Michele G. Sullivan

BOSTON — Atorvastatin significantly reduced the risk of stroke, cardiac events, and carotid endarterectomy in a large group of patients with carotid stenosis, Dr. Henrik Sillesen reported at the annual meeting of the American Academy of Neurology.

Over 5 years, the drug cut the incidence of stroke and heart attacks by more than 30%, and halved the incidence of endarterectomy in these high-risk patients, he said in an interview.

“Patients with carotid stenosis should certainly have aggressive treatment with atorvastatin at 80 mg per day,” said Dr. Sillesen, chairman of vascular surgery at Rigshospitalet, Copenhagen.

He presented the results of a subanalysis of the SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial, which focused on risk reduction in a subgroup of patients with existing coronary stenosis.

The Pfizer-supported SPARCL trial randomized 4,731 patients who had experienced an ischemic stroke, hemorrhagic stroke, or transient ischemic attack 1-6 months prior to either atorvastatin (Lipitor) 80 mg/day or placebo. After an average of 4.9 years of follow-up, stroke had occurred in 265 subjects in the atorvastatin group, compared with 311 in the placebo group, a 2.2% absolute difference. The drug also decreased the 5-year risk of other major cardiovascular events, with a 3.5% absolute difference and a 20% relative reduction in risk.

There was no difference between groups in overall mortality.

Patients in SPARCL were allowed to take other cardiovascular medications, including open-label statins, aspirin or other antiplatelet drugs, ACE inhibitors, dihydropyridine derivatives, β-blockers, angiotensin receptor antagonists, or vitamin K antagonists.

The subanalysis reported by Dr. Sillesen included 1,006 patients with a history of carotid stenosis. Compared with those taking placebo, patients taking the drug had a 34% reduction in the occurrence of stroke and a 36% reduction in major cardiovascular events (cardiac death, stroke, resuscitated cardiac arrest, and fatal and nonfatal myocardial infarction). Revascularization procedures were reduced by 50%, which included a 54% decrease in the number of carotid endarterectomies.

Atorvastatin stabilizes arterial plaque formation, thus preventing atherosclerotic disease progression, even in this subgroup of patients with more advanced disease, noted Dr. Sillesen, who has reported that he's received grant support from Pfizer and consulting and lecture fees from several other pharmaceutical companies.

ELSEVIER GLOBAL MEDICAL NEWS

BOSTON — Atorvastatin significantly reduced the risk of stroke, cardiac events, and carotid endarterectomy in a large group of patients with carotid stenosis, Dr. Henrik Sillesen reported at the annual meeting of the American Academy of Neurology.

Over 5 years, the drug cut the incidence of stroke and heart attacks by more than 30%, and halved the incidence of endarterectomy in these high-risk patients, he said in an interview.

“Patients with carotid stenosis should certainly have aggressive treatment with atorvastatin at 80 mg per day,” said Dr. Sillesen, chairman of vascular surgery at Rigshospitalet, Copenhagen.

He presented the results of a subanalysis of the SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial, which focused on risk reduction in a subgroup of patients with existing coronary stenosis.

The Pfizer-supported SPARCL trial randomized 4,731 patients who had experienced an ischemic stroke, hemorrhagic stroke, or transient ischemic attack 1-6 months prior to either atorvastatin (Lipitor) 80 mg/day or placebo. After an average of 4.9 years of follow-up, stroke had occurred in 265 subjects in the atorvastatin group, compared with 311 in the placebo group, a 2.2% absolute difference. The drug also decreased the 5-year risk of other major cardiovascular events, with a 3.5% absolute difference and a 20% relative reduction in risk.

There was no difference between groups in overall mortality.

Patients in SPARCL were allowed to take other cardiovascular medications, including open-label statins, aspirin or other antiplatelet drugs, ACE inhibitors, dihydropyridine derivatives, β-blockers, angiotensin receptor antagonists, or vitamin K antagonists.

The subanalysis reported by Dr. Sillesen included 1,006 patients with a history of carotid stenosis. Compared with those taking placebo, patients taking the drug had a 34% reduction in the occurrence of stroke and a 36% reduction in major cardiovascular events (cardiac death, stroke, resuscitated cardiac arrest, and fatal and nonfatal myocardial infarction). Revascularization procedures were reduced by 50%, which included a 54% decrease in the number of carotid endarterectomies.

Atorvastatin stabilizes arterial plaque formation, thus preventing atherosclerotic disease progression, even in this subgroup of patients with more advanced disease, noted Dr. Sillesen, who has reported that he's received grant support from Pfizer and consulting and lecture fees from several other pharmaceutical companies.

ELSEVIER GLOBAL MEDICAL NEWS

BOSTON — Atorvastatin significantly reduced the risk of stroke, cardiac events, and carotid endarterectomy in a large group of patients with carotid stenosis, Dr. Henrik Sillesen reported at the annual meeting of the American Academy of Neurology.

Over 5 years, the drug cut the incidence of stroke and heart attacks by more than 30%, and halved the incidence of endarterectomy in these high-risk patients, he said in an interview.

“Patients with carotid stenosis should certainly have aggressive treatment with atorvastatin at 80 mg per day,” said Dr. Sillesen, chairman of vascular surgery at Rigshospitalet, Copenhagen.

He presented the results of a subanalysis of the SPARCL (Stroke Prevention by Aggressive Reduction in Cholesterol Levels) trial, which focused on risk reduction in a subgroup of patients with existing coronary stenosis.

The Pfizer-supported SPARCL trial randomized 4,731 patients who had experienced an ischemic stroke, hemorrhagic stroke, or transient ischemic attack 1-6 months prior to either atorvastatin (Lipitor) 80 mg/day or placebo. After an average of 4.9 years of follow-up, stroke had occurred in 265 subjects in the atorvastatin group, compared with 311 in the placebo group, a 2.2% absolute difference. The drug also decreased the 5-year risk of other major cardiovascular events, with a 3.5% absolute difference and a 20% relative reduction in risk.

There was no difference between groups in overall mortality.

Patients in SPARCL were allowed to take other cardiovascular medications, including open-label statins, aspirin or other antiplatelet drugs, ACE inhibitors, dihydropyridine derivatives, β-blockers, angiotensin receptor antagonists, or vitamin K antagonists.

The subanalysis reported by Dr. Sillesen included 1,006 patients with a history of carotid stenosis. Compared with those taking placebo, patients taking the drug had a 34% reduction in the occurrence of stroke and a 36% reduction in major cardiovascular events (cardiac death, stroke, resuscitated cardiac arrest, and fatal and nonfatal myocardial infarction). Revascularization procedures were reduced by 50%, which included a 54% decrease in the number of carotid endarterectomies.

Atorvastatin stabilizes arterial plaque formation, thus preventing atherosclerotic disease progression, even in this subgroup of patients with more advanced disease, noted Dr. Sillesen, who has reported that he's received grant support from Pfizer and consulting and lecture fees from several other pharmaceutical companies.

ELSEVIER GLOBAL MEDICAL NEWS

A community-based push to create standardized response systems could decrease mortality and streamline acute care for patients suffering an ST-elevation myocardial infarction.

The American Heart Association's ambitious “Mission: Lifeline” program will go far beyond past efforts at improving treatment times through public outreach and education, Dr. Alice Jacobs said during a press conference. “Regrettably, prior public awareness campaigns and community-based interventions have not yet been effective in reducing the time from symptom onset to first medical contact, or in increasing the number of patients who use emergency medical services [EMS] to get to hospitals where they can receive the appropriate care.”

“Despite the proven benefits of quickly restoring blood flow to the heart muscle during a heart attack, 30% of STEMI patients do not receive any reperfusion therapy,” neither fibrinolytics nor primary percutaneous coronary intervention (PCI), said Dr. Jacobs, director of the cardiac catheterization lab at Boston Medical Center. “And only 50% of those who get fibrinolytics and 40% of those who undergo PCI do so within the recommended time frames.”

The group's recommendations are published in the journal Circulation (DOI: 10.1161/CIRCULATIONAHA.107.184043

The ideal system would combine several key elements, she said:

▸ Public education. “People need to understand the signs and symptoms of a heart attack, and the importance of activating the EMS system as quickly as possible,” Dr. Jacobs said.

▸ Improving EMS diagnosis of STEMI. “If EMS systems have the personnel, training, and appropriate resources, they can acquire, interpret, and transmit 12-lead electrocardiograms that can show the patient is having a STEMI heart attack,” she said.

▸ Quick, efficient transfer to hospitals equipped with cardiac catheterization teams. Under the proposed system, patients transported to a non-PCI-capable hospital would remain on the stretcher with EMS personnel in attendance until the decision is made about whether to transport to a PCI-capable receiving hospital.

▸ Hospital incentives and certification. “We will be working with payers and policy makers to ensure that mechanisms are in place for appropriate reimbursement,” Dr. Jacobs said. A STEMI Center Certification program will establish treatment and accountability protocols for both referring and receiving hospitals.

The AHA will play a pivotal role in bringing these parties together, said Dr. Raymond Gibbons, president of the AHA, beginning with an assessment of EMS effectiveness for STEMI patients. The AHA will use this information to construct a basic response system that can be tailored to different regions.

Funding these systems, Dr. Gibbons said, will be largely left to localities. AHA will provide support in seeking the money necessary for implementation–industry grants, for example–but the group won't be contributing financially to any individual project.

A few AHA-led pilot programs are already underway, Dr. Gibbons noted. A 2004 grant from The Annenberg Foundation made it possible for Los Angeles to create a response system that relies on 12-lead ECG readings by EMS providers. The AHA Greater Southeast Affiliate has convened a state-level STEMI task force and helped introduce a legislative bill to develop emergency angioplasty centers for STEMI patients. And in Texas, a task force met in January to discuss ways to more effectively manage STEMI patients.

Although establishing such a response system is an enormous challenge, the payoff is just as big, said Dr. Tim Henry, interventional cardiologist and director of research at the Minneapolis Heart Institute. Four years ago, the facility instituted a two-pronged standardized care system for STEMI patients based on their distance from a regional PCI-capable facility.

“Our approach involves different protocols for patients who live within either 60 miles [zone 1] or 60-210 miles [zone 2] from these hospitals. Our median time from the STEMI referral hospitals to balloon inflation at the receiving hospital is now 96 minutes for those in zone 1 and 118 minutes in zone 2.”

A community-based push to create standardized response systems could decrease mortality and streamline acute care for patients suffering an ST-elevation myocardial infarction.

The American Heart Association's ambitious “Mission: Lifeline” program will go far beyond past efforts at improving treatment times through public outreach and education, Dr. Alice Jacobs said during a press conference. “Regrettably, prior public awareness campaigns and community-based interventions have not yet been effective in reducing the time from symptom onset to first medical contact, or in increasing the number of patients who use emergency medical services [EMS] to get to hospitals where they can receive the appropriate care.”

“Despite the proven benefits of quickly restoring blood flow to the heart muscle during a heart attack, 30% of STEMI patients do not receive any reperfusion therapy,” neither fibrinolytics nor primary percutaneous coronary intervention (PCI), said Dr. Jacobs, director of the cardiac catheterization lab at Boston Medical Center. “And only 50% of those who get fibrinolytics and 40% of those who undergo PCI do so within the recommended time frames.”

The group's recommendations are published in the journal Circulation (DOI: 10.1161/CIRCULATIONAHA.107.184043

The ideal system would combine several key elements, she said:

▸ Public education. “People need to understand the signs and symptoms of a heart attack, and the importance of activating the EMS system as quickly as possible,” Dr. Jacobs said.

▸ Improving EMS diagnosis of STEMI. “If EMS systems have the personnel, training, and appropriate resources, they can acquire, interpret, and transmit 12-lead electrocardiograms that can show the patient is having a STEMI heart attack,” she said.

▸ Quick, efficient transfer to hospitals equipped with cardiac catheterization teams. Under the proposed system, patients transported to a non-PCI-capable hospital would remain on the stretcher with EMS personnel in attendance until the decision is made about whether to transport to a PCI-capable receiving hospital.

▸ Hospital incentives and certification. “We will be working with payers and policy makers to ensure that mechanisms are in place for appropriate reimbursement,” Dr. Jacobs said. A STEMI Center Certification program will establish treatment and accountability protocols for both referring and receiving hospitals.

The AHA will play a pivotal role in bringing these parties together, said Dr. Raymond Gibbons, president of the AHA, beginning with an assessment of EMS effectiveness for STEMI patients. The AHA will use this information to construct a basic response system that can be tailored to different regions.

Funding these systems, Dr. Gibbons said, will be largely left to localities. AHA will provide support in seeking the money necessary for implementation–industry grants, for example–but the group won't be contributing financially to any individual project.

A few AHA-led pilot programs are already underway, Dr. Gibbons noted. A 2004 grant from The Annenberg Foundation made it possible for Los Angeles to create a response system that relies on 12-lead ECG readings by EMS providers. The AHA Greater Southeast Affiliate has convened a state-level STEMI task force and helped introduce a legislative bill to develop emergency angioplasty centers for STEMI patients. And in Texas, a task force met in January to discuss ways to more effectively manage STEMI patients.

Although establishing such a response system is an enormous challenge, the payoff is just as big, said Dr. Tim Henry, interventional cardiologist and director of research at the Minneapolis Heart Institute. Four years ago, the facility instituted a two-pronged standardized care system for STEMI patients based on their distance from a regional PCI-capable facility.

“Our approach involves different protocols for patients who live within either 60 miles [zone 1] or 60-210 miles [zone 2] from these hospitals. Our median time from the STEMI referral hospitals to balloon inflation at the receiving hospital is now 96 minutes for those in zone 1 and 118 minutes in zone 2.”

A community-based push to create standardized response systems could decrease mortality and streamline acute care for patients suffering an ST-elevation myocardial infarction.

The American Heart Association's ambitious “Mission: Lifeline” program will go far beyond past efforts at improving treatment times through public outreach and education, Dr. Alice Jacobs said during a press conference. “Regrettably, prior public awareness campaigns and community-based interventions have not yet been effective in reducing the time from symptom onset to first medical contact, or in increasing the number of patients who use emergency medical services [EMS] to get to hospitals where they can receive the appropriate care.”

“Despite the proven benefits of quickly restoring blood flow to the heart muscle during a heart attack, 30% of STEMI patients do not receive any reperfusion therapy,” neither fibrinolytics nor primary percutaneous coronary intervention (PCI), said Dr. Jacobs, director of the cardiac catheterization lab at Boston Medical Center. “And only 50% of those who get fibrinolytics and 40% of those who undergo PCI do so within the recommended time frames.”

The group's recommendations are published in the journal Circulation (DOI: 10.1161/CIRCULATIONAHA.107.184043

The ideal system would combine several key elements, she said:

▸ Public education. “People need to understand the signs and symptoms of a heart attack, and the importance of activating the EMS system as quickly as possible,” Dr. Jacobs said.

▸ Improving EMS diagnosis of STEMI. “If EMS systems have the personnel, training, and appropriate resources, they can acquire, interpret, and transmit 12-lead electrocardiograms that can show the patient is having a STEMI heart attack,” she said.

▸ Quick, efficient transfer to hospitals equipped with cardiac catheterization teams. Under the proposed system, patients transported to a non-PCI-capable hospital would remain on the stretcher with EMS personnel in attendance until the decision is made about whether to transport to a PCI-capable receiving hospital.

▸ Hospital incentives and certification. “We will be working with payers and policy makers to ensure that mechanisms are in place for appropriate reimbursement,” Dr. Jacobs said. A STEMI Center Certification program will establish treatment and accountability protocols for both referring and receiving hospitals.

The AHA will play a pivotal role in bringing these parties together, said Dr. Raymond Gibbons, president of the AHA, beginning with an assessment of EMS effectiveness for STEMI patients. The AHA will use this information to construct a basic response system that can be tailored to different regions.

Funding these systems, Dr. Gibbons said, will be largely left to localities. AHA will provide support in seeking the money necessary for implementation–industry grants, for example–but the group won't be contributing financially to any individual project.

A few AHA-led pilot programs are already underway, Dr. Gibbons noted. A 2004 grant from The Annenberg Foundation made it possible for Los Angeles to create a response system that relies on 12-lead ECG readings by EMS providers. The AHA Greater Southeast Affiliate has convened a state-level STEMI task force and helped introduce a legislative bill to develop emergency angioplasty centers for STEMI patients. And in Texas, a task force met in January to discuss ways to more effectively manage STEMI patients.

Although establishing such a response system is an enormous challenge, the payoff is just as big, said Dr. Tim Henry, interventional cardiologist and director of research at the Minneapolis Heart Institute. Four years ago, the facility instituted a two-pronged standardized care system for STEMI patients based on their distance from a regional PCI-capable facility.

“Our approach involves different protocols for patients who live within either 60 miles [zone 1] or 60-210 miles [zone 2] from these hospitals. Our median time from the STEMI referral hospitals to balloon inflation at the receiving hospital is now 96 minutes for those in zone 1 and 118 minutes in zone 2.”

CHICAGO — Patients who gain at least 5% of body weight while taking prophylactic migraine medications experienced changes in clinical markers that could indicate increased risk of cardiovascular disease, said Dr. Marcelo Bigal at the annual meeting of the American Headache Society.

“Given that migraine and being overweight or obese are independent risk factors for cardiovascular disease, and obesity is a risk factor for migraine transformation and greater pain during migraine attacks, weight gain—including that associated with medical treatment—may have particularly important health implications in migraine patients,” said Dr. Bigal, of the Albert Einstein College of Medicine, New York.

He and his colleagues compared weight change with clinical markers of cardiovascular disease risk and headache treatment response in migraineurs participating in a large trial of topiramate and amitriptyline for migraine prophylaxis. The 331 patients were randomized to either topiramate 100 mg/day or amitriptyline 100 mg/day for 26 weeks. Most of the patients (67%) stayed at a steady weight. Weight gain occurred in 16% and weight loss in 17%. Most of those who lost weight (91%) were taking topiramate, and most of those who gained weight (87%) were taking amitriptyline.

There were no significant differences in medication response by weight change category. Patients with weight gain and loss had similar reductions in the mean frequency of monthly migraine episodes (−2.7 vs. −3.0).

However, weight change did influence the clinical markers of cardiovascular disease risk. Those who gained weight experienced significant elevations in mean diastolic blood pressure, glucose levels, heart rate, total cholesterol, and LDL cholesterol, compared with those who lost weight.

Patients who gained weight also had increases in their levels of C-reactive protein (CRP), gaining a mean of 1.8 mg/L. Patients who lost weight had a decline in CRP of 1.9 mg/L. Although the difference was not statistically significant, Dr. Bigal noted, it may be clinically meaningful. “CRP values of less than 1 mg/L predict low cardiovascular risk, values of 1–3 mg/L predict average risk, and values greater than 3 mg/L predict high risk [according to Centers for Disease Control and Prevention and the American Heart Association]. Given that migraine is itself is a risk factor for cardiovascular disease, weight gain in migraine patients may have particularly important health implications.”

The study was sponsored by Ortho-McNeil Janssen Scientific Affairs L.L.C. Dr. Bigal is a consultant for the company.

CHICAGO — Patients who gain at least 5% of body weight while taking prophylactic migraine medications experienced changes in clinical markers that could indicate increased risk of cardiovascular disease, said Dr. Marcelo Bigal at the annual meeting of the American Headache Society.

“Given that migraine and being overweight or obese are independent risk factors for cardiovascular disease, and obesity is a risk factor for migraine transformation and greater pain during migraine attacks, weight gain—including that associated with medical treatment—may have particularly important health implications in migraine patients,” said Dr. Bigal, of the Albert Einstein College of Medicine, New York.

He and his colleagues compared weight change with clinical markers of cardiovascular disease risk and headache treatment response in migraineurs participating in a large trial of topiramate and amitriptyline for migraine prophylaxis. The 331 patients were randomized to either topiramate 100 mg/day or amitriptyline 100 mg/day for 26 weeks. Most of the patients (67%) stayed at a steady weight. Weight gain occurred in 16% and weight loss in 17%. Most of those who lost weight (91%) were taking topiramate, and most of those who gained weight (87%) were taking amitriptyline.

There were no significant differences in medication response by weight change category. Patients with weight gain and loss had similar reductions in the mean frequency of monthly migraine episodes (−2.7 vs. −3.0).

However, weight change did influence the clinical markers of cardiovascular disease risk. Those who gained weight experienced significant elevations in mean diastolic blood pressure, glucose levels, heart rate, total cholesterol, and LDL cholesterol, compared with those who lost weight.

Patients who gained weight also had increases in their levels of C-reactive protein (CRP), gaining a mean of 1.8 mg/L. Patients who lost weight had a decline in CRP of 1.9 mg/L. Although the difference was not statistically significant, Dr. Bigal noted, it may be clinically meaningful. “CRP values of less than 1 mg/L predict low cardiovascular risk, values of 1–3 mg/L predict average risk, and values greater than 3 mg/L predict high risk [according to Centers for Disease Control and Prevention and the American Heart Association]. Given that migraine is itself is a risk factor for cardiovascular disease, weight gain in migraine patients may have particularly important health implications.”

The study was sponsored by Ortho-McNeil Janssen Scientific Affairs L.L.C. Dr. Bigal is a consultant for the company.

CHICAGO — Patients who gain at least 5% of body weight while taking prophylactic migraine medications experienced changes in clinical markers that could indicate increased risk of cardiovascular disease, said Dr. Marcelo Bigal at the annual meeting of the American Headache Society.

“Given that migraine and being overweight or obese are independent risk factors for cardiovascular disease, and obesity is a risk factor for migraine transformation and greater pain during migraine attacks, weight gain—including that associated with medical treatment—may have particularly important health implications in migraine patients,” said Dr. Bigal, of the Albert Einstein College of Medicine, New York.

He and his colleagues compared weight change with clinical markers of cardiovascular disease risk and headache treatment response in migraineurs participating in a large trial of topiramate and amitriptyline for migraine prophylaxis. The 331 patients were randomized to either topiramate 100 mg/day or amitriptyline 100 mg/day for 26 weeks. Most of the patients (67%) stayed at a steady weight. Weight gain occurred in 16% and weight loss in 17%. Most of those who lost weight (91%) were taking topiramate, and most of those who gained weight (87%) were taking amitriptyline.

There were no significant differences in medication response by weight change category. Patients with weight gain and loss had similar reductions in the mean frequency of monthly migraine episodes (−2.7 vs. −3.0).

However, weight change did influence the clinical markers of cardiovascular disease risk. Those who gained weight experienced significant elevations in mean diastolic blood pressure, glucose levels, heart rate, total cholesterol, and LDL cholesterol, compared with those who lost weight.

Patients who gained weight also had increases in their levels of C-reactive protein (CRP), gaining a mean of 1.8 mg/L. Patients who lost weight had a decline in CRP of 1.9 mg/L. Although the difference was not statistically significant, Dr. Bigal noted, it may be clinically meaningful. “CRP values of less than 1 mg/L predict low cardiovascular risk, values of 1–3 mg/L predict average risk, and values greater than 3 mg/L predict high risk [according to Centers for Disease Control and Prevention and the American Heart Association]. Given that migraine is itself is a risk factor for cardiovascular disease, weight gain in migraine patients may have particularly important health implications.”

The study was sponsored by Ortho-McNeil Janssen Scientific Affairs L.L.C. Dr. Bigal is a consultant for the company.

BOSTON — Two new data sets reinforce the recommendation to avoid valproate as a first-line therapy for any indication in women of childbearing years.

The findings, presented at the annual meeting of the American Academy of Neurology, strengthen evidence of a link between valproate use and an increased risk of major congenital malformations as well as impaired cognitive development of children exposed in utero.

“Not only our study, but nine other studies on valproate's anatomical and behavioral effects, have shown similar signals of poor outcome with this drug,” Dr. Kimford J Meador commented. “The drug should not be a first-line therapy for any indication in women of childbearing age. At the very minimum, women need to be aware of these risks if they are going to take this drug. We need to remember that half of U.S. pregnancies are unplanned.”

Dr. Meador, the Melvin Greer Professor of Neurology and director of the epilepsy program at the University of Florida, Gainesville, presented interim data from the ongoing Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study for which investigators enrolled 185 children whose mothers took carbamazepine (48), lamotrigine (66), phenytoin (42), or valproate (29) for epilepsy during pregnancy. Data were given on the children's mental development at 2 years; the prospective study will follow the cohort to age 6.

Mean IQ scores based on the Mental Development Index (MDI) from the Bayley Scale were lowest for children in the valproate group (81), Dr. Meador said. A score below 85 is considered to be below normal limits. Mean scores in the other groups were 94 for lamotrigine, 95 for phenytoin, and 96 for carbamazepine.

In addition, he said, the percentage of children in the valproate group with an MDI of less than 70 (correlating with mental retardation) was 24%, about double that seen in any of the other groups (carbamazepine, 13%; lamotrigine, 11%; and phenytoin, 12%).

The study also found an inverse relationship between maternal valproate blood levels during pregnancy and MDI scores in the children, Dr. Meador noted. All of the valproate relationships remained constant even after maternal IQ—an important driver of childhood IQ, maternal epilepsy type, and past medical history were controlled for.

The mechanism of brain injury in the valproate group is probably third-trimester neuronal apoptosis, Dr. Meador said in an interview. “We think it's similar to what's seen in fetal alcohol syndrome, and the apoptosis appears to occur at a relatively lower dose than it would with other drugs, such as phenytoin. I think that's why we see such an increased signal.”

NEAD only includes the children of women with epilepsy—the group that accounts for the smallest proportion of valproate scrips, he added. “Most of the prescriptions are written for other things, including psychotropic and pain indications. [Fewer] than half are for epilepsy.”

In the third quarter of 2006, about 16% of women of childbearing age with epilepsy were taking the drug, making it the fourth leading antiepileptic in the United States for this group. Valproate sales jumped 28% last year, an increase “that has to include some portion of women of childbearing age,” Dr. Meador said.

The second study, GlaxoSmithKline's lamotrigine pregnancy registry, found that valproate in conjunction with lamotrigine significantly increases the risk of a major birth defect. Lamotrigine is a GSK product.

The registry, now in its 14th year, has prospectively enrolled 2,400 pregnancies occurring in 32 countries. There are known outcome data on 1,539 pregnancies, said Marianne Cunnington, Ph.D., of GSK.

The risk of a major birth defect in the 908 first-trimester exposures to lamotrigine only was 2.9%, similar to the background population risk of 2%–3%. The risk associated with nonvalproate polytherapy was 2.6%. However, when lamotrigine polytherapy included valproate, the risk of a major congenital malformation jumped to more than 11%.

“We have a signal for an increased risk for polytherapy including valproate,” she said, although “it's unclear whether valproate is responsible for this increased risk.”

Dr. Meador noted, however, that six other studies have concluded that valproate significantly increases the risk of birth defects.

BOSTON — Two new data sets reinforce the recommendation to avoid valproate as a first-line therapy for any indication in women of childbearing years.

The findings, presented at the annual meeting of the American Academy of Neurology, strengthen evidence of a link between valproate use and an increased risk of major congenital malformations as well as impaired cognitive development of children exposed in utero.

“Not only our study, but nine other studies on valproate's anatomical and behavioral effects, have shown similar signals of poor outcome with this drug,” Dr. Kimford J Meador commented. “The drug should not be a first-line therapy for any indication in women of childbearing age. At the very minimum, women need to be aware of these risks if they are going to take this drug. We need to remember that half of U.S. pregnancies are unplanned.”

Dr. Meador, the Melvin Greer Professor of Neurology and director of the epilepsy program at the University of Florida, Gainesville, presented interim data from the ongoing Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study for which investigators enrolled 185 children whose mothers took carbamazepine (48), lamotrigine (66), phenytoin (42), or valproate (29) for epilepsy during pregnancy. Data were given on the children's mental development at 2 years; the prospective study will follow the cohort to age 6.

Mean IQ scores based on the Mental Development Index (MDI) from the Bayley Scale were lowest for children in the valproate group (81), Dr. Meador said. A score below 85 is considered to be below normal limits. Mean scores in the other groups were 94 for lamotrigine, 95 for phenytoin, and 96 for carbamazepine.

In addition, he said, the percentage of children in the valproate group with an MDI of less than 70 (correlating with mental retardation) was 24%, about double that seen in any of the other groups (carbamazepine, 13%; lamotrigine, 11%; and phenytoin, 12%).

The study also found an inverse relationship between maternal valproate blood levels during pregnancy and MDI scores in the children, Dr. Meador noted. All of the valproate relationships remained constant even after maternal IQ—an important driver of childhood IQ, maternal epilepsy type, and past medical history were controlled for.

The mechanism of brain injury in the valproate group is probably third-trimester neuronal apoptosis, Dr. Meador said in an interview. “We think it's similar to what's seen in fetal alcohol syndrome, and the apoptosis appears to occur at a relatively lower dose than it would with other drugs, such as phenytoin. I think that's why we see such an increased signal.”

NEAD only includes the children of women with epilepsy—the group that accounts for the smallest proportion of valproate scrips, he added. “Most of the prescriptions are written for other things, including psychotropic and pain indications. [Fewer] than half are for epilepsy.”

In the third quarter of 2006, about 16% of women of childbearing age with epilepsy were taking the drug, making it the fourth leading antiepileptic in the United States for this group. Valproate sales jumped 28% last year, an increase “that has to include some portion of women of childbearing age,” Dr. Meador said.

The second study, GlaxoSmithKline's lamotrigine pregnancy registry, found that valproate in conjunction with lamotrigine significantly increases the risk of a major birth defect. Lamotrigine is a GSK product.

The registry, now in its 14th year, has prospectively enrolled 2,400 pregnancies occurring in 32 countries. There are known outcome data on 1,539 pregnancies, said Marianne Cunnington, Ph.D., of GSK.

The risk of a major birth defect in the 908 first-trimester exposures to lamotrigine only was 2.9%, similar to the background population risk of 2%–3%. The risk associated with nonvalproate polytherapy was 2.6%. However, when lamotrigine polytherapy included valproate, the risk of a major congenital malformation jumped to more than 11%.

“We have a signal for an increased risk for polytherapy including valproate,” she said, although “it's unclear whether valproate is responsible for this increased risk.”

Dr. Meador noted, however, that six other studies have concluded that valproate significantly increases the risk of birth defects.

BOSTON — Two new data sets reinforce the recommendation to avoid valproate as a first-line therapy for any indication in women of childbearing years.

The findings, presented at the annual meeting of the American Academy of Neurology, strengthen evidence of a link between valproate use and an increased risk of major congenital malformations as well as impaired cognitive development of children exposed in utero.

“Not only our study, but nine other studies on valproate's anatomical and behavioral effects, have shown similar signals of poor outcome with this drug,” Dr. Kimford J Meador commented. “The drug should not be a first-line therapy for any indication in women of childbearing age. At the very minimum, women need to be aware of these risks if they are going to take this drug. We need to remember that half of U.S. pregnancies are unplanned.”

Dr. Meador, the Melvin Greer Professor of Neurology and director of the epilepsy program at the University of Florida, Gainesville, presented interim data from the ongoing Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study for which investigators enrolled 185 children whose mothers took carbamazepine (48), lamotrigine (66), phenytoin (42), or valproate (29) for epilepsy during pregnancy. Data were given on the children's mental development at 2 years; the prospective study will follow the cohort to age 6.

Mean IQ scores based on the Mental Development Index (MDI) from the Bayley Scale were lowest for children in the valproate group (81), Dr. Meador said. A score below 85 is considered to be below normal limits. Mean scores in the other groups were 94 for lamotrigine, 95 for phenytoin, and 96 for carbamazepine.

In addition, he said, the percentage of children in the valproate group with an MDI of less than 70 (correlating with mental retardation) was 24%, about double that seen in any of the other groups (carbamazepine, 13%; lamotrigine, 11%; and phenytoin, 12%).

The study also found an inverse relationship between maternal valproate blood levels during pregnancy and MDI scores in the children, Dr. Meador noted. All of the valproate relationships remained constant even after maternal IQ—an important driver of childhood IQ, maternal epilepsy type, and past medical history were controlled for.

The mechanism of brain injury in the valproate group is probably third-trimester neuronal apoptosis, Dr. Meador said in an interview. “We think it's similar to what's seen in fetal alcohol syndrome, and the apoptosis appears to occur at a relatively lower dose than it would with other drugs, such as phenytoin. I think that's why we see such an increased signal.”

NEAD only includes the children of women with epilepsy—the group that accounts for the smallest proportion of valproate scrips, he added. “Most of the prescriptions are written for other things, including psychotropic and pain indications. [Fewer] than half are for epilepsy.”

In the third quarter of 2006, about 16% of women of childbearing age with epilepsy were taking the drug, making it the fourth leading antiepileptic in the United States for this group. Valproate sales jumped 28% last year, an increase “that has to include some portion of women of childbearing age,” Dr. Meador said.

The second study, GlaxoSmithKline's lamotrigine pregnancy registry, found that valproate in conjunction with lamotrigine significantly increases the risk of a major birth defect. Lamotrigine is a GSK product.

The registry, now in its 14th year, has prospectively enrolled 2,400 pregnancies occurring in 32 countries. There are known outcome data on 1,539 pregnancies, said Marianne Cunnington, Ph.D., of GSK.

The risk of a major birth defect in the 908 first-trimester exposures to lamotrigine only was 2.9%, similar to the background population risk of 2%–3%. The risk associated with nonvalproate polytherapy was 2.6%. However, when lamotrigine polytherapy included valproate, the risk of a major congenital malformation jumped to more than 11%.

“We have a signal for an increased risk for polytherapy including valproate,” she said, although “it's unclear whether valproate is responsible for this increased risk.”

Dr. Meador noted, however, that six other studies have concluded that valproate significantly increases the risk of birth defects.

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“Both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads to them recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. And once there, if any lesions are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin, of the University of California, San Francisco, drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked them to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, Dr. Lin drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county. The PCPs and cardiologists were interviewed separately to encourage frank discussion.

The discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy.

One of the cases was that of a 45-year-old man with a family history of myocardial infarction. He worked out three times a week and was asymptomatic. However, his wife was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745. His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians ended up recommending PCI for all three of the case-study patients, even though they acknowledged that no clinical evidence suggested the procedure would be more beneficial than medical therapy.

Several major themes emerged from the physician discussions: They felt guilt over the possibility of missing a lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt was a particularly strong motivator for more tests and interventions. One PCP summed this when he said: “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist echoed that view: “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“I think it demonstrates the tendency of physicians to look for solutions based on action,” said Dr. Lin.

In addition, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. “We know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors,” said one cardiologist. “Nonetheless, when that patient leaves with an open artery, that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both PCPs and cardiologists said their patients expected testing regardless of what [the caregivers] thought of it.”

Concerns about medicolegal liability also strongly influenced the decision making. “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued,” said one PCP.

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said.

As the study shows, physicians tend to look for action-based solutions, Dr. Grace Lin said. Michele G. Sullivan/Elsevier Global Medical News

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“Both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads to them recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. And once there, if any lesions are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin, of the University of California, San Francisco, drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked them to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, Dr. Lin drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county. The PCPs and cardiologists were interviewed separately to encourage frank discussion.

The discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy.

One of the cases was that of a 45-year-old man with a family history of myocardial infarction. He worked out three times a week and was asymptomatic. However, his wife was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745. His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians ended up recommending PCI for all three of the case-study patients, even though they acknowledged that no clinical evidence suggested the procedure would be more beneficial than medical therapy.

Several major themes emerged from the physician discussions: They felt guilt over the possibility of missing a lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt was a particularly strong motivator for more tests and interventions. One PCP summed this when he said: “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist echoed that view: “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“I think it demonstrates the tendency of physicians to look for solutions based on action,” said Dr. Lin.

In addition, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. “We know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors,” said one cardiologist. “Nonetheless, when that patient leaves with an open artery, that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both PCPs and cardiologists said their patients expected testing regardless of what [the caregivers] thought of it.”

Concerns about medicolegal liability also strongly influenced the decision making. “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued,” said one PCP.

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said.

As the study shows, physicians tend to look for action-based solutions, Dr. Grace Lin said. Michele G. Sullivan/Elsevier Global Medical News

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“Both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads to them recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. And once there, if any lesions are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin, of the University of California, San Francisco, drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked them to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, Dr. Lin drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county. The PCPs and cardiologists were interviewed separately to encourage frank discussion.

The discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy.

One of the cases was that of a 45-year-old man with a family history of myocardial infarction. He worked out three times a week and was asymptomatic. However, his wife was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745. His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians ended up recommending PCI for all three of the case-study patients, even though they acknowledged that no clinical evidence suggested the procedure would be more beneficial than medical therapy.

Several major themes emerged from the physician discussions: They felt guilt over the possibility of missing a lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt was a particularly strong motivator for more tests and interventions. One PCP summed this when he said: “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist echoed that view: “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“I think it demonstrates the tendency of physicians to look for solutions based on action,” said Dr. Lin.

In addition, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. “We know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors,” said one cardiologist. “Nonetheless, when that patient leaves with an open artery, that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both PCPs and cardiologists said their patients expected testing regardless of what [the caregivers] thought of it.”

Concerns about medicolegal liability also strongly influenced the decision making. “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued,” said one PCP.

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said.

As the study shows, physicians tend to look for action-based solutions, Dr. Grace Lin said. Michele G. Sullivan/Elsevier Global Medical News

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“It appears that both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads them to recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. Once there, if any lesions at all are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked the participants to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, she drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county.

“We also interviewed PCPs and cardiologists separately, to encourage frank discussion,” said Dr. Lin of the University of California, San Francisco.

Group discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy. She described one of the cases: a 45-year-old male with a family history of myocardial infarction. The patient worked out three times each week and was asymptomatic. His wife, however, was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745.

His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians in each group ended up recommending PCI for all three of the hypothetical patients, Dr. Lin said—despite their acknowledgement that no clinical evidence supported the procedure as more beneficial than medical therapy in either the short or long term.

Several major themes emerged from the physician discussions: guilt over the possibility of missing a potentially lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt arising from a missed lesion was a particularly strong motivator for more tests and interventions. One PCP spoke quite eloquently of this, Dr. Lin said. “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist expressed a similar view. Despite the data suggesting that PCI is no better than medical therapy for these patients, “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“This belief was shared by most of the physicians in our groups,” Dr. Lin said. “I think it demonstrates the tendency of physicians to look for solutions based on action.”

Interestingly, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. According to one cardiologist, “I think we know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors. But nonetheless, when that patient leaves with an open artery—that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both our PCPs and cardiologists said their patients expected testing regardless of what they themselves thought of it.”

One cardiologist put it this way: “If the patient is worried enough to come in and see me, we need to do this testing to reassure him.”

Concerns about medicolegal liability also strongly influenced the decision making. A PCP noted, “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued. With a jury of laypeople, it's hard to justify not stenting despite the evidence, and because of that it's hard to just treat medically and not be afraid of a lawsuit.”

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said, citing a PCP who referred to the hypothetical patient's elevated calcium load. “This guy's wife has bought him much more than a scan—she has bought him an entrée to the whole garden path of testing. Any equivocal test and he's ending up in the cath lab.”

“This demonstrates that once a patient has any positive screen, it's very difficult to prevent a referral to a cardiologist and eventually, to the cath lab,” Dr. Lin said. “Once he reaches there, the cardiologists told us that if any amenable lesion is found, that person is almost certain to get a PCI.”

The culture of the catheterization lab also plays into this inevitable progression. A cardiologist explained, “By this time the die is cast. In our practice, where we don't get paid per procedure, we would have difficulty getting out of the lab because the cath lab staff wouldn't let us out unless we did something with that lesion.”

The cascade of emotion and worry is what appears to drive the patient with stable CAD to a PCI, Dr. Lin said. Even considering the possible complications of the procedure and the evidence that it probably yields no additional benefit wasn't enough to sway physicians to medical therapy alone.

“One cardiologist put it like this,” she said. “'If you do the procedure and there's a complication, that's a complication. But if you don't do it and there's an event—that's a mistake.'”

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“It appears that both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads them to recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. Once there, if any lesions at all are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked the participants to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, she drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county.

“We also interviewed PCPs and cardiologists separately, to encourage frank discussion,” said Dr. Lin of the University of California, San Francisco.

Group discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy. She described one of the cases: a 45-year-old male with a family history of myocardial infarction. The patient worked out three times each week and was asymptomatic. His wife, however, was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745.

His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians in each group ended up recommending PCI for all three of the hypothetical patients, Dr. Lin said—despite their acknowledgement that no clinical evidence supported the procedure as more beneficial than medical therapy in either the short or long term.

Several major themes emerged from the physician discussions: guilt over the possibility of missing a potentially lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt arising from a missed lesion was a particularly strong motivator for more tests and interventions. One PCP spoke quite eloquently of this, Dr. Lin said. “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist expressed a similar view. Despite the data suggesting that PCI is no better than medical therapy for these patients, “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“This belief was shared by most of the physicians in our groups,” Dr. Lin said. “I think it demonstrates the tendency of physicians to look for solutions based on action.”

Interestingly, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. According to one cardiologist, “I think we know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors. But nonetheless, when that patient leaves with an open artery—that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both our PCPs and cardiologists said their patients expected testing regardless of what they themselves thought of it.”

One cardiologist put it this way: “If the patient is worried enough to come in and see me, we need to do this testing to reassure him.”

Concerns about medicolegal liability also strongly influenced the decision making. A PCP noted, “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued. With a jury of laypeople, it's hard to justify not stenting despite the evidence, and because of that it's hard to just treat medically and not be afraid of a lawsuit.”

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said, citing a PCP who referred to the hypothetical patient's elevated calcium load. “This guy's wife has bought him much more than a scan—she has bought him an entrée to the whole garden path of testing. Any equivocal test and he's ending up in the cath lab.”

“This demonstrates that once a patient has any positive screen, it's very difficult to prevent a referral to a cardiologist and eventually, to the cath lab,” Dr. Lin said. “Once he reaches there, the cardiologists told us that if any amenable lesion is found, that person is almost certain to get a PCI.”

The culture of the catheterization lab also plays into this inevitable progression. A cardiologist explained, “By this time the die is cast. In our practice, where we don't get paid per procedure, we would have difficulty getting out of the lab because the cath lab staff wouldn't let us out unless we did something with that lesion.”

The cascade of emotion and worry is what appears to drive the patient with stable CAD to a PCI, Dr. Lin said. Even considering the possible complications of the procedure and the evidence that it probably yields no additional benefit wasn't enough to sway physicians to medical therapy alone.

“One cardiologist put it like this,” she said. “'If you do the procedure and there's a complication, that's a complication. But if you don't do it and there's an event—that's a mistake.'”

WASHINGTON — When it comes to recommending angioplasty for stable coronary artery disease, evidence can take a backseat to worry, guilt, and the fear of legal liability.

“It appears that both cardiologists and primary care physicians [PCPs] have trouble balancing these psychological and emotional factors with scientific evidence in decision making, and this leads them to recommending more tests and procedures,” which eventually culminate in a trip to the cardiac catheterization lab, Dr. Grace Lin said at a conference sponsored by the American Heart Association. Once there, if any lesions at all are identified, “the die is cast” for percutaneous coronary intervention (PCI), she said.

Dr. Lin drew these conclusions from a series of six focus-group meetings she held with 28 primary care providers and 20 cardiologists (13 interventional and 7 noninterventional). She presented each group with three case scenarios based on actual patients with symptoms of stable coronary artery disease (CAD), and asked the participants to describe how they would arrive at a treatment recommendation.

All of the physicians lived in California; their mean duration of practice was 17 years. To help identify any regional differences, she drew one-third from San Francisco, one-third from the city's suburbs, and one-third from a rural county.

“We also interviewed PCPs and cardiologists separately, to encourage frank discussion,” said Dr. Lin of the University of California, San Francisco.

Group discussions were set around three case scenarios representing minimally symptomatic or asymptomatic patients for whom the current evidence shows no benefit of PCI over optimal medical therapy. She described one of the cases: a 45-year-old male with a family history of myocardial infarction. The patient worked out three times each week and was asymptomatic. His wife, however, was worried about his family history and bought him a coronary calcium scan for his birthday. The scan showed a calcium score of 745.

His stress test showed ST-segment depressions of 1–2 mm. A catheterization revealed a tight lesion in the left anterior descending artery.

Dr. Lin asked the group to discuss a range of recommendations, from reassurance and risk reduction interventions to medical therapy, PCI, and coronary artery bypass grafting.

All of the physicians in each group ended up recommending PCI for all three of the hypothetical patients, Dr. Lin said—despite their acknowledgement that no clinical evidence supported the procedure as more beneficial than medical therapy in either the short or long term.

Several major themes emerged from the physician discussions: guilt over the possibility of missing a potentially lethal lesion, patient expectation of testing and intervention, and liability fears.

The fear of guilt arising from a missed lesion was a particularly strong motivator for more tests and interventions. One PCP spoke quite eloquently of this, Dr. Lin said. “I had a healthy 42-year-old who dropped dead while jogging. I'm always afraid of missing that widow-maker lesion.”

A cardiologist expressed a similar view. Despite the data suggesting that PCI is no better than medical therapy for these patients, “I don't think you can ignore a lesion, because then, if something happens, it's your fault.”

“This belief was shared by most of the physicians in our groups,” Dr. Lin said. “I think it demonstrates the tendency of physicians to look for solutions based on action.”

Interestingly, the participants stuck to their recommendations despite their intellectual understanding of the clinical evidence. According to one cardiologist, “I think we know we are not necessarily preventing heart attacks by treating asymptomatic stenosis with PCI. We are going to prevent future heart attacks with lipid-lowering drugs, aspirin, and ACE inhibitors. But nonetheless, when that patient leaves with an open artery—that is the best that my interventional partners can deliver.”

Physicians aren't alone in wanting some concrete action in these cases, Dr Lin said. “Patient expectations are a frequent reason for testing. Both our PCPs and cardiologists said their patients expected testing regardless of what they themselves thought of it.”

One cardiologist put it this way: “If the patient is worried enough to come in and see me, we need to do this testing to reassure him.”

Concerns about medicolegal liability also strongly influenced the decision making. A PCP noted, “We all would feel more comfortable treating more patients medically if we weren't afraid of being sued. With a jury of laypeople, it's hard to justify not stenting despite the evidence, and because of that it's hard to just treat medically and not be afraid of a lawsuit.”

Again, Dr Lin observed, physicians felt very strongly about this despite evidence to the contrary. “There are no data linking additional testing with fewer lawsuits.”

All of these factors “culminate in a cascade effect where screening leads to more testing and eventually to the cath lab,” she said, citing a PCP who referred to the hypothetical patient's elevated calcium load. “This guy's wife has bought him much more than a scan—she has bought him an entrée to the whole garden path of testing. Any equivocal test and he's ending up in the cath lab.”

“This demonstrates that once a patient has any positive screen, it's very difficult to prevent a referral to a cardiologist and eventually, to the cath lab,” Dr. Lin said. “Once he reaches there, the cardiologists told us that if any amenable lesion is found, that person is almost certain to get a PCI.”

The culture of the catheterization lab also plays into this inevitable progression. A cardiologist explained, “By this time the die is cast. In our practice, where we don't get paid per procedure, we would have difficulty getting out of the lab because the cath lab staff wouldn't let us out unless we did something with that lesion.”

The cascade of emotion and worry is what appears to drive the patient with stable CAD to a PCI, Dr. Lin said. Even considering the possible complications of the procedure and the evidence that it probably yields no additional benefit wasn't enough to sway physicians to medical therapy alone.

“One cardiologist put it like this,” she said. “'If you do the procedure and there's a complication, that's a complication. But if you don't do it and there's an event—that's a mistake.'”

ORLANDO — Laparoscopic uterine artery occlusion is an effective way to manage patients with symptomatic fibroids, and may offer better outcomes than uterine artery embolization for women desiring pregnancy after the surgery, Dr. Zdenek Holub said at a meeting on laparoscopy and minimally invasive surgery.

In a prospective follow-up study, Dr. Holub found only a 9% miscarriage rate among women who became pregnant after the procedure.

That compares very favorably with the 14% rate he and his colleagues found in a previous study they performed of uterine artery embolization for symptomatic fibroids, he said.

The laparoscopic occlusion study included 161 women (mean age 37 years). All of them had one to three symptomatic fibroids with a mean size of 6 cm. The mean follow-up time was 34 months, with postoperative visits at 3, 6, and 12 months, followed by yearly visits.

The mean operative time was 35 minutes, and patients had minimal blood loss, said Dr. Holub, chairman of obstetrics and gynecology at the Baby Friendly Hospital in Kladno, Czech Republic.

Postoperative complications occurred in 11 patients, and included port-site bleeding, hemorrhage, fever, and fibroid necrosis. There were no life-threatening complications.

At 12 months' follow-up, the mean reduction in fibroid volume was 56%, with the size of the dominant fibroid reduced by a mean of 72%. At 34 months, 87% of the group was without fibroid recurrence.

Sixty-three patients desired pregnancy after their surgery. A total of 32 pregnancies occurred; 29 women conceived naturally. There were three miscarriages (9%).

The preterm delivery rate was 10%, and 50% of the babies were delivered by cesarean section

“Our miscarriage rate was significantly lower than the rate we see associated with uterine artery embolization in the literature,” said Dr. Holub at the meeting sponsored by the Society of Laparoendoscopic Surgeons. “In a control group of women who got embolization at our hospital, we had a 14% miscarriage rate.”

A more detailed account of the study has been published (Int. J. Gynaecol. Obstet. 2007;1:44–5).

ORLANDO — Laparoscopic uterine artery occlusion is an effective way to manage patients with symptomatic fibroids, and may offer better outcomes than uterine artery embolization for women desiring pregnancy after the surgery, Dr. Zdenek Holub said at a meeting on laparoscopy and minimally invasive surgery.

In a prospective follow-up study, Dr. Holub found only a 9% miscarriage rate among women who became pregnant after the procedure.

That compares very favorably with the 14% rate he and his colleagues found in a previous study they performed of uterine artery embolization for symptomatic fibroids, he said.

The laparoscopic occlusion study included 161 women (mean age 37 years). All of them had one to three symptomatic fibroids with a mean size of 6 cm. The mean follow-up time was 34 months, with postoperative visits at 3, 6, and 12 months, followed by yearly visits.

The mean operative time was 35 minutes, and patients had minimal blood loss, said Dr. Holub, chairman of obstetrics and gynecology at the Baby Friendly Hospital in Kladno, Czech Republic.

Postoperative complications occurred in 11 patients, and included port-site bleeding, hemorrhage, fever, and fibroid necrosis. There were no life-threatening complications.

At 12 months' follow-up, the mean reduction in fibroid volume was 56%, with the size of the dominant fibroid reduced by a mean of 72%. At 34 months, 87% of the group was without fibroid recurrence.

Sixty-three patients desired pregnancy after their surgery. A total of 32 pregnancies occurred; 29 women conceived naturally. There were three miscarriages (9%).

The preterm delivery rate was 10%, and 50% of the babies were delivered by cesarean section

“Our miscarriage rate was significantly lower than the rate we see associated with uterine artery embolization in the literature,” said Dr. Holub at the meeting sponsored by the Society of Laparoendoscopic Surgeons. “In a control group of women who got embolization at our hospital, we had a 14% miscarriage rate.”

A more detailed account of the study has been published (Int. J. Gynaecol. Obstet. 2007;1:44–5).

ORLANDO — Laparoscopic uterine artery occlusion is an effective way to manage patients with symptomatic fibroids, and may offer better outcomes than uterine artery embolization for women desiring pregnancy after the surgery, Dr. Zdenek Holub said at a meeting on laparoscopy and minimally invasive surgery.

In a prospective follow-up study, Dr. Holub found only a 9% miscarriage rate among women who became pregnant after the procedure.

That compares very favorably with the 14% rate he and his colleagues found in a previous study they performed of uterine artery embolization for symptomatic fibroids, he said.

The laparoscopic occlusion study included 161 women (mean age 37 years). All of them had one to three symptomatic fibroids with a mean size of 6 cm. The mean follow-up time was 34 months, with postoperative visits at 3, 6, and 12 months, followed by yearly visits.

The mean operative time was 35 minutes, and patients had minimal blood loss, said Dr. Holub, chairman of obstetrics and gynecology at the Baby Friendly Hospital in Kladno, Czech Republic.

Postoperative complications occurred in 11 patients, and included port-site bleeding, hemorrhage, fever, and fibroid necrosis. There were no life-threatening complications.

At 12 months' follow-up, the mean reduction in fibroid volume was 56%, with the size of the dominant fibroid reduced by a mean of 72%. At 34 months, 87% of the group was without fibroid recurrence.

Sixty-three patients desired pregnancy after their surgery. A total of 32 pregnancies occurred; 29 women conceived naturally. There were three miscarriages (9%).

The preterm delivery rate was 10%, and 50% of the babies were delivered by cesarean section

“Our miscarriage rate was significantly lower than the rate we see associated with uterine artery embolization in the literature,” said Dr. Holub at the meeting sponsored by the Society of Laparoendoscopic Surgeons. “In a control group of women who got embolization at our hospital, we had a 14% miscarriage rate.”

A more detailed account of the study has been published (Int. J. Gynaecol. Obstet. 2007;1:44–5).

HOT SPRINGS, VA. — Complex aphthosis may be the cause of noninfectious vulvar ulcers in young females, Dr. Judith Burgis said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“When we see vulvar ulcers in these girls, especially after their sexual debut, we tend to immediately think of an infectious etiology like herpes simplex,” said Dr. Burgis, of the department of ob.gyn. at the University of South Carolina, Columbia.

“But the differential diagnosis for these types of lesions is actually quite diverse,” she said.

Dr. Burgis presented a case series of 12 girls, aged 6–16 years, with vulvar ulcers; 11 of the girls were premenarcheal and sexually naive. The one postmenarcheal patient was sexually active. All 12 of the patients had been referred by their pediatricians for management of the ulcers, and many had been told that they had a herpes simplex infection. “This is a very anxiety-provoking diagnosis for both the girl and her parents.”

None of the ulcers was positive for viral, bacterial, or fungal pathogens.

Two girls, both of whom had recurrent oral and genital ulcers, were referred for a rheumatology evaluation with a presumed diagnosis of Behçet's disease.

The ulcers in three other patients had identifiable etiology. An 11-year-old with a several-month history of severe itching and a periclitoral ulcer unresponsive to topical yeast medication had lichen simplex. The large ulcer on a 6-year-old was related to chemotherapy for acute lymphocytic leukemia. Another 11-year-old had myelodysplasia and sacral agenesis; her ulcers were related to incontinence and diaper use.

But the final seven cases had no readily identifiable cause, Dr. Burgis said. Six of these girls were premenarcheal; one was postmenarcheal. Epstein-Barr serology and testing for infections were negative in all of them. There were no reasons to suspect trauma or sexual abuse in any patient, and all other laboratory testing was unrevealing. None of the girls had inflammatory bowel disease or Crohn's disease, both of which can cause vulvar ulcers.

“Since we found no common pathogen and no sign of systemic illness, we concluded the diagnosis was probably complex aphthosis,” Dr. Burgis said. “The etiology is unknown; it may be primary or may be secondary due to a systemic illness, perhaps of viral etiology.”

All these girls had an unremarkable course of recovery over 1–3 weeks, Dr. Burgis said. They were treated with superpotent topical corticosteroids, clobetasol ointment, and 2% topical Xylocaine for pain. Those with an accompanying cellulitis also received antibiotics.

Since we found no common pathogen and no sign of systemic illness, we diagnosed complex aphthosis. DR. BURGIS

None of the ulcers was positive for viral, bacterial, or fungal pathogens. Courtesy Dr. Judith Burgis

HOT SPRINGS, VA. — Complex aphthosis may be the cause of noninfectious vulvar ulcers in young females, Dr. Judith Burgis said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“When we see vulvar ulcers in these girls, especially after their sexual debut, we tend to immediately think of an infectious etiology like herpes simplex,” said Dr. Burgis, of the department of ob.gyn. at the University of South Carolina, Columbia.

“But the differential diagnosis for these types of lesions is actually quite diverse,” she said.

Dr. Burgis presented a case series of 12 girls, aged 6–16 years, with vulvar ulcers; 11 of the girls were premenarcheal and sexually naive. The one postmenarcheal patient was sexually active. All 12 of the patients had been referred by their pediatricians for management of the ulcers, and many had been told that they had a herpes simplex infection. “This is a very anxiety-provoking diagnosis for both the girl and her parents.”

None of the ulcers was positive for viral, bacterial, or fungal pathogens.

Two girls, both of whom had recurrent oral and genital ulcers, were referred for a rheumatology evaluation with a presumed diagnosis of Behçet's disease.

The ulcers in three other patients had identifiable etiology. An 11-year-old with a several-month history of severe itching and a periclitoral ulcer unresponsive to topical yeast medication had lichen simplex. The large ulcer on a 6-year-old was related to chemotherapy for acute lymphocytic leukemia. Another 11-year-old had myelodysplasia and sacral agenesis; her ulcers were related to incontinence and diaper use.

But the final seven cases had no readily identifiable cause, Dr. Burgis said. Six of these girls were premenarcheal; one was postmenarcheal. Epstein-Barr serology and testing for infections were negative in all of them. There were no reasons to suspect trauma or sexual abuse in any patient, and all other laboratory testing was unrevealing. None of the girls had inflammatory bowel disease or Crohn's disease, both of which can cause vulvar ulcers.

“Since we found no common pathogen and no sign of systemic illness, we concluded the diagnosis was probably complex aphthosis,” Dr. Burgis said. “The etiology is unknown; it may be primary or may be secondary due to a systemic illness, perhaps of viral etiology.”

All these girls had an unremarkable course of recovery over 1–3 weeks, Dr. Burgis said. They were treated with superpotent topical corticosteroids, clobetasol ointment, and 2% topical Xylocaine for pain. Those with an accompanying cellulitis also received antibiotics.

Since we found no common pathogen and no sign of systemic illness, we diagnosed complex aphthosis. DR. BURGIS

None of the ulcers was positive for viral, bacterial, or fungal pathogens. Courtesy Dr. Judith Burgis

HOT SPRINGS, VA. — Complex aphthosis may be the cause of noninfectious vulvar ulcers in young females, Dr. Judith Burgis said at the annual meeting of the South Atlantic Association of Obstetricians and Gynecologists.

“When we see vulvar ulcers in these girls, especially after their sexual debut, we tend to immediately think of an infectious etiology like herpes simplex,” said Dr. Burgis, of the department of ob.gyn. at the University of South Carolina, Columbia.

“But the differential diagnosis for these types of lesions is actually quite diverse,” she said.

Dr. Burgis presented a case series of 12 girls, aged 6–16 years, with vulvar ulcers; 11 of the girls were premenarcheal and sexually naive. The one postmenarcheal patient was sexually active. All 12 of the patients had been referred by their pediatricians for management of the ulcers, and many had been told that they had a herpes simplex infection. “This is a very anxiety-provoking diagnosis for both the girl and her parents.”

None of the ulcers was positive for viral, bacterial, or fungal pathogens.

Two girls, both of whom had recurrent oral and genital ulcers, were referred for a rheumatology evaluation with a presumed diagnosis of Behçet's disease.

The ulcers in three other patients had identifiable etiology. An 11-year-old with a several-month history of severe itching and a periclitoral ulcer unresponsive to topical yeast medication had lichen simplex. The large ulcer on a 6-year-old was related to chemotherapy for acute lymphocytic leukemia. Another 11-year-old had myelodysplasia and sacral agenesis; her ulcers were related to incontinence and diaper use.

But the final seven cases had no readily identifiable cause, Dr. Burgis said. Six of these girls were premenarcheal; one was postmenarcheal. Epstein-Barr serology and testing for infections were negative in all of them. There were no reasons to suspect trauma or sexual abuse in any patient, and all other laboratory testing was unrevealing. None of the girls had inflammatory bowel disease or Crohn's disease, both of which can cause vulvar ulcers.

“Since we found no common pathogen and no sign of systemic illness, we concluded the diagnosis was probably complex aphthosis,” Dr. Burgis said. “The etiology is unknown; it may be primary or may be secondary due to a systemic illness, perhaps of viral etiology.”

All these girls had an unremarkable course of recovery over 1–3 weeks, Dr. Burgis said. They were treated with superpotent topical corticosteroids, clobetasol ointment, and 2% topical Xylocaine for pain. Those with an accompanying cellulitis also received antibiotics.

Since we found no common pathogen and no sign of systemic illness, we diagnosed complex aphthosis. DR. BURGIS

None of the ulcers was positive for viral, bacterial, or fungal pathogens. Courtesy Dr. Judith Burgis

SAN ANTONIO — Monthly ibandronate appears to prevent, and perhaps even reverse, bone loss in women who are taking anastrozole for estrogen receptor-positive breast cancers, Dr. J.E. Lester reported in a poster presentation at the Sixth International Meeting on Cancer-Induced Bone Disease.

While she said that further follow-up is required, her randomized placebo-controlled trial showed that after 1 year, women taking the bisphosphonate showed a significant increase in bone mineral density (BMD) at both the hip and spine, while those taking the placebo experienced a significant decrease at both sites.

Dr. Lester, of the Cancer Research Centre of Weston Park Hospital, Sheffield, England, examined ibandronate's effects in 131 postmenopausal women who had estrogen receptor-positive breast cancer.

The women were grouped according to baseline BMD: 68 had normal BMD (mean age 63 years), 50 were osteopenic (mean age 67 years), and 13 were osteoporotic (mean age 71 years).

All patients were taking calcium and vitamin D supplements in addition to anastrozole. Those with normal BMD continued on the supplements.

Osteopenic patients were randomized to either 150 mg oral ibandronate every 28 days (25 patients) or placebo (25 patients). All osteoporotic women received the same monthly ibandronate treatment.

Ibandronate significantly increased BMD at the hip and spine in both treated groups. At 1 year, osteopenic women had a mean increase of 2.8% at the lumbar spine and 1.4% at the hip. After 1 year, five of the previously osteopenic women were found to have normal BMD.

Women in the placebo group had a decrease of BMD at both sites (mean -2.6% at the lumbar spine and −2.3% at the hip).

During the blinded period, two osteopenic patients lost more than 10% of their BMD at either the spine or hip. They were withdrawn from the study and unblinded; both had been taking the placebo and both were offered open-label ibandronate.

Among the osteoporotic women, the mean increase in BMD was 2.6% at the lumbar spine and 2.6% at the hip. Seven previously osteoporotic patients were found to be osteopenic at 1-year follow-up.

Of the 68 women with initially normal BMD who had not been treated with ibandronate, 20 were followed for 2 years.

Follow-up scans showed a mean decrease in BMD of −4% at the lumbar spine and −3% at the hip.

Despite these changes, however, none of the women who had not been treated with idandronate developed osteoporosis.

ELSEVIER GLOBAL MEDICAL NEWS

SAN ANTONIO — Monthly ibandronate appears to prevent, and perhaps even reverse, bone loss in women who are taking anastrozole for estrogen receptor-positive breast cancers, Dr. J.E. Lester reported in a poster presentation at the Sixth International Meeting on Cancer-Induced Bone Disease.

While she said that further follow-up is required, her randomized placebo-controlled trial showed that after 1 year, women taking the bisphosphonate showed a significant increase in bone mineral density (BMD) at both the hip and spine, while those taking the placebo experienced a significant decrease at both sites.

Dr. Lester, of the Cancer Research Centre of Weston Park Hospital, Sheffield, England, examined ibandronate's effects in 131 postmenopausal women who had estrogen receptor-positive breast cancer.

The women were grouped according to baseline BMD: 68 had normal BMD (mean age 63 years), 50 were osteopenic (mean age 67 years), and 13 were osteoporotic (mean age 71 years).

All patients were taking calcium and vitamin D supplements in addition to anastrozole. Those with normal BMD continued on the supplements.

Osteopenic patients were randomized to either 150 mg oral ibandronate every 28 days (25 patients) or placebo (25 patients). All osteoporotic women received the same monthly ibandronate treatment.

Ibandronate significantly increased BMD at the hip and spine in both treated groups. At 1 year, osteopenic women had a mean increase of 2.8% at the lumbar spine and 1.4% at the hip. After 1 year, five of the previously osteopenic women were found to have normal BMD.

Women in the placebo group had a decrease of BMD at both sites (mean -2.6% at the lumbar spine and −2.3% at the hip).

During the blinded period, two osteopenic patients lost more than 10% of their BMD at either the spine or hip. They were withdrawn from the study and unblinded; both had been taking the placebo and both were offered open-label ibandronate.

Among the osteoporotic women, the mean increase in BMD was 2.6% at the lumbar spine and 2.6% at the hip. Seven previously osteoporotic patients were found to be osteopenic at 1-year follow-up.

Of the 68 women with initially normal BMD who had not been treated with ibandronate, 20 were followed for 2 years.

Follow-up scans showed a mean decrease in BMD of −4% at the lumbar spine and −3% at the hip.

Despite these changes, however, none of the women who had not been treated with idandronate developed osteoporosis.

ELSEVIER GLOBAL MEDICAL NEWS

SAN ANTONIO — Monthly ibandronate appears to prevent, and perhaps even reverse, bone loss in women who are taking anastrozole for estrogen receptor-positive breast cancers, Dr. J.E. Lester reported in a poster presentation at the Sixth International Meeting on Cancer-Induced Bone Disease.

While she said that further follow-up is required, her randomized placebo-controlled trial showed that after 1 year, women taking the bisphosphonate showed a significant increase in bone mineral density (BMD) at both the hip and spine, while those taking the placebo experienced a significant decrease at both sites.

Dr. Lester, of the Cancer Research Centre of Weston Park Hospital, Sheffield, England, examined ibandronate's effects in 131 postmenopausal women who had estrogen receptor-positive breast cancer.

The women were grouped according to baseline BMD: 68 had normal BMD (mean age 63 years), 50 were osteopenic (mean age 67 years), and 13 were osteoporotic (mean age 71 years).

All patients were taking calcium and vitamin D supplements in addition to anastrozole. Those with normal BMD continued on the supplements.

Osteopenic patients were randomized to either 150 mg oral ibandronate every 28 days (25 patients) or placebo (25 patients). All osteoporotic women received the same monthly ibandronate treatment.

Ibandronate significantly increased BMD at the hip and spine in both treated groups. At 1 year, osteopenic women had a mean increase of 2.8% at the lumbar spine and 1.4% at the hip. After 1 year, five of the previously osteopenic women were found to have normal BMD.

Women in the placebo group had a decrease of BMD at both sites (mean -2.6% at the lumbar spine and −2.3% at the hip).

During the blinded period, two osteopenic patients lost more than 10% of their BMD at either the spine or hip. They were withdrawn from the study and unblinded; both had been taking the placebo and both were offered open-label ibandronate.

Among the osteoporotic women, the mean increase in BMD was 2.6% at the lumbar spine and 2.6% at the hip. Seven previously osteoporotic patients were found to be osteopenic at 1-year follow-up.

Of the 68 women with initially normal BMD who had not been treated with ibandronate, 20 were followed for 2 years.

Follow-up scans showed a mean decrease in BMD of −4% at the lumbar spine and −3% at the hip.

Despite these changes, however, none of the women who had not been treated with idandronate developed osteoporosis.

ELSEVIER GLOBAL MEDICAL NEWS

RIVIERA MAYA, MEXICO — Expect the unexpected during a fetal ultrasound exam, and if you find it, be kind but unambiguous in describing your observations and concerns.

“The ambiguity we sometimes use to try and soften what we are saying doesn't change the message, but it can change the interpretation,” Dr. Nancy Chescheir said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“If there is no fetal heart activity, tell the patient her baby's heart is not beating and that the fetus has died. If you see findings suggestive of a fetal anomaly, describe exactly what you see, express your concern, and refer the patient to an expert as quickly as possible,” said Dr. Chescheir, the Betty and Lonnie S. Burnett Professor of obstetrics and gynecology at Vanderbilt University, Nashville, Tenn.

Many diagnoses of fetal demise or anomaly will be discovered during a detailed anatomic scan ordered on the basis of some increased risk, including a poor past pregnancy outcome, family history of genetic disorders, or abnormal early biomarker studies. In these cases, the patient probably already has an idea that there may be a serious problem.

“The patient is already suspicious. They watch the ultrasound; they may have had scans before, and they know what fetal heart activity looks like. If you are certain of the diagnosis of fetal demise, be very kind, do it in private, but be unambiguous about what you are seeing.”

In cases of uncertainty, the 5–10–20 rules can be a help, Dr. Chescheir said. “If you have a 5-mm crown-rump length, you have to see a heartbeat or you have a dead baby. There's no need to have her come back in 48 hours for a repeat scan or to do hormone levels.”

If the fetus measures only 4.5 mm from crown to rump, however, you should ask the woman to come back for a repeat scan when you anticipate a length of 5 mm. “You will probably have to wait at least 3 days to see this growth. If at that time, you have a 5-mm length and still no heartbeat, make the diagnosis and get on with your therapeutic options.”

For a gestational sac with a mean diameter of 10 mm, you must see a yolk sac; if you don't, the pregnancy is not viable. Similarly, for a 20-mm mean gestational sac, you must see a fetal pole. The absence of one means the pregnancy is not viable, Dr. Chescheir said at the meeting, which was sponsored by Boston University.

Surveys about patient satisfaction with fetal ultrasound diagnosis agree on one thing, Dr. Chescheir said: Women don't appreciate the delay between the moment a problem is identified and the moment the doctor communicates the problem.

“They really don't like it if the sonographer is not allowed to say anything during the exam,” Dr. Chescheir said. “If the sonographer is fairly certain about a fetal demise, she should be able to say something. You may not want her making the diagnosis, but she should be allowed to tell the patient something.”

Having very clear office procedures can avert problems in this area, she said.

RIVIERA MAYA, MEXICO — Expect the unexpected during a fetal ultrasound exam, and if you find it, be kind but unambiguous in describing your observations and concerns.

“The ambiguity we sometimes use to try and soften what we are saying doesn't change the message, but it can change the interpretation,” Dr. Nancy Chescheir said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“If there is no fetal heart activity, tell the patient her baby's heart is not beating and that the fetus has died. If you see findings suggestive of a fetal anomaly, describe exactly what you see, express your concern, and refer the patient to an expert as quickly as possible,” said Dr. Chescheir, the Betty and Lonnie S. Burnett Professor of obstetrics and gynecology at Vanderbilt University, Nashville, Tenn.

Many diagnoses of fetal demise or anomaly will be discovered during a detailed anatomic scan ordered on the basis of some increased risk, including a poor past pregnancy outcome, family history of genetic disorders, or abnormal early biomarker studies. In these cases, the patient probably already has an idea that there may be a serious problem.

“The patient is already suspicious. They watch the ultrasound; they may have had scans before, and they know what fetal heart activity looks like. If you are certain of the diagnosis of fetal demise, be very kind, do it in private, but be unambiguous about what you are seeing.”

In cases of uncertainty, the 5–10–20 rules can be a help, Dr. Chescheir said. “If you have a 5-mm crown-rump length, you have to see a heartbeat or you have a dead baby. There's no need to have her come back in 48 hours for a repeat scan or to do hormone levels.”

If the fetus measures only 4.5 mm from crown to rump, however, you should ask the woman to come back for a repeat scan when you anticipate a length of 5 mm. “You will probably have to wait at least 3 days to see this growth. If at that time, you have a 5-mm length and still no heartbeat, make the diagnosis and get on with your therapeutic options.”

For a gestational sac with a mean diameter of 10 mm, you must see a yolk sac; if you don't, the pregnancy is not viable. Similarly, for a 20-mm mean gestational sac, you must see a fetal pole. The absence of one means the pregnancy is not viable, Dr. Chescheir said at the meeting, which was sponsored by Boston University.

Surveys about patient satisfaction with fetal ultrasound diagnosis agree on one thing, Dr. Chescheir said: Women don't appreciate the delay between the moment a problem is identified and the moment the doctor communicates the problem.

“They really don't like it if the sonographer is not allowed to say anything during the exam,” Dr. Chescheir said. “If the sonographer is fairly certain about a fetal demise, she should be able to say something. You may not want her making the diagnosis, but she should be allowed to tell the patient something.”

Having very clear office procedures can avert problems in this area, she said.

RIVIERA MAYA, MEXICO — Expect the unexpected during a fetal ultrasound exam, and if you find it, be kind but unambiguous in describing your observations and concerns.

“The ambiguity we sometimes use to try and soften what we are saying doesn't change the message, but it can change the interpretation,” Dr. Nancy Chescheir said at a conference on obstetrics, gynecology, perinatal medicine, neonatology, and the law.

“If there is no fetal heart activity, tell the patient her baby's heart is not beating and that the fetus has died. If you see findings suggestive of a fetal anomaly, describe exactly what you see, express your concern, and refer the patient to an expert as quickly as possible,” said Dr. Chescheir, the Betty and Lonnie S. Burnett Professor of obstetrics and gynecology at Vanderbilt University, Nashville, Tenn.

Many diagnoses of fetal demise or anomaly will be discovered during a detailed anatomic scan ordered on the basis of some increased risk, including a poor past pregnancy outcome, family history of genetic disorders, or abnormal early biomarker studies. In these cases, the patient probably already has an idea that there may be a serious problem.

“The patient is already suspicious. They watch the ultrasound; they may have had scans before, and they know what fetal heart activity looks like. If you are certain of the diagnosis of fetal demise, be very kind, do it in private, but be unambiguous about what you are seeing.”

In cases of uncertainty, the 5–10–20 rules can be a help, Dr. Chescheir said. “If you have a 5-mm crown-rump length, you have to see a heartbeat or you have a dead baby. There's no need to have her come back in 48 hours for a repeat scan or to do hormone levels.”

If the fetus measures only 4.5 mm from crown to rump, however, you should ask the woman to come back for a repeat scan when you anticipate a length of 5 mm. “You will probably have to wait at least 3 days to see this growth. If at that time, you have a 5-mm length and still no heartbeat, make the diagnosis and get on with your therapeutic options.”

For a gestational sac with a mean diameter of 10 mm, you must see a yolk sac; if you don't, the pregnancy is not viable. Similarly, for a 20-mm mean gestational sac, you must see a fetal pole. The absence of one means the pregnancy is not viable, Dr. Chescheir said at the meeting, which was sponsored by Boston University.

Surveys about patient satisfaction with fetal ultrasound diagnosis agree on one thing, Dr. Chescheir said: Women don't appreciate the delay between the moment a problem is identified and the moment the doctor communicates the problem.

“They really don't like it if the sonographer is not allowed to say anything during the exam,” Dr. Chescheir said. “If the sonographer is fairly certain about a fetal demise, she should be able to say something. You may not want her making the diagnosis, but she should be allowed to tell the patient something.”

Having very clear office procedures can avert problems in this area, she said.