatment.
Dr. Berland is director of outpatient vascular interventions at NYU Langone Medical Center.
References
1. Circulation 2012;125:188.
2. JAMA 1995:273:1421-8.
3. Lancet 2004;363:1491-502.
NO: General screening is not appropriate.
By R. Eugene Zierler, M.D.
To most vascular specialists, the concept of detecting asymptomatic carotid stenosis and intervening to prevent stroke makes intuitive sense, but is it consistent with the evidence? In 2007, the USPSTF concluded that the general asymptomatic adult population should not be screened for carotid stenosis, and this recommendation has been reiterated in a 2014 draft recommendation statement.1,2 Other groups, including our own Society for Vascular Surgery, have published similar recommendations.3,4
Arguments in favor of screening for asymptomatic carotid stenosis are often based on the results of randomized controlled trials such as the Asymptomatic Carotid Atherosclerosis Study, which was reported in 1995.5 However, while these trials are historically important, they are no longer clinically relevant. Surgical and catheter-based interventions for carotid atherosclerosis have evolved significantly in the last 2 decades, but the outcomes associated with modern intensive medical therapy have also improved dramatically.6,7 It is not clear that carotid endarterectomy or stenting is superior to current medical management for asymptomatic carotid stenosis, and new trials such as the recently announced CREST-2 are designed to answer these important questions.
The relatively poor reliability and accuracy of duplex ultrasound as a screening test for carotid stenosis is a major theme in the USPSTF draft recommendations, but in spite of this criticism, carotid duplex scanning has served as a clinically valuable method for classifying the severity of carotid stenosis for more than 30 years.8 As pointed out by others, the best way to ensure quality in the vascular laboratory is to recognize the importance of certified vascular sonographers, accredited vascular laboratories, and qualified medical staff. But despite high-quality ultrasound testing, relying on carotid stenosis as a marker of stroke risk has significant limitations. While there is an association between the degree of carotid stenosis and risk of stroke, many patients with severe carotid stenosis do not have strokes and some with moderate stenosis do have strokes. For example, it was reported that 61% of the symptomatic patients in the North American Symptomatic Carotid Endarterectomy Trial had less than 50% carotid stenosis.9 This suggests that stenosis severity alone does not identify those patients who are at the highest risk for stroke. Fortunately, the concept of the "vulnerable plaque" is promising as a means for more accurate risk stratification, and features such as intraplaque hemorrhage and thin or ruptured fibrous caps do correlate with a high risk for stroke.10 Experience has shown that these features can be characterized by ultrasound.11
So although screening of the general population for asymptomatic carotid stenosis is not justified, there still may be subgroups of patients with specific risk factors and plaque features that could benefit from early intervention, and future clinical trials will establish whether or not this hypothesis has merit. Until more data are available the issue of screening for asymptomatic carotid stenosis will continue to provoke debate on multiple levels. Carotid disease screening is not covered by insurance, so cost and ability to pay are key factors to consider. In these discussions, the health of the patient and the population must always be the first priority, and clinical decision-making should be evidence based.
Dr. Zierler is professor of surgery at the University of Washington and medical director of the D.E. Strandness Jr. Vascular Laboratory at the university’s medical center and Harborview Medical Center, Seattle. He is also an associate medical editor of Vascular Specialist.
References
1. Ann. Intern. Med. 2007;147:860-70.
2. uspreventiveservicestaskforce.org/.htm.
3. JACC 2011;57:e16-94.
4. J. Vasc. Surg. 2011;54:e1-31.
5. JAMA 1995:273:1421-8.
6. Circulation 2013;127:739-42.
7. Stroke 2009;40:e573-83.
8. Vasc. Endovascular Surg. 2012;46:466-74.
9. N. Engl. J. Med. 1998;339:1415-25.
10. Imaging Med. 2010;2:63-75.
11. J. Vasc. Surg. 2010;52:1486-96.
Introduction
The U.S. Preventive Services Task Force has just published its latest guidance on carotid screening for asymptomatic disease, basically stating that it should not be done (see story page 1). In this Point-Counterpoint Dr. Zierler and Dr. Berland provide their views on this controversial issue. From my perspective the debate must revolve around the following questions: The gist of the USPSTF statement seems to be that screening is being performed only to detect patients with critical carotid stenosis so that an intervention (CEA or CAS) can be performed. However, shouldn’t screening also be used to identify atherosclerotic burden in order to prevent cardiovascular morbidity? Whatever the reasons for screening, should national health systems pay for screening? If not, what about individual physicians charging for screenings on selected/nonselected patients? What about free screenings? And as Dr. Zierler and Dr. Berland suggest, is screening getting a bad rap just because screening and subsequent CEA or CAS are being poorly performed? Finally, I wouldn\'t be surprised if some of the task force members have had their own carotids screened despite their negative recommendation. We would be interested in your viewpoint, so please take our online, interactive poll on our home page (bottom right) to weigh in on this important issue.
Dr. Russell Samson is the Medical Editor of Vascular Specialist.
YES: Screen, but screen well.
By Todd Berland, M.D.
Every patient with symptomatic carotid artery stenosis was asymptomatic the day before. The impact of stroke can be devastating, with a 20% mortality from the acute event and 40%-50% survival over the next 5 years. Of those surviving the initial event, a significant percentage of patients are unable to return to work, and up to 25% over the age of 65 require long-term institutional care.1 There is no doubt that the emotional, financial, and societal burden of caring for stroke patients is significant. The Asymptomatic Carotid Atherosclerosis Study and the Asymptomatic Carotid Surgery Trial demonstrated a significant reduction in stroke in asymptomatic, high-grade carotid artery stenosis patients treated with carotid endarterectomy compared to medical management alone.2,3 So wouldn’t it seem as if carotid artery screening would be beneficial?
The U.S. Preventive Services Task Force recommended against routine carotid screening because of its "high risk" and low reward. I believe that when a certified lab screens the appropriate population such as individuals over 55 with cardiovascular risk factors that include hypertension, diabetes, smoking, and hypercholesterolemia, and combines this with an intervention that has a low stroke and morbidity rate, then the balance is tipped and carotid screening becomes both low risk and high reward.
One of the problems with carotid ultrasound is that too many entrepreneurs have made a business of it. Suboptimal equipment is being used by uncertified technicians in medical offices and church parking lots all across this country. It’s no surprise that the false positives are going to be high in these situations. Also, when one combines all of the above with the screening of those who aren’t at risk, where the general prevalence of disease is low, it can be a recipe for disaster. This is going to lead to additional studies such as CT angiograms or possibly even cerebral angiograms, both of which have inherent risks.
Even though it’s possible to understand why the USPSTF may have concluded against routine screening, I believe that at-risk patients should be screened by a certified lab, and that physicians performing the interventions should be able to do so with low morbidity and mortality. Vascular surgeons have been marginalized over recent years as many others have become interested in finding and treating carotid disease. Most of us are either registered vascular technologists or registered physicians in vascular interpretation, and our labs are certified by the Intersocietal Accreditation Commission. We go through hours of continuing medical education in regard to vascular ultrasound, and our labs’ results are tested and certified for accuracy.
We need to convince insurance companies and the Centers for Medicare & Medicaid Services that these studies should be permitted only in certified labs and the results interpreted by certified physicians such as vascular surgeons.
Moreover, when indicated, the interventions should be carried out by vascular surgeons who are trained to perform both carotid endarter- ectomy and carotid artery stenting to be able to offer the patient the best individualized treatment.
Dr. Berland is director of outpatient vascular interventions at NYU Langone Medical Center.
References
1. Circulation 2012;125:188.
2. JAMA 1995:273:1421-8.
3. Lancet 2004;363:1491-502.
NO: General screening is not appropriate.
By R. Eugene Zierler, M.D.
To most vascular specialists, the concept of detecting asymptomatic carotid stenosis and intervening to prevent stroke makes intuitive sense, but is it consistent with the evidence? In 2007, the USPSTF concluded that the general asymptomatic adult population should not be screened for carotid stenosis, and this recommendation has been reiterated in a 2014 draft recommendation statement.1,2 Other groups, including our own Society for Vascular Surgery, have published similar recommendations.3,4
Arguments in favor of screening for asymptomatic carotid stenosis are often based on the results of randomized controlled trials such as the Asymptomatic Carotid Atherosclerosis Study, which was reported in 1995.5 However, while these trials are historically important, they are no longer clinically relevant. Surgical and catheter-based interventions for carotid atherosclerosis have evolved significantly in the last 2 decades, but the outcomes associated with modern intensive medical therapy have also improved dramatically.6,7 It is not clear that carotid endarterectomy or stenting is superior to current medical management for asymptomatic carotid stenosis, and new trials such as the recently announced CREST-2 are designed to answer these important questions.
The relatively poor reliability and accuracy of duplex ultrasound as a screening test for carotid stenosis is a major theme in the USPSTF draft recommendations, but in spite of this criticism, carotid duplex scanning has served as a clinically valuable method for classifying the severity of carotid stenosis for more than 30 years.8 As pointed out by others, the best way to ensure quality in the vascular laboratory is to recognize the importance of certified vascular sonographers, accredited vascular laboratories, and qualified medical staff. But despite high-quality ultrasound testing, relying on carotid stenosis as a marker of stroke risk has significant limitations. While there is an association between the degree of carotid stenosis and risk of stroke, many patients with severe carotid stenosis do not have strokes and some with moderate stenosis do have strokes. For example, it was reported that 61% of the symptomatic patients in the North American Symptomatic Carotid Endarterectomy Trial had less than 50% carotid stenosis.9 This suggests that stenosis severity alone does not identify those patients who are at the highest risk for stroke. Fortunately, the concept of the "vulnerable plaque" is promising as a means for more accurate risk stratification, and features such as intraplaque hemorrhage and thin or ruptured fibrous caps do correlate with a high risk for stroke.10 Experience has shown that these features can be characterized by ultrasound.11
So although screening of the general population for asymptomatic carotid stenosis is not justified, there still may be subgroups of patients with specific risk factors and plaque features that could benefit from early intervention, and future clinical trials will establish whether or not this hypothesis has merit. Until more data are available the issue of screening for asymptomatic carotid stenosis will continue to provoke debate on multiple levels. Carotid disease screening is not covered by insurance, so cost and ability to pay are key factors to consider. In these discussions, the health of the patient and the population must always be the first priority, and clinical decision-making should be evidence based.
Dr. Zierler is professor of surgery at the University of Washington and medical director of the D.E. Strandness Jr. Vascular Laboratory at the university’s medical center and Harborview Medical Center, Seattle. He is also an associate medical editor of Vascular Specialist.
References
1. Ann. Intern. Med. 2007;147:860-70.
2. uspreventiveservicestaskforce.org/.htm.
3. JACC 2011;57:e16-94.
4. J. Vasc. Surg. 2011;54:e1-31.
5. JAMA 1995:273:1421-8.
6. Circulation 2013;127:739-42.
7. Stroke 2009;40:e573-83.
8. Vasc. Endovascular Surg. 2012;46:466-74.
9. N. Engl. J. Med. 1998;339:1415-25.
10. Imaging Med. 2010;2:63-75.
11. J. Vasc. Surg. 2010;52:1486-96.
Another surgeon’s error – Must you tell the patient?
YES: Surgeons have a duty to tell patients when a medical error has been made by a physician colleague.
Surgeons have a moral and ethical obligation to inform a patient when a medical error has occurred, including cases when the error was made by another surgeon.
Principles that support complete and honest disclosure to the patient and/or the patient’s family in such cases include professional obligation on the part of both the surgeon who made the error and the surgeon who discovered the error, the integrity of both surgeons, the patient’s right to informed care throughout the continuum of care, and the patient’s right to informed consent.
With respect to the first, the American Medical Association’s code of ethics provides a framework for disclosure; it clearly states that situations occur in which a patient experiences significant complications that may have resulted from a physician’s mistake or judgment and that the physician is ethically required to inform the patient of all facts necessary to ensure understanding of the error that occurred.
The American College of Physicians’ ethics manual also states that physicians should disclose to patients information about procedural or judgment errors made during the course of care, as long as that information is pertinent and material to the patient’s well-being.
Errors do not necessarily imply negligence or unethical behavior, but failure to disclose may.
As for patients’ rights, I think that patients are entitled to honest information. They shouldn’t bear the burden of determining how they came to be in another surgeon’s care.
Patients with complications may have impactful financial burdens that result from the additional treatment that is needed, and without all pertinent information, they may have difficulty understanding the benefits, such as deferment of payments, to which they are entitled.
The patient must also be kept informed as to the long-term care plan, and honest and timely disclosure will facilitate moving beyond blame and toward patient advocacy.
The patient is entitled to informed consent, and this requires an understanding of the conditions under which they arrived in another surgeon’s care. If a second procedure is required, the patient must be made aware of potential complications – including how the effects of the initial error might impact outcomes.
Although surgeons have an ethical obligation to disclose errors made by another surgeon, this is a difficult task. Pressures from society and medical professionals can make disclosure difficult, but the benefits of disclosure are real; studies show that open, honest communication improves patient satisfaction, strengthens the physician-patient relationship, and can improve outcomes.
Disclosure also has the potential to improve the well-being of the surgeons involved, through relieving feelings of guilt, and satisfying the need to fulfill one’s obligations. Furthermore, data suggest that error disclosure reduces long-term litigation and costs. Admittedly, however, there are little data on how disclosure of another surgeon’s errors ultimately reduces litigation and costs.
Ultimately, supporting a just culture allows us to emphasize the importance of disclosing errors and to be accountable in setting a standard that involves exploring errors rather than ignoring them; it must be remembered, though, that this process of disclosure involves obtaining facts to help both surgeons and patients understand what truly happened.
Surgeon-to-surgeon discussions can be productive and can facilitate disclosure. However, if the doctor who made the error declines to be part of the disclosure process, one still has an obligation to disclose the error and to answer the patient’s questions honestly.
This approach requires a commitment to support surgeons in their efforts to promote transparency, and it requires a clear understanding of our obligations and the role of disclosure during training; we need to engage medical students and residents.
Dr. Susan D. Moffatt-Bruce is an associate professor at the Ohio State University, Columbus.
NO: Surgeons are not required to inform a patient of another physician’s possible error.
Surgeons do not have an obligation to disclose to a patient another surgeon’s possible medical error.
A consensus has been reached in medicine about our ethical duty to inform patients about our own medical errors. Although nondisclosure has previously been rationalized by concerns about invoking anxiety or confusion in the patient, this approach has largely been discredited; disclosure preserves patient trust and bolsters the physician-patient relationship.
However, it is an entirely different story when it comes to disclosing another surgeon’s mistake – a situation that is quite common. A recent survey showed that two-thirds of respondents had encountered a similar dilemma in the past 6 months (Qual. Saf. Health Care 2009;18:209-12).
The approach that physicians have previously taken when faced with this dilemma is an important measure of what they believe represents an ethical or just response. A poll of many of my colleagues across the country and at my own institution suggests that the preferred approach is to provide appropriate care for the patient and to answer their questions honestly, but to not proactively disclose the perceived medical error.
In fact, this was the preferred approach of every surgeon who responded.
A recent article in the New England Journal of Medicine addressed this very topic. The authors noted that there is little guidance available regarding the reporting of another physician’s error (2013;369:1752-7).
Among the challenges inherent in disclosing another’s mistake is the difficulty in determining exactly what happened. Uncertainty inevitably exists regarding the conversations that took place between the patient and the surgeon, and also about what actually defines a medical error. Incidents regarded as medical errors may comprise a large spectrum, ranging from "not what I would have done – but within the standard of care," to "blatant negligence."
Several studies suggest that highly trained physicians and surgeons routinely disagree about whether negligence has occurred in a given case. In one study, two reviewers disagreed 38% of the time as to whether appropriate care was provided.
Physicians have difficulty judging if the standard of care has been met. Therefore, it is not acceptable for each of us to assume we are the medical expert capable of rendering an opinion of whether previous care was appropriate and informing patients of our opinion.
Physicians overwhelmingly report that in the event they are responsible for a medical error discovered by another physician, they would prefer that the physician come to them first to discuss the matter. In fact, 93% of 400 respondents in one survey reported this preference.
The most acceptable approach when dealing with a peer’s medical error is to discuss the error with the responsible physician and to encourage the physician to disclose any error with the patient.
If there is disagreement as to whether an error occurred, institutional guidance should be applied. Only a collaborative approach can appropriately meet the needs of the patient and family after harmful medical errors.
Dr. Chadrick E. Denlinger is an associate professor at the Medical University of South Carolina, Charleston.
YES: Surgeons have a duty to tell patients when a medical error has been made by a physician colleague.
Surgeons have a moral and ethical obligation to inform a patient when a medical error has occurred, including cases when the error was made by another surgeon.
Principles that support complete and honest disclosure to the patient and/or the patient’s family in such cases include professional obligation on the part of both the surgeon who made the error and the surgeon who discovered the error, the integrity of both surgeons, the patient’s right to informed care throughout the continuum of care, and the patient’s right to informed consent.
With respect to the first, the American Medical Association’s code of ethics provides a framework for disclosure; it clearly states that situations occur in which a patient experiences significant complications that may have resulted from a physician’s mistake or judgment and that the physician is ethically required to inform the patient of all facts necessary to ensure understanding of the error that occurred.
The American College of Physicians’ ethics manual also states that physicians should disclose to patients information about procedural or judgment errors made during the course of care, as long as that information is pertinent and material to the patient’s well-being.
Errors do not necessarily imply negligence or unethical behavior, but failure to disclose may.
As for patients’ rights, I think that patients are entitled to honest information. They shouldn’t bear the burden of determining how they came to be in another surgeon’s care.
Patients with complications may have impactful financial burdens that result from the additional treatment that is needed, and without all pertinent information, they may have difficulty understanding the benefits, such as deferment of payments, to which they are entitled.
The patient must also be kept informed as to the long-term care plan, and honest and timely disclosure will facilitate moving beyond blame and toward patient advocacy.
The patient is entitled to informed consent, and this requires an understanding of the conditions under which they arrived in another surgeon’s care. If a second procedure is required, the patient must be made aware of potential complications – including how the effects of the initial error might impact outcomes.
Although surgeons have an ethical obligation to disclose errors made by another surgeon, this is a difficult task. Pressures from society and medical professionals can make disclosure difficult, but the benefits of disclosure are real; studies show that open, honest communication improves patient satisfaction, strengthens the physician-patient relationship, and can improve outcomes.
Disclosure also has the potential to improve the well-being of the surgeons involved, through relieving feelings of guilt, and satisfying the need to fulfill one’s obligations. Furthermore, data suggest that error disclosure reduces long-term litigation and costs. Admittedly, however, there are little data on how disclosure of another surgeon’s errors ultimately reduces litigation and costs.
Ultimately, supporting a just culture allows us to emphasize the importance of disclosing errors and to be accountable in setting a standard that involves exploring errors rather than ignoring them; it must be remembered, though, that this process of disclosure involves obtaining facts to help both surgeons and patients understand what truly happened.
Surgeon-to-surgeon discussions can be productive and can facilitate disclosure. However, if the doctor who made the error declines to be part of the disclosure process, one still has an obligation to disclose the error and to answer the patient’s questions honestly.
This approach requires a commitment to support surgeons in their efforts to promote transparency, and it requires a clear understanding of our obligations and the role of disclosure during training; we need to engage medical students and residents.
Dr. Susan D. Moffatt-Bruce is an associate professor at the Ohio State University, Columbus.
NO: Surgeons are not required to inform a patient of another physician’s possible error.
Surgeons do not have an obligation to disclose to a patient another surgeon’s possible medical error.
A consensus has been reached in medicine about our ethical duty to inform patients about our own medical errors. Although nondisclosure has previously been rationalized by concerns about invoking anxiety or confusion in the patient, this approach has largely been discredited; disclosure preserves patient trust and bolsters the physician-patient relationship.
However, it is an entirely different story when it comes to disclosing another surgeon’s mistake – a situation that is quite common. A recent survey showed that two-thirds of respondents had encountered a similar dilemma in the past 6 months (Qual. Saf. Health Care 2009;18:209-12).
The approach that physicians have previously taken when faced with this dilemma is an important measure of what they believe represents an ethical or just response. A poll of many of my colleagues across the country and at my own institution suggests that the preferred approach is to provide appropriate care for the patient and to answer their questions honestly, but to not proactively disclose the perceived medical error.
In fact, this was the preferred approach of every surgeon who responded.
A recent article in the New England Journal of Medicine addressed this very topic. The authors noted that there is little guidance available regarding the reporting of another physician’s error (2013;369:1752-7).
Among the challenges inherent in disclosing another’s mistake is the difficulty in determining exactly what happened. Uncertainty inevitably exists regarding the conversations that took place between the patient and the surgeon, and also about what actually defines a medical error. Incidents regarded as medical errors may comprise a large spectrum, ranging from "not what I would have done – but within the standard of care," to "blatant negligence."
Several studies suggest that highly trained physicians and surgeons routinely disagree about whether negligence has occurred in a given case. In one study, two reviewers disagreed 38% of the time as to whether appropriate care was provided.
Physicians have difficulty judging if the standard of care has been met. Therefore, it is not acceptable for each of us to assume we are the medical expert capable of rendering an opinion of whether previous care was appropriate and informing patients of our opinion.
Physicians overwhelmingly report that in the event they are responsible for a medical error discovered by another physician, they would prefer that the physician come to them first to discuss the matter. In fact, 93% of 400 respondents in one survey reported this preference.
The most acceptable approach when dealing with a peer’s medical error is to discuss the error with the responsible physician and to encourage the physician to disclose any error with the patient.
If there is disagreement as to whether an error occurred, institutional guidance should be applied. Only a collaborative approach can appropriately meet the needs of the patient and family after harmful medical errors.
Dr. Chadrick E. Denlinger is an associate professor at the Medical University of South Carolina, Charleston.
YES: Surgeons have a duty to tell patients when a medical error has been made by a physician colleague.
Surgeons have a moral and ethical obligation to inform a patient when a medical error has occurred, including cases when the error was made by another surgeon.
Principles that support complete and honest disclosure to the patient and/or the patient’s family in such cases include professional obligation on the part of both the surgeon who made the error and the surgeon who discovered the error, the integrity of both surgeons, the patient’s right to informed care throughout the continuum of care, and the patient’s right to informed consent.
With respect to the first, the American Medical Association’s code of ethics provides a framework for disclosure; it clearly states that situations occur in which a patient experiences significant complications that may have resulted from a physician’s mistake or judgment and that the physician is ethically required to inform the patient of all facts necessary to ensure understanding of the error that occurred.
The American College of Physicians’ ethics manual also states that physicians should disclose to patients information about procedural or judgment errors made during the course of care, as long as that information is pertinent and material to the patient’s well-being.
Errors do not necessarily imply negligence or unethical behavior, but failure to disclose may.
As for patients’ rights, I think that patients are entitled to honest information. They shouldn’t bear the burden of determining how they came to be in another surgeon’s care.
Patients with complications may have impactful financial burdens that result from the additional treatment that is needed, and without all pertinent information, they may have difficulty understanding the benefits, such as deferment of payments, to which they are entitled.
The patient must also be kept informed as to the long-term care plan, and honest and timely disclosure will facilitate moving beyond blame and toward patient advocacy.
The patient is entitled to informed consent, and this requires an understanding of the conditions under which they arrived in another surgeon’s care. If a second procedure is required, the patient must be made aware of potential complications – including how the effects of the initial error might impact outcomes.
Although surgeons have an ethical obligation to disclose errors made by another surgeon, this is a difficult task. Pressures from society and medical professionals can make disclosure difficult, but the benefits of disclosure are real; studies show that open, honest communication improves patient satisfaction, strengthens the physician-patient relationship, and can improve outcomes.
Disclosure also has the potential to improve the well-being of the surgeons involved, through relieving feelings of guilt, and satisfying the need to fulfill one’s obligations. Furthermore, data suggest that error disclosure reduces long-term litigation and costs. Admittedly, however, there are little data on how disclosure of another surgeon’s errors ultimately reduces litigation and costs.
Ultimately, supporting a just culture allows us to emphasize the importance of disclosing errors and to be accountable in setting a standard that involves exploring errors rather than ignoring them; it must be remembered, though, that this process of disclosure involves obtaining facts to help both surgeons and patients understand what truly happened.
Surgeon-to-surgeon discussions can be productive and can facilitate disclosure. However, if the doctor who made the error declines to be part of the disclosure process, one still has an obligation to disclose the error and to answer the patient’s questions honestly.
This approach requires a commitment to support surgeons in their efforts to promote transparency, and it requires a clear understanding of our obligations and the role of disclosure during training; we need to engage medical students and residents.
Dr. Susan D. Moffatt-Bruce is an associate professor at the Ohio State University, Columbus.
NO: Surgeons are not required to inform a patient of another physician’s possible error.
Surgeons do not have an obligation to disclose to a patient another surgeon’s possible medical error.
A consensus has been reached in medicine about our ethical duty to inform patients about our own medical errors. Although nondisclosure has previously been rationalized by concerns about invoking anxiety or confusion in the patient, this approach has largely been discredited; disclosure preserves patient trust and bolsters the physician-patient relationship.
However, it is an entirely different story when it comes to disclosing another surgeon’s mistake – a situation that is quite common. A recent survey showed that two-thirds of respondents had encountered a similar dilemma in the past 6 months (Qual. Saf. Health Care 2009;18:209-12).
The approach that physicians have previously taken when faced with this dilemma is an important measure of what they believe represents an ethical or just response. A poll of many of my colleagues across the country and at my own institution suggests that the preferred approach is to provide appropriate care for the patient and to answer their questions honestly, but to not proactively disclose the perceived medical error.
In fact, this was the preferred approach of every surgeon who responded.
A recent article in the New England Journal of Medicine addressed this very topic. The authors noted that there is little guidance available regarding the reporting of another physician’s error (2013;369:1752-7).
Among the challenges inherent in disclosing another’s mistake is the difficulty in determining exactly what happened. Uncertainty inevitably exists regarding the conversations that took place between the patient and the surgeon, and also about what actually defines a medical error. Incidents regarded as medical errors may comprise a large spectrum, ranging from "not what I would have done – but within the standard of care," to "blatant negligence."
Several studies suggest that highly trained physicians and surgeons routinely disagree about whether negligence has occurred in a given case. In one study, two reviewers disagreed 38% of the time as to whether appropriate care was provided.
Physicians have difficulty judging if the standard of care has been met. Therefore, it is not acceptable for each of us to assume we are the medical expert capable of rendering an opinion of whether previous care was appropriate and informing patients of our opinion.
Physicians overwhelmingly report that in the event they are responsible for a medical error discovered by another physician, they would prefer that the physician come to them first to discuss the matter. In fact, 93% of 400 respondents in one survey reported this preference.
The most acceptable approach when dealing with a peer’s medical error is to discuss the error with the responsible physician and to encourage the physician to disclose any error with the patient.
If there is disagreement as to whether an error occurred, institutional guidance should be applied. Only a collaborative approach can appropriately meet the needs of the patient and family after harmful medical errors.
Dr. Chadrick E. Denlinger is an associate professor at the Medical University of South Carolina, Charleston.
Is an MI following CEA or CAS just as clinically important as stroke?
The answer is yes!
I was not involved in the design of CREST, but I do have a responsibility to interpret the results and incorporate them into my clinical approach. When MI occurred after carotid endarterectomy (CEA) or carotid artery stenting (CAS) in CREST, the 1-year mortality was 14.2% versus 2.2% among those who did not have an MI (Blackshear et al. Circulation 2011;123:2571). This is consistent with the vascular literature, which is chock-full of strongly compelling data showing that we should take cardiac risk into account when planning our therapy.
It is not a mystery as to who is at risk for an MI. The significant independent risk factors for MI in CREST were known coronary artery disease or previous coronary revascularization. Since this is well known to us prior to treatment, shouldn’t this information be part of our therapeutic plan?
Suppose I said that perioperative MI is not important after abdominal aortic aneurysm repair, fem-pop bypass, or distal bypass?
A large part of the growth of endovascular approaches in recent years has been motivated by our best efforts to avoid MI. Think of the early days of endovascular aneurysm repair, prior to establishment of this as standard of care for most patients, and how many patients were treated with stent-grafts in an attempt to avoid cardiac risk. How could we now claim that it is unimportant?
There were two independent risk factors for mortality during CREST that increased the hazard ratio more than two times: stroke and MI (FDA panel presentation, Jan. 26, 2011).
The reason to revascularize the carotid is to prevent stroke, and this is a worthwhile endeavor. However, if the patient is harmed in some other way, especially in a manner associated with dramatically increased mortality, shouldn’t we understand that?
At some point, with further technological development, mesh-covered carotid stents, customized protection devices, and more informed patient selection, the stroke risk of CAS is likely to decrease. At that point, our relative concern about the risk of MI and the importance of MI as an endpoint is likely to increase, not decrease.
There is no doubt that we all fear stroke. Unfortunately, when something bad happens to a patient, they don’t get to select which complication they are going to have. We owe it to our patients to do what we can to diminish all the risks they face. I cannot envision an honest and useful future carotid trial design in which MI is not considered an endpoint.
Dr. Peter A. Schneider is chief of the division of vascular surgery, Hawaii Permanente Medical Group and Kaiser Foundation Hospital, Honolulu.
The answer is no!
Being given a choice between MI and stroke is like asking someone if they would rather be rich and healthy or poor and sick. The best option is to have neither an MI nor a stroke following carotid intervention. However, when given this unpleasant choice, the participants in CREST clearly stated that MI was preferable to either major or minor stroke. How often have we heard our patients state, "Doc, I’m not afraid to die, but I don’t want to live disabled from a stroke"?
A quality-of-life assessment was carried out in CREST patients using an SF-36.
This questionnaire looked at both the physical and the emotional effect of the complications of stroke and MI compared with those who were complication free.
One year after a complication, the patients stated that the worst thing that happened was a major stroke. The next worse thing was a minor stroke.
Myocardial infarction, 1 year later, from the patient’s perspective, was a nonevent. The argument that has been used regarding the importance of MI is that it has an adverse effect on life expectancy.
This is true, and it has been confirmed in several trials including CREST. The surprise finding is that stroke, including so-called minor strokes, also reduced life expectancy.
In CREST, 4 years following an adjudicated MI, the mortality rate was 19.1% versus 6.7% for those not suffering an MI.
However, the 4-year mortality rate among patients having suffered a stroke was 20%.
Therefore, compromised survival occurred equally among those patients following either stroke or MI.
However, not only did patients suffering a stroke have an equally high mortality, the group was further compromised by neurologic disability among the survivors, whereas the survivors following MI returned to their precomplication status.
Therefore, from the patients’ subjective status as well as objective clinical considerations, stroke is clearly more deleterious than MI.
Dr. Wesley S. Moore is a vascular and endovascular surgeon, and professor and chief, emeritus, of the division of vascular surgery, University of California, Los Angeles, Medical Center.
The answer is yes!
I was not involved in the design of CREST, but I do have a responsibility to interpret the results and incorporate them into my clinical approach. When MI occurred after carotid endarterectomy (CEA) or carotid artery stenting (CAS) in CREST, the 1-year mortality was 14.2% versus 2.2% among those who did not have an MI (Blackshear et al. Circulation 2011;123:2571). This is consistent with the vascular literature, which is chock-full of strongly compelling data showing that we should take cardiac risk into account when planning our therapy.
It is not a mystery as to who is at risk for an MI. The significant independent risk factors for MI in CREST were known coronary artery disease or previous coronary revascularization. Since this is well known to us prior to treatment, shouldn’t this information be part of our therapeutic plan?
Suppose I said that perioperative MI is not important after abdominal aortic aneurysm repair, fem-pop bypass, or distal bypass?
A large part of the growth of endovascular approaches in recent years has been motivated by our best efforts to avoid MI. Think of the early days of endovascular aneurysm repair, prior to establishment of this as standard of care for most patients, and how many patients were treated with stent-grafts in an attempt to avoid cardiac risk. How could we now claim that it is unimportant?
There were two independent risk factors for mortality during CREST that increased the hazard ratio more than two times: stroke and MI (FDA panel presentation, Jan. 26, 2011).
The reason to revascularize the carotid is to prevent stroke, and this is a worthwhile endeavor. However, if the patient is harmed in some other way, especially in a manner associated with dramatically increased mortality, shouldn’t we understand that?
At some point, with further technological development, mesh-covered carotid stents, customized protection devices, and more informed patient selection, the stroke risk of CAS is likely to decrease. At that point, our relative concern about the risk of MI and the importance of MI as an endpoint is likely to increase, not decrease.
There is no doubt that we all fear stroke. Unfortunately, when something bad happens to a patient, they don’t get to select which complication they are going to have. We owe it to our patients to do what we can to diminish all the risks they face. I cannot envision an honest and useful future carotid trial design in which MI is not considered an endpoint.
Dr. Peter A. Schneider is chief of the division of vascular surgery, Hawaii Permanente Medical Group and Kaiser Foundation Hospital, Honolulu.
The answer is no!
Being given a choice between MI and stroke is like asking someone if they would rather be rich and healthy or poor and sick. The best option is to have neither an MI nor a stroke following carotid intervention. However, when given this unpleasant choice, the participants in CREST clearly stated that MI was preferable to either major or minor stroke. How often have we heard our patients state, "Doc, I’m not afraid to die, but I don’t want to live disabled from a stroke"?
A quality-of-life assessment was carried out in CREST patients using an SF-36.
This questionnaire looked at both the physical and the emotional effect of the complications of stroke and MI compared with those who were complication free.
One year after a complication, the patients stated that the worst thing that happened was a major stroke. The next worse thing was a minor stroke.
Myocardial infarction, 1 year later, from the patient’s perspective, was a nonevent. The argument that has been used regarding the importance of MI is that it has an adverse effect on life expectancy.
This is true, and it has been confirmed in several trials including CREST. The surprise finding is that stroke, including so-called minor strokes, also reduced life expectancy.
In CREST, 4 years following an adjudicated MI, the mortality rate was 19.1% versus 6.7% for those not suffering an MI.
However, the 4-year mortality rate among patients having suffered a stroke was 20%.
Therefore, compromised survival occurred equally among those patients following either stroke or MI.
However, not only did patients suffering a stroke have an equally high mortality, the group was further compromised by neurologic disability among the survivors, whereas the survivors following MI returned to their precomplication status.
Therefore, from the patients’ subjective status as well as objective clinical considerations, stroke is clearly more deleterious than MI.
Dr. Wesley S. Moore is a vascular and endovascular surgeon, and professor and chief, emeritus, of the division of vascular surgery, University of California, Los Angeles, Medical Center.
The answer is yes!
I was not involved in the design of CREST, but I do have a responsibility to interpret the results and incorporate them into my clinical approach. When MI occurred after carotid endarterectomy (CEA) or carotid artery stenting (CAS) in CREST, the 1-year mortality was 14.2% versus 2.2% among those who did not have an MI (Blackshear et al. Circulation 2011;123:2571). This is consistent with the vascular literature, which is chock-full of strongly compelling data showing that we should take cardiac risk into account when planning our therapy.
It is not a mystery as to who is at risk for an MI. The significant independent risk factors for MI in CREST were known coronary artery disease or previous coronary revascularization. Since this is well known to us prior to treatment, shouldn’t this information be part of our therapeutic plan?
Suppose I said that perioperative MI is not important after abdominal aortic aneurysm repair, fem-pop bypass, or distal bypass?
A large part of the growth of endovascular approaches in recent years has been motivated by our best efforts to avoid MI. Think of the early days of endovascular aneurysm repair, prior to establishment of this as standard of care for most patients, and how many patients were treated with stent-grafts in an attempt to avoid cardiac risk. How could we now claim that it is unimportant?
There were two independent risk factors for mortality during CREST that increased the hazard ratio more than two times: stroke and MI (FDA panel presentation, Jan. 26, 2011).
The reason to revascularize the carotid is to prevent stroke, and this is a worthwhile endeavor. However, if the patient is harmed in some other way, especially in a manner associated with dramatically increased mortality, shouldn’t we understand that?
At some point, with further technological development, mesh-covered carotid stents, customized protection devices, and more informed patient selection, the stroke risk of CAS is likely to decrease. At that point, our relative concern about the risk of MI and the importance of MI as an endpoint is likely to increase, not decrease.
There is no doubt that we all fear stroke. Unfortunately, when something bad happens to a patient, they don’t get to select which complication they are going to have. We owe it to our patients to do what we can to diminish all the risks they face. I cannot envision an honest and useful future carotid trial design in which MI is not considered an endpoint.
Dr. Peter A. Schneider is chief of the division of vascular surgery, Hawaii Permanente Medical Group and Kaiser Foundation Hospital, Honolulu.
The answer is no!
Being given a choice between MI and stroke is like asking someone if they would rather be rich and healthy or poor and sick. The best option is to have neither an MI nor a stroke following carotid intervention. However, when given this unpleasant choice, the participants in CREST clearly stated that MI was preferable to either major or minor stroke. How often have we heard our patients state, "Doc, I’m not afraid to die, but I don’t want to live disabled from a stroke"?
A quality-of-life assessment was carried out in CREST patients using an SF-36.
This questionnaire looked at both the physical and the emotional effect of the complications of stroke and MI compared with those who were complication free.
One year after a complication, the patients stated that the worst thing that happened was a major stroke. The next worse thing was a minor stroke.
Myocardial infarction, 1 year later, from the patient’s perspective, was a nonevent. The argument that has been used regarding the importance of MI is that it has an adverse effect on life expectancy.
This is true, and it has been confirmed in several trials including CREST. The surprise finding is that stroke, including so-called minor strokes, also reduced life expectancy.
In CREST, 4 years following an adjudicated MI, the mortality rate was 19.1% versus 6.7% for those not suffering an MI.
However, the 4-year mortality rate among patients having suffered a stroke was 20%.
Therefore, compromised survival occurred equally among those patients following either stroke or MI.
However, not only did patients suffering a stroke have an equally high mortality, the group was further compromised by neurologic disability among the survivors, whereas the survivors following MI returned to their precomplication status.
Therefore, from the patients’ subjective status as well as objective clinical considerations, stroke is clearly more deleterious than MI.
Dr. Wesley S. Moore is a vascular and endovascular surgeon, and professor and chief, emeritus, of the division of vascular surgery, University of California, Los Angeles, Medical Center.
Point-Counterpoint: Type II Endoleaks - To treat or not to treat
The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.
– Dr. Russell Samson is the medical editor of Vascular Specialist.
A slow start can be salvaged
Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.1 Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.
Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.2-4 In light of this data, one might logically question why I continue to support intervention in this setting.
The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.2 The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.
Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.
How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx® (EV3-Covidien), as championed by Abularrage and Bosiers,7,8 offers the potential to achieve full treatment with a single intervention.
Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.
T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.
Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.
3. J Endovasc Ther, 2012. 19(2): p. 182-92.
4. J Vasc Surg, 2012. 55(1): p. 33-40.
5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.
6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.
7. J Vasc Surg, 2012. 56(3): p. 630-6.
8. J Cardiovasc Surg (Torino), 2013.
A call for a prospective randomized trial
While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,1 I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."2
Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.
Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.3 The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.
These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.
We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.
Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.
3. J Vasc Surg, 2012. 55(1): p. 33-40.
4. J Vasc Surg, 2012. 56(3): p. 630-6.
The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.
– Dr. Russell Samson is the medical editor of Vascular Specialist.
A slow start can be salvaged
Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.1 Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.
Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.2-4 In light of this data, one might logically question why I continue to support intervention in this setting.
The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.2 The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.
Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.
How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx® (EV3-Covidien), as championed by Abularrage and Bosiers,7,8 offers the potential to achieve full treatment with a single intervention.
Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.
T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.
Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.
3. J Endovasc Ther, 2012. 19(2): p. 182-92.
4. J Vasc Surg, 2012. 55(1): p. 33-40.
5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.
6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.
7. J Vasc Surg, 2012. 56(3): p. 630-6.
8. J Cardiovasc Surg (Torino), 2013.
A call for a prospective randomized trial
While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,1 I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."2
Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.
Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.3 The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.
These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.
We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.
Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.
3. J Vasc Surg, 2012. 55(1): p. 33-40.
4. J Vasc Surg, 2012. 56(3): p. 630-6.
The management of Type II endoleaks remains controversial. At the Charing Cross meeting this year Jean- Pierre Becquemin and Hence Vehagen debated whether Type II endoleaks should be treated. Dr. Verhagen suggested that results of endoleak treatment are so poor and the natural history of Type II endoleaks so benign that perhaps we shouldn’t even try to treat them. Dr. Becquemin felt that an attempt at treatment for some endoleaks was still necessary. This prompted our editors to suggest a U.S. version of the debate. As you will see both Dr. Geraghty and Dr. Kwolek feel that there is merit in pursuing treatment but with certain caveats. We appreciate their insight into this important subject.
– Dr. Russell Samson is the medical editor of Vascular Specialist.
A slow start can be salvaged
Our group recently published the midterm outcomes of our series of percutaneous glue and /or coil embolizations to treat type II endoleaks (T2EL) accompanied by continued aneurysm sac growth.1 Painstaking retrospective data collection, augmented by blinded review of all follow-up CT scans, demonstrated that at 23 months post intervention, T2EL had persisted or recurred in 72% of patients. Furthermore, the rate of aneurysm sac growth was not altered by the percutaneous intervention.
Other institutions have also reported significant rates of T2EL persistence/recurrence following embolization, and in the Cleveland Clinic experience, continued sac growth in excess of 5 mm in diameter was documented in 56% of patients who had undergone an attempt at T2EL ablation.2-4 In light of this data, one might logically question why I continue to support intervention in this setting.
The midterm reappraisals of T2EL interventions are certainly sobering. We can no longer accept apparent procedural success as a guarantee that these endoleaks will remain clinically and radiographically dormant. Yet these studies were not without their bright spots. In our series, diagnostic angiography (via transfemoral and translumbar approaches) detected occult type I or type III endoleaks in 21% of patients, prompting definitive repair by additional endograft placement. Similar angiographic elucidation of type I and III endoleaks was confirmed by the University of Chicago experience, with a 16% detection rate.2 The diagnosis and treatment of these highly pressurized leaks likely contributed to the low incidence of aneurysm rupture and aneurysm-related mortality seen in most of these series.
Bright spots aside, current midterm results for T2EL intervention leave much to be desired. I would contend, however, that these interventions should be refined, not abandoned. We now appreciate that T2EL mimic the behavior of complex arteriovenous malformations in several ways: the presence of multiple feeding and draining branches, the finding that solitary branch vessel embolization often leads to inflow recruitment from less prominent branches, and the presence of a nidus whose ablation is critical. In retrospect, then, it is not surprising that treatment approaches consisting of single-vessel coiling, or simple embolization of the nidus without concomitant treatment of all feeding branches, failed to produce the desired result. The aggressiveness of early T2EL embolization procedures may have been tempered by the potential for visceral and spinal cord complications.5,6 However, current midterm outcomes data suggest that predictable and durable success in T2EL treatment will require complete nidus ablation and occlusion of all arterial branches of the sac.
How can we pursue this more aggressive goal while maintaining an appropriate safety profile? In several instances, we have pursued this objective via staged interventions: initial angiographic coil/glue deployment, followed by laparoscopic clipping of persistent feeding vessels. The use of Onyx® (EV3-Covidien), as championed by Abularrage and Bosiers,7,8 offers the potential to achieve full treatment with a single intervention.
Advantages of Onyx include predictable polymerization times and lack of adhesion to the delivery catheter. These features permit deliberate and complete obliteration of the nidus, with intentional extension of the polymerizing mixture into the feeding vessels.
T2EL intervention has thus completed its first iteration. The value of routine angiographic examination is clear, particularly as regards the detection of occult type I and III endoleaks. Failure analysis of first-generation T2EL interventions suggests that incomplete obliteration of the endoleak complex (nidus and all feeding branches) sets the stage for vessel recruitment and reestablishment of sac flow. Promising alternative therapies have been identified, and we await their thorough evaluation.
Dr. Geraghty is an associate professor, surgery and radiology, in the division of general surgery, vascular surgery section at Washington University School of Medicine, St. Louis, Mo., and co-director of the Washington University Limb Preservation Center.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. J Vasc Interv Radiol, 2012. 23(7): p. 866-72; quiz 872.
3. J Endovasc Ther, 2012. 19(2): p. 182-92.
4. J Vasc Surg, 2012. 55(1): p. 33-40.
5. Ann Vasc Surg, 2012. 26(6): p. 860 e1-7.
6. J Vasc Interv Radiol, 2013. 24(1): p. 49-55.
7. J Vasc Surg, 2012. 56(3): p. 630-6.
8. J Cardiovasc Surg (Torino), 2013.
A call for a prospective randomized trial
While I agree with Dr. Geraghty’s comments concerning the initial poor results reported for the percutaneous treatment of Type II endoleaks,1 I disagree with comments made in April 2013 at the Charing Cross meeting by Dr. Hence Verhagen that there is "no need to worry about Type II endoleaks since they are low pressure."2
Early on in our experience we began measuring sac pressures after trans- lumbar catheterization and have found that some aneurysm sacs may in fact have systolic arterial pressures of 8-90 mm HG from large lumbar or IMA collaterals. Furthermore, we and others have described the treatment of patients with ruptured AAA after EVAR who upon open exploration where found to have large patent lumbar arteries as the sole etiology of the ruptured AAA.
Dr. Geraghty and Dr. Sarac at Cleveland Clinic have also described the important observation that these Type II endoleaks may be associated with a Type I or III endoleaks and thus put patients at even higher risk of rupture.3 The extent of these leaks may not be completely elucidated until the time of angiography, again emphasizing the importance of a more aggressive approach to diagnosis and treatment in patients with an enlarging aneurysm sac.
These authors have also appropriately pointed out that overall treatment success rates are low with persistence of type II endoleaks on long–term follow-up. While we initially described an overall success rate of 30%, our approach has changed over time to include direct access to the endoleak nidus with the injection of a flow directed glue (Onyx) to obliterate the flow channel and feeding vessels.
We have found this approach to be more successful than attempting to cannulate each of the feeding lumbar vessels or coil embolization of the aneurysm sac, and can be performed via either a translumbar or transarterial approach using SMA to IMA collaterals. While our success rate using this technique has improved to nearly 80%, several words of caution should be noted. 1) Onyx glue is approved for use in the treatment of intracerebral vascular malformations and does not have a peripheral indication at this time. 2) It is critically important that the interventionalist obtains access into the nidus/flow channel to allow the embolic agent to flow. Otherwise you are injecting glue directly into the sac thrombus and wasting time and an expensive embolic agent. 3) There are often multiple levels of lumbar vessels involved and we have found that we often have to go back several times at different levels to treat extensive Type II endoleaks. All of these observations emphasize the need to further study the treatment of Type II endoleaks and the need for a prospective randomized trial to better identify the best treatment options.
Dr. Kwolek is the director of the vascular and endovascular training program at Massachusetts General Hospital, Boston, and the chief of vascular surgery at Newton Wellesley Hospital.
1. J Vasc Surg, 2012. 55(5): p. 1263-7.
2. Management of Type II endoleaks divides the experts at CX 35. Vascular News International,58, May 2012, BIBA publishing.
3. J Vasc Surg, 2012. 55(1): p. 33-40.
4. J Vasc Surg, 2012. 56(3): p. 630-6.
