Cardiology

Discovery of substantial atrial fibrillation (AFib) is usually an indication to start oral anticoagulation (OAC) for stroke prevention, but it’s far from settled whether such AFib is actually a direct cause of thromboembolic stroke. And that has implications for whether patients with occasional bouts of the arrhythmia need to be on continuous OAC.  

It’s possible that some with infrequent paroxysmal AFib can get away with OAC maintained only about as long as the arrhythmia persists, and then go off the drugs, say researchers based on their study, which, they caution, would need the support of prospective trials before such a strategy could be considered.

But importantly, in their patients who had been continuously monitored by their cardiac implantable electronic devices (CIEDs) prior to experiencing a stroke, the 30-day risk of that stroke more than tripled if their AFib burden on 1 day reached at least 5-6 hours. The risk jumped especially high within the first few days after accumulating that amount of AFib in a day, but then fell off sharply over the next few days.

Based on the study, “Your risk of stroke goes up acutely when you have an episode of AFib, and it decreases rapidly, back to baseline – certainly by 30 days and it looked like in our data by 5 days,” Daniel E. Singer, MD, of Massachusetts General Hospital, Boston, said in an interview.

Increasingly, he noted, “there’s a widespread belief that AFib is a risk marker, not a causal risk factor.” In that scenario, most embolic strokes are caused by thrombi formed as a result of an atrial myopathy, characterized by fibrosis and inflammation, that also happens to trigger AFib.

But the current findings are, “from a mechanistic point of view, very much in favor of AFib being a causal risk factor, acutely raising the risk of stroke,” said Dr. Singer, who is lead author on the analysis published online Sept. 29 in JAMA Cardiology.

Some studies have “shown that anticoagulants seem to lower stroke risk even in patients without atrial fib, and even from sources not likely to be coming from the atrium,” Mintu P. Turakhia, MD, of Stanford (Calif.) University, Palo Alto, said in an interview. Collectively they point to “atrial fibrillation as a cause of and a noncausal marker for stroke.”

For example, Dr. Turakhia pointed out in an editorial accompanying the current report that stroke in patients with CIEDs “may occur during prolonged periods of sinus rhythm.”

The current study, he said in an interview, doesn’t preclude atrial myopathy as one direct cause of stroke-associated thrombus, because probably both the myopathy and AFib can be culprits. Still, AFib itself it may bear more responsibility for strokes in patients with fewer competing risks for stroke.

In such patients at lower vascular risk, who may have a CHA2DS2-VASc score of only 1 or 2, for example, “AFib can become a more important cause” of ischemic stroke, Dr. Turakhia said. That’s when AFib is more likely to be temporally related to stroke as the likely culprit, the mechanism addressed by Dr. Singer and associates.

“I think we’re all trying to grapple with what the truth is,” Dr. Singer observed. Still, the current study was unusual for primarily looking at the temporal relationship between AFib and stroke, rather than stroke risk. “And once again, as we found in our earlier study, but now a much larger study, it’s a tight relationship.”

Based on the current results, he said, the risk is “high when you have AFib, and it decreases very rapidly after the AFib is over.” And, “it takes multiple hours of AFib to raise stroke risk.” Inclusion in the analysis required accumulation of at least 5.5 hours of AFib on at least 1 day in a month, the cut point at which stroke risk started to climb significantly in an earlier trial.  

In the current analysis, however, the 30-day odds ratio for stroke was a nonsignificant 2.75 for an AFib burden of 6-23 hours in a day and jumped to a significant 5.0 for a burden in excess of 23 hours in a day. “That’s a lot of AFib” before the risk actually goes up, and supports AFib as causative, Dr. Singer said. If it were the myopathy itself triggering stroke in these particular patients, the risk would be ongoing and not subject to a threshold of AFib burden.
 

Implications for noncontinuous OAC

“The hope is that there are people who have very little AFib: They may have several hours, and then they have nothing for 6 months. Do they have to be anticoagulated or not?” Dr. Singer asked.

“If you believe the risk-marker story, you might say they have to be anticoagulated. But if you believe our results, you would certainly think there’s a good chance they don’t have to be anticoagulated,” he said.

“So it is logical to think, if you have the right people and continuous monitoring, that you could have time-delimited anticoagulation.” That is, patients might start right away on a direct OAC once reaching the AFib threshold in a day, Dr. Singer said, “going on and off anticoagulants in parallel with their episodes of AFib.”

The strategy wouldn’t be feasible in patients who often experience AFib, Dr. Singer noted, “but it might work for people who have infrequent paroxysmal AFib.” It certainly would first have to be tested in prospective trials, he said. Such trials would be more practical than ever to carry out given the growing availability of continuous AFib monitoring by wearables.

“We need a trial to make the case whether it’s safe or not,” Dr. Turakhia said of such a rhythm-guided approach to OAC for AFib. The population to start with, he said, would be patients with paroxysmal AFib and low CHA2DS2-VASc scores. “If you think CHA2DS2-VASc as an integrated score of vascular risk, such patients would have a lot fewer reasons to have strokes. And if they do have a stroke, it’s more reasonable to assume that it’s likely caused by atrial fib and not just a marker.”

Importantly, such a strategy could well be safer than continuous OAC for some patients – those at the lowest vascular risk and with the most occasional AFib and lowest AFib burden “who are otherwise doing fine,” Dr. Turakhia said. In such patients on continuous OAC, he proposed, the risks of bleeding and intracranial hemorrhage could potentially exceed the expected degree of protection from ischemic events.
 

Discordant periods of AFib burden

Dr. Singer and his colleagues linked a national electronic health record database with Medtronic CareLink records covering 10 years to identify 891 patients who experienced an ischemic stroke preceded by at least 120 days of continuous heart-rhythm monitoring.

The patients were then categorized by their pattern of AFib, if any, within each of two prestroke periods: the most recent 30 days, which was the test period, and the preceding 91-120 days, the control period.

The analysis then excluded any patients who reached an AFib-burden threshold of at least 5.5 hours on any day during both the test and control periods, and those who did not attain that threshold in either period.

“The ones who had AFib in both periods mostly had permanent AFib, and ones that didn’t have AFib in either period mostly were in sinus rhythm,” Dr. Singer said. It was “close to 100%” in both cases.

Those exclusions left 66 patients, 7.4% of the total, who reached the AFib-burden threshold on at least 1 day during either the test or control periods, but not both. They included 52 and 14 patients, respectively, with “discordant” periods, that is, at least that burden of AFib in a day during either the test or control period, but not both.

Comparing AFib burden at test versus control periods among patients for whom the two periods were discordant yielded an OR for stroke of 3.71 (95% confidence interval, 2.06-6.70).

Stroke risk levels were not evenly spread throughout the 24-hour periods that met the AFib-burden threshold or the 30 days preceding the patients’ strokes. The OR for stroke was 5.00 (95% CI, 2.62-9.55) during days 1-5 following the day in which the AFib-burden threshold was met. And it was 5.00 (95% CI, 2.08-12.01) over 30 days if the AFib burden exceeded 23 hours on any day of the test period.

The study’s case-crossover design, in which each patient served as their own control, is one of its advantages, Dr. Singer observed. Most patient features, including CHA2DS2-VASc score and comorbidities, did not change appreciably from earliest to the latest 30-day period, which strengthens the comparison of the two because “you don’t have to worry about long-term confounding.”

Dr. Singer was supported by the Eliot B. and Edith C. Shoolman fund of the Massachusetts General Hospital. He discloses receiving grants from Boehringer Ingelheim and Bristol-Myers Squibb; personal fees from Boehringer Ingelheim, Bristol-Myers Squibb, Fitbit, Johnson & Johnson, Merck, and Pfizer; and royalties from UpToDate.

Dr. Turakhia discloses personal fees from Medtronic, Abbott, Sanofi, Pfizer, Myokardia, Johnson & Johnson, Milestone Pharmaceuticals, InCarda Therapeutics, 100Plus, Forward Pharma, and AliveCor; and grants from Bristol-Myers Squibb, the American Heart Association, Apple, and Bayer.

A version of this article first appeared on Medscape.com.

Discovery of substantial atrial fibrillation (AFib) is usually an indication to start oral anticoagulation (OAC) for stroke prevention, but it’s far from settled whether such AFib is actually a direct cause of thromboembolic stroke. And that has implications for whether patients with occasional bouts of the arrhythmia need to be on continuous OAC.  

It’s possible that some with infrequent paroxysmal AFib can get away with OAC maintained only about as long as the arrhythmia persists, and then go off the drugs, say researchers based on their study, which, they caution, would need the support of prospective trials before such a strategy could be considered.

But importantly, in their patients who had been continuously monitored by their cardiac implantable electronic devices (CIEDs) prior to experiencing a stroke, the 30-day risk of that stroke more than tripled if their AFib burden on 1 day reached at least 5-6 hours. The risk jumped especially high within the first few days after accumulating that amount of AFib in a day, but then fell off sharply over the next few days.

Based on the study, “Your risk of stroke goes up acutely when you have an episode of AFib, and it decreases rapidly, back to baseline – certainly by 30 days and it looked like in our data by 5 days,” Daniel E. Singer, MD, of Massachusetts General Hospital, Boston, said in an interview.

Increasingly, he noted, “there’s a widespread belief that AFib is a risk marker, not a causal risk factor.” In that scenario, most embolic strokes are caused by thrombi formed as a result of an atrial myopathy, characterized by fibrosis and inflammation, that also happens to trigger AFib.

But the current findings are, “from a mechanistic point of view, very much in favor of AFib being a causal risk factor, acutely raising the risk of stroke,” said Dr. Singer, who is lead author on the analysis published online Sept. 29 in JAMA Cardiology.

Some studies have “shown that anticoagulants seem to lower stroke risk even in patients without atrial fib, and even from sources not likely to be coming from the atrium,” Mintu P. Turakhia, MD, of Stanford (Calif.) University, Palo Alto, said in an interview. Collectively they point to “atrial fibrillation as a cause of and a noncausal marker for stroke.”

For example, Dr. Turakhia pointed out in an editorial accompanying the current report that stroke in patients with CIEDs “may occur during prolonged periods of sinus rhythm.”

The current study, he said in an interview, doesn’t preclude atrial myopathy as one direct cause of stroke-associated thrombus, because probably both the myopathy and AFib can be culprits. Still, AFib itself it may bear more responsibility for strokes in patients with fewer competing risks for stroke.

In such patients at lower vascular risk, who may have a CHA2DS2-VASc score of only 1 or 2, for example, “AFib can become a more important cause” of ischemic stroke, Dr. Turakhia said. That’s when AFib is more likely to be temporally related to stroke as the likely culprit, the mechanism addressed by Dr. Singer and associates.

“I think we’re all trying to grapple with what the truth is,” Dr. Singer observed. Still, the current study was unusual for primarily looking at the temporal relationship between AFib and stroke, rather than stroke risk. “And once again, as we found in our earlier study, but now a much larger study, it’s a tight relationship.”

Based on the current results, he said, the risk is “high when you have AFib, and it decreases very rapidly after the AFib is over.” And, “it takes multiple hours of AFib to raise stroke risk.” Inclusion in the analysis required accumulation of at least 5.5 hours of AFib on at least 1 day in a month, the cut point at which stroke risk started to climb significantly in an earlier trial.  

In the current analysis, however, the 30-day odds ratio for stroke was a nonsignificant 2.75 for an AFib burden of 6-23 hours in a day and jumped to a significant 5.0 for a burden in excess of 23 hours in a day. “That’s a lot of AFib” before the risk actually goes up, and supports AFib as causative, Dr. Singer said. If it were the myopathy itself triggering stroke in these particular patients, the risk would be ongoing and not subject to a threshold of AFib burden.
 

Implications for noncontinuous OAC

“The hope is that there are people who have very little AFib: They may have several hours, and then they have nothing for 6 months. Do they have to be anticoagulated or not?” Dr. Singer asked.

“If you believe the risk-marker story, you might say they have to be anticoagulated. But if you believe our results, you would certainly think there’s a good chance they don’t have to be anticoagulated,” he said.

“So it is logical to think, if you have the right people and continuous monitoring, that you could have time-delimited anticoagulation.” That is, patients might start right away on a direct OAC once reaching the AFib threshold in a day, Dr. Singer said, “going on and off anticoagulants in parallel with their episodes of AFib.”

The strategy wouldn’t be feasible in patients who often experience AFib, Dr. Singer noted, “but it might work for people who have infrequent paroxysmal AFib.” It certainly would first have to be tested in prospective trials, he said. Such trials would be more practical than ever to carry out given the growing availability of continuous AFib monitoring by wearables.

“We need a trial to make the case whether it’s safe or not,” Dr. Turakhia said of such a rhythm-guided approach to OAC for AFib. The population to start with, he said, would be patients with paroxysmal AFib and low CHA2DS2-VASc scores. “If you think CHA2DS2-VASc as an integrated score of vascular risk, such patients would have a lot fewer reasons to have strokes. And if they do have a stroke, it’s more reasonable to assume that it’s likely caused by atrial fib and not just a marker.”

Importantly, such a strategy could well be safer than continuous OAC for some patients – those at the lowest vascular risk and with the most occasional AFib and lowest AFib burden “who are otherwise doing fine,” Dr. Turakhia said. In such patients on continuous OAC, he proposed, the risks of bleeding and intracranial hemorrhage could potentially exceed the expected degree of protection from ischemic events.
 

Discordant periods of AFib burden

Dr. Singer and his colleagues linked a national electronic health record database with Medtronic CareLink records covering 10 years to identify 891 patients who experienced an ischemic stroke preceded by at least 120 days of continuous heart-rhythm monitoring.

The patients were then categorized by their pattern of AFib, if any, within each of two prestroke periods: the most recent 30 days, which was the test period, and the preceding 91-120 days, the control period.

The analysis then excluded any patients who reached an AFib-burden threshold of at least 5.5 hours on any day during both the test and control periods, and those who did not attain that threshold in either period.

“The ones who had AFib in both periods mostly had permanent AFib, and ones that didn’t have AFib in either period mostly were in sinus rhythm,” Dr. Singer said. It was “close to 100%” in both cases.

Those exclusions left 66 patients, 7.4% of the total, who reached the AFib-burden threshold on at least 1 day during either the test or control periods, but not both. They included 52 and 14 patients, respectively, with “discordant” periods, that is, at least that burden of AFib in a day during either the test or control period, but not both.

Comparing AFib burden at test versus control periods among patients for whom the two periods were discordant yielded an OR for stroke of 3.71 (95% confidence interval, 2.06-6.70).

Stroke risk levels were not evenly spread throughout the 24-hour periods that met the AFib-burden threshold or the 30 days preceding the patients’ strokes. The OR for stroke was 5.00 (95% CI, 2.62-9.55) during days 1-5 following the day in which the AFib-burden threshold was met. And it was 5.00 (95% CI, 2.08-12.01) over 30 days if the AFib burden exceeded 23 hours on any day of the test period.

The study’s case-crossover design, in which each patient served as their own control, is one of its advantages, Dr. Singer observed. Most patient features, including CHA2DS2-VASc score and comorbidities, did not change appreciably from earliest to the latest 30-day period, which strengthens the comparison of the two because “you don’t have to worry about long-term confounding.”

Dr. Singer was supported by the Eliot B. and Edith C. Shoolman fund of the Massachusetts General Hospital. He discloses receiving grants from Boehringer Ingelheim and Bristol-Myers Squibb; personal fees from Boehringer Ingelheim, Bristol-Myers Squibb, Fitbit, Johnson & Johnson, Merck, and Pfizer; and royalties from UpToDate.

Dr. Turakhia discloses personal fees from Medtronic, Abbott, Sanofi, Pfizer, Myokardia, Johnson & Johnson, Milestone Pharmaceuticals, InCarda Therapeutics, 100Plus, Forward Pharma, and AliveCor; and grants from Bristol-Myers Squibb, the American Heart Association, Apple, and Bayer.

A version of this article first appeared on Medscape.com.

Discovery of substantial atrial fibrillation (AFib) is usually an indication to start oral anticoagulation (OAC) for stroke prevention, but it’s far from settled whether such AFib is actually a direct cause of thromboembolic stroke. And that has implications for whether patients with occasional bouts of the arrhythmia need to be on continuous OAC.  

It’s possible that some with infrequent paroxysmal AFib can get away with OAC maintained only about as long as the arrhythmia persists, and then go off the drugs, say researchers based on their study, which, they caution, would need the support of prospective trials before such a strategy could be considered.

But importantly, in their patients who had been continuously monitored by their cardiac implantable electronic devices (CIEDs) prior to experiencing a stroke, the 30-day risk of that stroke more than tripled if their AFib burden on 1 day reached at least 5-6 hours. The risk jumped especially high within the first few days after accumulating that amount of AFib in a day, but then fell off sharply over the next few days.

Based on the study, “Your risk of stroke goes up acutely when you have an episode of AFib, and it decreases rapidly, back to baseline – certainly by 30 days and it looked like in our data by 5 days,” Daniel E. Singer, MD, of Massachusetts General Hospital, Boston, said in an interview.

Increasingly, he noted, “there’s a widespread belief that AFib is a risk marker, not a causal risk factor.” In that scenario, most embolic strokes are caused by thrombi formed as a result of an atrial myopathy, characterized by fibrosis and inflammation, that also happens to trigger AFib.

But the current findings are, “from a mechanistic point of view, very much in favor of AFib being a causal risk factor, acutely raising the risk of stroke,” said Dr. Singer, who is lead author on the analysis published online Sept. 29 in JAMA Cardiology.

Some studies have “shown that anticoagulants seem to lower stroke risk even in patients without atrial fib, and even from sources not likely to be coming from the atrium,” Mintu P. Turakhia, MD, of Stanford (Calif.) University, Palo Alto, said in an interview. Collectively they point to “atrial fibrillation as a cause of and a noncausal marker for stroke.”

For example, Dr. Turakhia pointed out in an editorial accompanying the current report that stroke in patients with CIEDs “may occur during prolonged periods of sinus rhythm.”

The current study, he said in an interview, doesn’t preclude atrial myopathy as one direct cause of stroke-associated thrombus, because probably both the myopathy and AFib can be culprits. Still, AFib itself it may bear more responsibility for strokes in patients with fewer competing risks for stroke.

In such patients at lower vascular risk, who may have a CHA2DS2-VASc score of only 1 or 2, for example, “AFib can become a more important cause” of ischemic stroke, Dr. Turakhia said. That’s when AFib is more likely to be temporally related to stroke as the likely culprit, the mechanism addressed by Dr. Singer and associates.

“I think we’re all trying to grapple with what the truth is,” Dr. Singer observed. Still, the current study was unusual for primarily looking at the temporal relationship between AFib and stroke, rather than stroke risk. “And once again, as we found in our earlier study, but now a much larger study, it’s a tight relationship.”

Based on the current results, he said, the risk is “high when you have AFib, and it decreases very rapidly after the AFib is over.” And, “it takes multiple hours of AFib to raise stroke risk.” Inclusion in the analysis required accumulation of at least 5.5 hours of AFib on at least 1 day in a month, the cut point at which stroke risk started to climb significantly in an earlier trial.  

In the current analysis, however, the 30-day odds ratio for stroke was a nonsignificant 2.75 for an AFib burden of 6-23 hours in a day and jumped to a significant 5.0 for a burden in excess of 23 hours in a day. “That’s a lot of AFib” before the risk actually goes up, and supports AFib as causative, Dr. Singer said. If it were the myopathy itself triggering stroke in these particular patients, the risk would be ongoing and not subject to a threshold of AFib burden.
 

Implications for noncontinuous OAC

“The hope is that there are people who have very little AFib: They may have several hours, and then they have nothing for 6 months. Do they have to be anticoagulated or not?” Dr. Singer asked.

“If you believe the risk-marker story, you might say they have to be anticoagulated. But if you believe our results, you would certainly think there’s a good chance they don’t have to be anticoagulated,” he said.

“So it is logical to think, if you have the right people and continuous monitoring, that you could have time-delimited anticoagulation.” That is, patients might start right away on a direct OAC once reaching the AFib threshold in a day, Dr. Singer said, “going on and off anticoagulants in parallel with their episodes of AFib.”

The strategy wouldn’t be feasible in patients who often experience AFib, Dr. Singer noted, “but it might work for people who have infrequent paroxysmal AFib.” It certainly would first have to be tested in prospective trials, he said. Such trials would be more practical than ever to carry out given the growing availability of continuous AFib monitoring by wearables.

“We need a trial to make the case whether it’s safe or not,” Dr. Turakhia said of such a rhythm-guided approach to OAC for AFib. The population to start with, he said, would be patients with paroxysmal AFib and low CHA2DS2-VASc scores. “If you think CHA2DS2-VASc as an integrated score of vascular risk, such patients would have a lot fewer reasons to have strokes. And if they do have a stroke, it’s more reasonable to assume that it’s likely caused by atrial fib and not just a marker.”

Importantly, such a strategy could well be safer than continuous OAC for some patients – those at the lowest vascular risk and with the most occasional AFib and lowest AFib burden “who are otherwise doing fine,” Dr. Turakhia said. In such patients on continuous OAC, he proposed, the risks of bleeding and intracranial hemorrhage could potentially exceed the expected degree of protection from ischemic events.
 

Discordant periods of AFib burden

Dr. Singer and his colleagues linked a national electronic health record database with Medtronic CareLink records covering 10 years to identify 891 patients who experienced an ischemic stroke preceded by at least 120 days of continuous heart-rhythm monitoring.

The patients were then categorized by their pattern of AFib, if any, within each of two prestroke periods: the most recent 30 days, which was the test period, and the preceding 91-120 days, the control period.

The analysis then excluded any patients who reached an AFib-burden threshold of at least 5.5 hours on any day during both the test and control periods, and those who did not attain that threshold in either period.

“The ones who had AFib in both periods mostly had permanent AFib, and ones that didn’t have AFib in either period mostly were in sinus rhythm,” Dr. Singer said. It was “close to 100%” in both cases.

Those exclusions left 66 patients, 7.4% of the total, who reached the AFib-burden threshold on at least 1 day during either the test or control periods, but not both. They included 52 and 14 patients, respectively, with “discordant” periods, that is, at least that burden of AFib in a day during either the test or control period, but not both.

Comparing AFib burden at test versus control periods among patients for whom the two periods were discordant yielded an OR for stroke of 3.71 (95% confidence interval, 2.06-6.70).

Stroke risk levels were not evenly spread throughout the 24-hour periods that met the AFib-burden threshold or the 30 days preceding the patients’ strokes. The OR for stroke was 5.00 (95% CI, 2.62-9.55) during days 1-5 following the day in which the AFib-burden threshold was met. And it was 5.00 (95% CI, 2.08-12.01) over 30 days if the AFib burden exceeded 23 hours on any day of the test period.

The study’s case-crossover design, in which each patient served as their own control, is one of its advantages, Dr. Singer observed. Most patient features, including CHA2DS2-VASc score and comorbidities, did not change appreciably from earliest to the latest 30-day period, which strengthens the comparison of the two because “you don’t have to worry about long-term confounding.”

Dr. Singer was supported by the Eliot B. and Edith C. Shoolman fund of the Massachusetts General Hospital. He discloses receiving grants from Boehringer Ingelheim and Bristol-Myers Squibb; personal fees from Boehringer Ingelheim, Bristol-Myers Squibb, Fitbit, Johnson & Johnson, Merck, and Pfizer; and royalties from UpToDate.

Dr. Turakhia discloses personal fees from Medtronic, Abbott, Sanofi, Pfizer, Myokardia, Johnson & Johnson, Milestone Pharmaceuticals, InCarda Therapeutics, 100Plus, Forward Pharma, and AliveCor; and grants from Bristol-Myers Squibb, the American Heart Association, Apple, and Bayer.

A version of this article first appeared on Medscape.com.

Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.

“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.

Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.

“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.

“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
 

Convenience is key

The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.

Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.

Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.

Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.

All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.

The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.

Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.

Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.

Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.

The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.

“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.

“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.

“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.

Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.

“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.

Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.

“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.

“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
 

Convenience is key

The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.

Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.

Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.

Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.

All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.

The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.

Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.

Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.

Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.

The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.

“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.

“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.

“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.

Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Adults who need to track their blood pressure to find out if they have hypertension prefer to do it at home rather than at a clinic or kiosk or with 24-hour ambulatory BP monitoring (ABPM), according to a new study.

“From a patient-centered perspective, home BP monitoring is the most acceptable method for diagnosing hypertension, although participants were willing to complete ABPM and appreciated its accuracy,” said Beverly Green, MD, MPH, of Kaiser Permanente Washington, Seattle.

Dr. Green presented the study Sept. 29 during the virtual American Heart Association Hypertension Scientific Sessions 2021.

“Health care professionals should work toward relying less on in-clinic visits to diagnose hypertension and supporting their patients in taking their blood pressure measurements at home,” Dr. Green said in an AHA news release.

“Home blood pressure monitoring is empowering and improves our ability to identify and treat hypertension, and to prevent strokes, heart attacks, heart failure, and cardiovascular death,” she added.
 

Convenience is key

The BP-CHECK study was a three-group, randomized, controlled diagnostic study that tested the accuracy and acceptability of office, home, and kiosk BP monitoring against the gold-standard – ABPM – for diagnosing hypertension. Dr. Green presented the results on patient adherence and acceptability of these methods.

Those assigned to clinic measurements were asked to return to the clinic for at least one additional BP check, as is routine in diagnosing hypertension in clinical practice.

Those in the home group were given and trained to use a Bluetooth/web-enabled home BP monitor and were asked to take their BP twice a day (morning and evening, with two measurements each time) for 5 days.

Those in the kiosk group were trained to use a BP kiosk with a smart card and were asked to return to the kiosk (or a nearby pharmacy with the same kiosk) on 3 separate days and measure their BP three times at each visit.

All participants were asked to complete their group-assigned diagnostic regimens in 3 weeks and then to complete 24-hour ABPM.

The trial enrolled 510 adults who presented to Kaiser Permanente Washington primary care clinics with elevated BP (mean, 150/88 mm Hg) but who had not yet been diagnosed with hypertension. Their mean age was 59 years, 80% of the study participants were White, and 51% were male.

Adherence to the monitoring regimen was highest in the home BP group (90.6%), followed by the clinic group (87.2%), and lowest in the kiosk group (67.9%). Adherence to ABPM among all participants was 91.6%.

Overall, acceptability was highest for the home BP group, followed by the clinic and kiosk groups; 24-hour ABPM monitoring was the least acceptable option.

Home was the “overwhelming” stated preference when asked before randomization and after, Dr. Green said.

The findings come as no surprise to Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee. “Patients will do what’s most convenient for them,” he told this news organization.

“We know from other studies that really all you need to do is measure the blood pressure twice a day for 3 days. That will give you a good idea what that patient’s blood pressure is as it relates to future cardiac events,” said Dr. Lawrence, who wasn’t involved in the study.

“We should really begin to focus more on these home, self-measured blood pressures using validated devices, and that’s important because a lot of the devices out there aren’t validated,” he explained.

“Patients with hypertension should have a blood pressure monitor at home that is validated and should be instructed in how to use it properly,” Dr. Lawrence concluded.

Funding for the study was provided by the Patient-Centered Outcomes Research Institute. Dr. Green and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.

“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.

“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.

Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Scarce data

Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.

“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.

To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.

Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.

The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.

Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.

During a median follow-up of 21 years, 136 patients died (39%). 

Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.

During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).

There was no significant difference in all-cause mortality risk between dippers and nondippers.

Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).

Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
 

Important underused diagnostic tool

“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.

There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”

Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”

“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.

“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.

“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.

The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.

“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.

“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.

Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Scarce data

Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.

“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.

To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.

Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.

The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.

Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.

During a median follow-up of 21 years, 136 patients died (39%). 

Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.

During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).

There was no significant difference in all-cause mortality risk between dippers and nondippers.

Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).

Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
 

Important underused diagnostic tool

“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.

There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”

Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”

“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.

“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.

“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.

The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Adults with diabetes whose blood pressure does not drop as expected at night (nondipping), or whose BP increases during the night (reverse dipping) are at higher risk of dying than peers with normal nighttime BP patterns, a longitudinal study has shown.

“Reverse dippers have more than double the risk of death for any cause over 20 years, irrespective of blood pressure control,” study investigator Martina Chiriacò, MD, University of Pisa (Italy), said in an interview.

“Primary physicians and diabetologists should look for abnormal blood pressure dipping patterns in patients with diabetes through 24-hour ambulatory blood pressure monitoring,” she added.

Dr. Chiriacò presented the research Sept. 28 at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Scarce data

Previous studies have shown that a nondipping BP pattern is linked to renal and cardiovascular disease, both in healthy individuals and in patients with hypertension or diabetes.

“Nevertheless, the long-term effect of nondipping on mortality in diabetes is still unclear; in particular, data on reverse dippers are extremely scarce,” Dr. Chiriacò explained.

To investigate, the researchers analyzed data on 349 adults with diabetes (81% type 2 diabetes) who were followed for more than 2 decades as part of the CHAMPION study, all with available 24-hour ambulatory BP monitoring (ABPM) and heart rate variability monitoring.

Dipping, nondipping, and reverse dipping were defined as a decline of at least 10%, a decline of less than 10%, and an increase of at least 0.1% in average night-time systolic BP, compared with average daytime SBP, respectively.

The cohort involved 166 (47.6%) dippers, 144 (41.2%) nondippers, and 39 (11.2%) reverse dippers.

Compared with dippers, nondippers and reverse dippers showed a progressively higher prevalence of cardiac autonomic neuropathy, low heart rate variability, 24-hour hypertension, isolated nocturnal hypertension, postural hypotension, and lower prevalence of white-coat hypertension.

During a median follow-up of 21 years, 136 patients died (39%). 

Compared with dippers, reverse dippers and nondippers had an average reduction in survival of 2.5 years and 1.1 years, respectively, Dr. Chiriacò reported.

During follow-up, risk for all-cause mortality was about twofold higher for reverse dippers than for dippers (adjusted hazard ratio, 2.2; 95% confidence interval, 1.3-3.8; P = .003) and than for nondippers (adjusted HR, 1.8; 95% CI, 1.1-2.9; P = .34).

There was no significant difference in all-cause mortality risk between dippers and nondippers.

Notably, said Dr. Chiriacò, the one in five patients with isolated nocturnal hypertension had a reduction in survival similar to that seen in individuals with 24-hour sustained hypertension (average, 1.2 years).

Individuals with low heart rate variability over 24 hours had an average reduction in survival of 1.8 years.
 

Important underused diagnostic tool

“We believe that our study is important since it is the only available study with a follow-up longer than 20 years that explores the role of blood pressure patterns and heart rate variability as risk factors for all-cause mortality in diabetes,” Dr. Chiriacò said in an interview.

There are some available strategies to reduce BP during the night, she added. “The most tested and effective is the administration of anti-hypertensive medications in the evening rather than in the morning.”

Weighing in on the study, Maryann McLaughlin, MD, cardiologist at Mount Sinai Hospital, New York, said: “Interestingly, most physicians do not do 24-hour ambulatory blood pressure monitoring when they’re making the diagnosis of hypertension.”

“And really, the correct way to make a diagnosis of hypertension and rule out white-coat hypertension is either with a 24-hour ambulatory blood pressure monitor or use of home blood pressure monitors,” she said in an interview.

“The 24-hour ambulatory blood pressure monitor is an important diagnostic tool and a great way to really look at this issue of dipping, which is a very important physiologic parameter,” Dr. McLaughlin said.

“In our offices, we offer the 24-hour home ambulatory blood pressure monitor routinely. Most patients are receptive to it and they usually tolerate it pretty well,” Dr. McLaughlin said.

The study was funded by the University of Pisa. Dr. Chiriacò and Dr. McLaughlin have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Introduction

There have been incident reports of cardiac-related adverse events (CrAE) from immune checkpoint inhibitors (ICPI); however, the true incidence and subsequent management of these potential side effects have not been defined. It is therefore important to study ICPI related cardiac dysfunction to assist in monitoring and surveillance of these patients.

Methods

63 patients who received nivolumab and pembrolizumab at Stratton VAMC Albany between January 2015 to December 2018 were studied. Retrospective chart review was done to identify the CrAE up to two-year post-therapy completion or discontinuation. Naranjo score was used to assess drug-related side effect. IRB approval was obtained.

Results 

CrAE were defined as new onset arrythmia identified on electrocardiogram, evidence of cardiomyopathy on echocardiogram, an acute coronary event, and hospitalizations from primary cardiac disorder following ICPI administration. Of the 63 patients, 6 patients developed CrAE. Our review showed 3 patients developed new arrythmias including 1 with atrial fibrillation, and 2 with atrial flutter. There was 1 case each of new heart failure with reduced ejection fraction and pericarditis with pericardial tamponade. 1 patient developed acute coronary syndrome in addition to complete heart block. Of the 6 patients, 2 had elevated brain natriuretic peptide (BNP) prior to onset of CrAE. Elevated markers including BNP and troponin-I were also seen in 13 patients with preexisting heart conditions without CrAE. Duration of therapy was variable for all patients with CrAE. Therapy was continued for 3 patients without recurrence of CrAE. Therapy was permanently discontinued in the patient who developed pericardial effusion (grade IV toxicity). The remaining 2 patients had additional concurrent immune-related toxicities that required discontinuation of therapy. Our analysis showed 25/63 patients with pre-existing cardiac conditions (including arrhythmia, heart failure or coronary artery disease) who did not develop new CrAE; however 6 of these patients required hospitalization for exacerbation related to these pre-existing conditions.

Conclusions

CrAE can occur with ICPIs, and vigilance is required in high-risk patient including those with pre-existing cardiac comorbidity. Further studies are required to establish if baseline screening EKG and echocardiogram should be obtained for all patients starting ICPI.

Introduction

There have been incident reports of cardiac-related adverse events (CrAE) from immune checkpoint inhibitors (ICPI); however, the true incidence and subsequent management of these potential side effects have not been defined. It is therefore important to study ICPI related cardiac dysfunction to assist in monitoring and surveillance of these patients.

Methods

63 patients who received nivolumab and pembrolizumab at Stratton VAMC Albany between January 2015 to December 2018 were studied. Retrospective chart review was done to identify the CrAE up to two-year post-therapy completion or discontinuation. Naranjo score was used to assess drug-related side effect. IRB approval was obtained.

Results 

CrAE were defined as new onset arrythmia identified on electrocardiogram, evidence of cardiomyopathy on echocardiogram, an acute coronary event, and hospitalizations from primary cardiac disorder following ICPI administration. Of the 63 patients, 6 patients developed CrAE. Our review showed 3 patients developed new arrythmias including 1 with atrial fibrillation, and 2 with atrial flutter. There was 1 case each of new heart failure with reduced ejection fraction and pericarditis with pericardial tamponade. 1 patient developed acute coronary syndrome in addition to complete heart block. Of the 6 patients, 2 had elevated brain natriuretic peptide (BNP) prior to onset of CrAE. Elevated markers including BNP and troponin-I were also seen in 13 patients with preexisting heart conditions without CrAE. Duration of therapy was variable for all patients with CrAE. Therapy was continued for 3 patients without recurrence of CrAE. Therapy was permanently discontinued in the patient who developed pericardial effusion (grade IV toxicity). The remaining 2 patients had additional concurrent immune-related toxicities that required discontinuation of therapy. Our analysis showed 25/63 patients with pre-existing cardiac conditions (including arrhythmia, heart failure or coronary artery disease) who did not develop new CrAE; however 6 of these patients required hospitalization for exacerbation related to these pre-existing conditions.

Conclusions

CrAE can occur with ICPIs, and vigilance is required in high-risk patient including those with pre-existing cardiac comorbidity. Further studies are required to establish if baseline screening EKG and echocardiogram should be obtained for all patients starting ICPI.

Introduction

There have been incident reports of cardiac-related adverse events (CrAE) from immune checkpoint inhibitors (ICPI); however, the true incidence and subsequent management of these potential side effects have not been defined. It is therefore important to study ICPI related cardiac dysfunction to assist in monitoring and surveillance of these patients.

Methods

63 patients who received nivolumab and pembrolizumab at Stratton VAMC Albany between January 2015 to December 2018 were studied. Retrospective chart review was done to identify the CrAE up to two-year post-therapy completion or discontinuation. Naranjo score was used to assess drug-related side effect. IRB approval was obtained.

Results 

CrAE were defined as new onset arrythmia identified on electrocardiogram, evidence of cardiomyopathy on echocardiogram, an acute coronary event, and hospitalizations from primary cardiac disorder following ICPI administration. Of the 63 patients, 6 patients developed CrAE. Our review showed 3 patients developed new arrythmias including 1 with atrial fibrillation, and 2 with atrial flutter. There was 1 case each of new heart failure with reduced ejection fraction and pericarditis with pericardial tamponade. 1 patient developed acute coronary syndrome in addition to complete heart block. Of the 6 patients, 2 had elevated brain natriuretic peptide (BNP) prior to onset of CrAE. Elevated markers including BNP and troponin-I were also seen in 13 patients with preexisting heart conditions without CrAE. Duration of therapy was variable for all patients with CrAE. Therapy was continued for 3 patients without recurrence of CrAE. Therapy was permanently discontinued in the patient who developed pericardial effusion (grade IV toxicity). The remaining 2 patients had additional concurrent immune-related toxicities that required discontinuation of therapy. Our analysis showed 25/63 patients with pre-existing cardiac conditions (including arrhythmia, heart failure or coronary artery disease) who did not develop new CrAE; however 6 of these patients required hospitalization for exacerbation related to these pre-existing conditions.

Conclusions

CrAE can occur with ICPIs, and vigilance is required in high-risk patient including those with pre-existing cardiac comorbidity. Further studies are required to establish if baseline screening EKG and echocardiogram should be obtained for all patients starting ICPI.

Sexual harassment or assault during military service among young and middle-aged veterans is associated with an increased risk for hypertension, a new study suggests.

“Understanding a patient’s trauma history is invaluable for treating the whole person,” Allison E. Gaffey, PhD, Yale University, New Haven, Conn., and the Veterans Affairs Connecticut Healthcare System, told this news organization.

“Assessing men and women’s history of trauma, including sexual trauma, is critical for recognizing nontraditional factors that contribute to their cardiovascular risk and to gain a more comprehensive understanding of their mental and physical health,” Dr. Gaffey added.

She presented her research at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Lasting impact on physical health

Dr. Gaffey and colleagues analyzed data from the VA for roughly 1.2 million veterans (mean age, 30.2 years; 12% female) who were discharged from the military after Sept. 30, 2001, and who received health care services at VA medical centers from 2001 to 2017. 

All were screened for sexual harassment and assault, known as military sexual trauma (MST), when they first began receiving VA care.

During 16 years of follow-up, 33,881 veterans screened positive for MST (65% women), and 307,332 developed hypertension (15% women).

Overall, MST was associated with a 30% increase in risk for incident hypertension in unadjusted models (hazard ratio, 1.30; 95% confidence interval, 1.28-1.33; P < .001).

After adjustment for demographic characteristics, lifestyle factors, cardiovascular comorbidities, PTSD, anxiety, and depression, MST remained significantly associated with hypertension (adjusted HR, 1.10; 95% CI, 1.08-1.12; P < .001).

When women and men were examined separately, the link between MST and risk for hypertension remained for both groups, but was slightly stronger among women.

“Sexual trauma has been associated with autonomic dysfunction, inflammation, and dysregulation in the hypothalamic pituitary adrenal axis and renin-angiotensin-aldosterone system, which could lead to elevations in BP over time,” Dr. Gaffey told this news organization.

“These findings show that even many years after being discharged from military service, exposure to military sexual trauma can continue to significantly influence veterans’ physical health,” she added.

Dr. Gaffey said it will be important to determine if early treatment of MST improves hypertension risk, particularly among those showing elevated blood pressure or stage 1 hypertension.
 

Social determinants of health

Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee, said the findings in this study are “in line with what we know about the impact of social determinants of health on high blood pressure.”

“There are studies that suggest that things that we historically don’t look at as risk factors for hypertension – lifelong racism, crime, mental health status – do in fact predict your risk of developing hypertension,” Dr. Lawrence, from Spectrum Health in Benton Harbor, Mich., told this news organization.

“It’s not just your genetics that will determine your health, and there are a lot of things that will affect your blood pressure. Your blood pressure is really just a barometer of everything that’s going on in your life and some of the things that have gone on in your life in the past,” added Dr. Lawrence, who wasn’t involved in the study.

Funding for the study was provided by the Department of Veterans Affairs. Dr. Gaffey and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Sexual harassment or assault during military service among young and middle-aged veterans is associated with an increased risk for hypertension, a new study suggests.

“Understanding a patient’s trauma history is invaluable for treating the whole person,” Allison E. Gaffey, PhD, Yale University, New Haven, Conn., and the Veterans Affairs Connecticut Healthcare System, told this news organization.

“Assessing men and women’s history of trauma, including sexual trauma, is critical for recognizing nontraditional factors that contribute to their cardiovascular risk and to gain a more comprehensive understanding of their mental and physical health,” Dr. Gaffey added.

She presented her research at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Lasting impact on physical health

Dr. Gaffey and colleagues analyzed data from the VA for roughly 1.2 million veterans (mean age, 30.2 years; 12% female) who were discharged from the military after Sept. 30, 2001, and who received health care services at VA medical centers from 2001 to 2017. 

All were screened for sexual harassment and assault, known as military sexual trauma (MST), when they first began receiving VA care.

During 16 years of follow-up, 33,881 veterans screened positive for MST (65% women), and 307,332 developed hypertension (15% women).

Overall, MST was associated with a 30% increase in risk for incident hypertension in unadjusted models (hazard ratio, 1.30; 95% confidence interval, 1.28-1.33; P < .001).

After adjustment for demographic characteristics, lifestyle factors, cardiovascular comorbidities, PTSD, anxiety, and depression, MST remained significantly associated with hypertension (adjusted HR, 1.10; 95% CI, 1.08-1.12; P < .001).

When women and men were examined separately, the link between MST and risk for hypertension remained for both groups, but was slightly stronger among women.

“Sexual trauma has been associated with autonomic dysfunction, inflammation, and dysregulation in the hypothalamic pituitary adrenal axis and renin-angiotensin-aldosterone system, which could lead to elevations in BP over time,” Dr. Gaffey told this news organization.

“These findings show that even many years after being discharged from military service, exposure to military sexual trauma can continue to significantly influence veterans’ physical health,” she added.

Dr. Gaffey said it will be important to determine if early treatment of MST improves hypertension risk, particularly among those showing elevated blood pressure or stage 1 hypertension.
 

Social determinants of health

Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee, said the findings in this study are “in line with what we know about the impact of social determinants of health on high blood pressure.”

“There are studies that suggest that things that we historically don’t look at as risk factors for hypertension – lifelong racism, crime, mental health status – do in fact predict your risk of developing hypertension,” Dr. Lawrence, from Spectrum Health in Benton Harbor, Mich., told this news organization.

“It’s not just your genetics that will determine your health, and there are a lot of things that will affect your blood pressure. Your blood pressure is really just a barometer of everything that’s going on in your life and some of the things that have gone on in your life in the past,” added Dr. Lawrence, who wasn’t involved in the study.

Funding for the study was provided by the Department of Veterans Affairs. Dr. Gaffey and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Sexual harassment or assault during military service among young and middle-aged veterans is associated with an increased risk for hypertension, a new study suggests.

“Understanding a patient’s trauma history is invaluable for treating the whole person,” Allison E. Gaffey, PhD, Yale University, New Haven, Conn., and the Veterans Affairs Connecticut Healthcare System, told this news organization.

“Assessing men and women’s history of trauma, including sexual trauma, is critical for recognizing nontraditional factors that contribute to their cardiovascular risk and to gain a more comprehensive understanding of their mental and physical health,” Dr. Gaffey added.

She presented her research at the joint scientific sessions of the American Heart Association Council on Hypertension, AHA Council on Kidney in Cardiovascular Disease, and American Society of Hypertension.
 

Lasting impact on physical health

Dr. Gaffey and colleagues analyzed data from the VA for roughly 1.2 million veterans (mean age, 30.2 years; 12% female) who were discharged from the military after Sept. 30, 2001, and who received health care services at VA medical centers from 2001 to 2017. 

All were screened for sexual harassment and assault, known as military sexual trauma (MST), when they first began receiving VA care.

During 16 years of follow-up, 33,881 veterans screened positive for MST (65% women), and 307,332 developed hypertension (15% women).

Overall, MST was associated with a 30% increase in risk for incident hypertension in unadjusted models (hazard ratio, 1.30; 95% confidence interval, 1.28-1.33; P < .001).

After adjustment for demographic characteristics, lifestyle factors, cardiovascular comorbidities, PTSD, anxiety, and depression, MST remained significantly associated with hypertension (adjusted HR, 1.10; 95% CI, 1.08-1.12; P < .001).

When women and men were examined separately, the link between MST and risk for hypertension remained for both groups, but was slightly stronger among women.

“Sexual trauma has been associated with autonomic dysfunction, inflammation, and dysregulation in the hypothalamic pituitary adrenal axis and renin-angiotensin-aldosterone system, which could lead to elevations in BP over time,” Dr. Gaffey told this news organization.

“These findings show that even many years after being discharged from military service, exposure to military sexual trauma can continue to significantly influence veterans’ physical health,” she added.

Dr. Gaffey said it will be important to determine if early treatment of MST improves hypertension risk, particularly among those showing elevated blood pressure or stage 1 hypertension.
 

Social determinants of health

Willie Lawrence Jr., MD, head of the AHA National Hypertension Control Initiative oversight committee, said the findings in this study are “in line with what we know about the impact of social determinants of health on high blood pressure.”

“There are studies that suggest that things that we historically don’t look at as risk factors for hypertension – lifelong racism, crime, mental health status – do in fact predict your risk of developing hypertension,” Dr. Lawrence, from Spectrum Health in Benton Harbor, Mich., told this news organization.

“It’s not just your genetics that will determine your health, and there are a lot of things that will affect your blood pressure. Your blood pressure is really just a barometer of everything that’s going on in your life and some of the things that have gone on in your life in the past,” added Dr. Lawrence, who wasn’t involved in the study.

Funding for the study was provided by the Department of Veterans Affairs. Dr. Gaffey and Dr. Lawrence have no relevant disclosures.

A version of this article first appeared on Medscape.com.

Carrying excess weight is associated with an increased risk for certain heart problems even when there are no metabolic disturbances, data from a large French longitudinal study have shown.

In an analysis of almost 3 million people with no prior heart issues, there was a 34% increased risk for developing heart failure and a 33% increased risk for developing atrial fibrillation, it was reported at the annual meeting of the European Association for the Study of Diabetes.

There appeared to be no increase in the risk for heart attacks, ischemic stroke, or cardiovascular death, but the study’s 5-year follow-up period may have been too short to see such differences.

“Our findings highlight the importance of preventing poor metabolic health,” study investigator Laurent Fauchier, MD, PhD, of Centre Hospitalier Universitaire Trousseau (France), observed in a press release that highlighted his EASD presentation.

“Encouraging weight loss in people with obesity, regardless of whether or not they are ‘metabolically healthy,’ will help prevent atrial fibrillation and heart failure,” he suggested.
 

‘Metabolically healthy obesity’ – a misnomer?

‘Metabolically healthy obesity’, or MHO, has been suggested as a term to describe those who have a body mass index greater than 30 mg/m² but no obvious metabolic abnormalities, such as hypertension, dyslipidemia, or diabetes. It’s a term that could cover around a third of people with obesity, but it’s one that not everyone agrees with.

“I don’t feel the label ‘MHO’ is useful,” Frederick Ho, PhD, who is part of team at the University of Glasgow (Scotland) that has done similar research in a U.K. population, said in an interview.

Courtesy Dr. Ho

“Even if – and this is a big if– [people with obesity] are at no higher risk of heart attack or stroke, they are still at higher risk of many other diseases, including heart failure and respiratory diseases. The term ‘healthy’ is sometimes interpreted as no additional health risk at all, which is not true,” Dr. Ho, a research fellow in public health, qualified.
 

Hospital discharge records checked

For their analysis Dr. Fauchier and coinvestigators obtained the medical records of all patients who had been discharged from French hospitals in 2013 and who had at least 5 years’ worth of follow-up data. For inclusion, there had to be no prior history of major cardiovascular events (MACE), which included myocardial infarction (MI), heart failure, and ischemic stroke. Patients who were underweight or malnourished were excluded.

In all, around 2.8 million patients were included for the analysis, of whom 9.5% (n = 272,838) were classified as being obese and the remainder as ‘nonobese’ (n = 2,600,201). Patients were then subdivided according to whether they had diabetes, hypertension, and hyperlipidemia, with those who did not have any of these conditions being classified as ‘metabolically healthy’ and those who had all three as ‘metabolically unhealthy.’

The results, published in Diabetes, Obesity and Metabolism, showed that just under a third (32.8%) of the obese patients were ‘metabolically healthy,’ compared with 72.7% of those who were not obese.

The adjusted hazard ratio (aHR) for experiencing MACE with heart failure was 1.22 comparing those who were obese and ‘metabolically healthy’ with those who were not obese and had no metabolic abnormalities (95% confidence interval, 1.19-1.24). Corresponding aHRs for new-onset heart failure and new-onset atrial fibrillation were 1.34 (CI, 1.31-1.37) and 1.33 (CI, 1.30-1.37). For MI, ischemic stroke, and cardiovascular death aHRs were a respective 0.92 (CI, 0.87-0.98), 0.93 (CI, 0.88-0.98), and 0.99 (CI, 0.93-1.0).
 

Findings consistent with UK Biobank data

While these are observational associations that do not show cause and effect, they do agree with other recently published data from the UK Biobank as Dr. Ho pointed out. These data are “quite interesting and partly consistent with what we found previously, e.g., a higher heart failure risk,” he said.

“We’d expect people with ‘metabolically healthy’ obesity to develop heart attack and stroke a little later than those who were initially metabolically unhealthy,” Dr. Ho noted, observing that the study was very large, but it does has a relatively short period of follow up.

“This is partly because quite a few of those with ‘MHO’ would become metabolically unhealthy after a few years,” Dr. Ho added.

Importantly, he noted, “this study has omitted several important confounders, such as physical activity and diet, which are both strong predictors of MHO and cardiovascular outcomes.”

Naveed Sattar, FMedSci, FRCPath, FRCPGlas, FRSE, professor and honorary consultant in cardiovascular and medical sciences at the University of Glasgow, with whom Dr. Ho has collaborated, gave his thoughts on the topic in an interview.

“Carrying excess weight can give considerable risks for conditions such as heart failure or respiratory disease in ways (not yet fully understood) that are not captured by metabolic health factors,” he said.

“This means that even if someone were to be labeled as living with metabolically healthy obesity, losing weight may still benefit that individual in many ways and reduce their risk of several other important health outcomes. They may also feel better.” 

Furthermore, he added: “Our Glasgow team has therefore strongly cautioned on the use of the term metabolically healthy obesity, and these new data do not change our view.”

Dr. Fauchier has acted as a speaker or consultant for AstraZeneca, Bayer, Bristol Myers Squibb Pfizer, Boehringer Ingelheim, Medtronic, Novartis, and XO. Dr. Ho had no relevant conflicts of interest. Dr. Sattar has received grants and personal fees from Boehringer Ingelheim, and personal fees from Amgen, AstraZeneca, Eli Lilly, Merck Sharp & Dohme, Novartis, Novo Nordisk, Pfizer, and Sanofi.

Carrying excess weight is associated with an increased risk for certain heart problems even when there are no metabolic disturbances, data from a large French longitudinal study have shown.

In an analysis of almost 3 million people with no prior heart issues, there was a 34% increased risk for developing heart failure and a 33% increased risk for developing atrial fibrillation, it was reported at the annual meeting of the European Association for the Study of Diabetes.

There appeared to be no increase in the risk for heart attacks, ischemic stroke, or cardiovascular death, but the study’s 5-year follow-up period may have been too short to see such differences.

“Our findings highlight the importance of preventing poor metabolic health,” study investigator Laurent Fauchier, MD, PhD, of Centre Hospitalier Universitaire Trousseau (France), observed in a press release that highlighted his EASD presentation.

“Encouraging weight loss in people with obesity, regardless of whether or not they are ‘metabolically healthy,’ will help prevent atrial fibrillation and heart failure,” he suggested.
 

‘Metabolically healthy obesity’ – a misnomer?

‘Metabolically healthy obesity’, or MHO, has been suggested as a term to describe those who have a body mass index greater than 30 mg/m² but no obvious metabolic abnormalities, such as hypertension, dyslipidemia, or diabetes. It’s a term that could cover around a third of people with obesity, but it’s one that not everyone agrees with.

“I don’t feel the label ‘MHO’ is useful,” Frederick Ho, PhD, who is part of team at the University of Glasgow (Scotland) that has done similar research in a U.K. population, said in an interview.

Courtesy Dr. Ho

“Even if – and this is a big if– [people with obesity] are at no higher risk of heart attack or stroke, they are still at higher risk of many other diseases, including heart failure and respiratory diseases. The term ‘healthy’ is sometimes interpreted as no additional health risk at all, which is not true,” Dr. Ho, a research fellow in public health, qualified.
 

Hospital discharge records checked

For their analysis Dr. Fauchier and coinvestigators obtained the medical records of all patients who had been discharged from French hospitals in 2013 and who had at least 5 years’ worth of follow-up data. For inclusion, there had to be no prior history of major cardiovascular events (MACE), which included myocardial infarction (MI), heart failure, and ischemic stroke. Patients who were underweight or malnourished were excluded.

In all, around 2.8 million patients were included for the analysis, of whom 9.5% (n = 272,838) were classified as being obese and the remainder as ‘nonobese’ (n = 2,600,201). Patients were then subdivided according to whether they had diabetes, hypertension, and hyperlipidemia, with those who did not have any of these conditions being classified as ‘metabolically healthy’ and those who had all three as ‘metabolically unhealthy.’

The results, published in Diabetes, Obesity and Metabolism, showed that just under a third (32.8%) of the obese patients were ‘metabolically healthy,’ compared with 72.7% of those who were not obese.

The adjusted hazard ratio (aHR) for experiencing MACE with heart failure was 1.22 comparing those who were obese and ‘metabolically healthy’ with those who were not obese and had no metabolic abnormalities (95% confidence interval, 1.19-1.24). Corresponding aHRs for new-onset heart failure and new-onset atrial fibrillation were 1.34 (CI, 1.31-1.37) and 1.33 (CI, 1.30-1.37). For MI, ischemic stroke, and cardiovascular death aHRs were a respective 0.92 (CI, 0.87-0.98), 0.93 (CI, 0.88-0.98), and 0.99 (CI, 0.93-1.0).
 

Findings consistent with UK Biobank data

While these are observational associations that do not show cause and effect, they do agree with other recently published data from the UK Biobank as Dr. Ho pointed out. These data are “quite interesting and partly consistent with what we found previously, e.g., a higher heart failure risk,” he said.

“We’d expect people with ‘metabolically healthy’ obesity to develop heart attack and stroke a little later than those who were initially metabolically unhealthy,” Dr. Ho noted, observing that the study was very large, but it does has a relatively short period of follow up.

“This is partly because quite a few of those with ‘MHO’ would become metabolically unhealthy after a few years,” Dr. Ho added.

Importantly, he noted, “this study has omitted several important confounders, such as physical activity and diet, which are both strong predictors of MHO and cardiovascular outcomes.”

Naveed Sattar, FMedSci, FRCPath, FRCPGlas, FRSE, professor and honorary consultant in cardiovascular and medical sciences at the University of Glasgow, with whom Dr. Ho has collaborated, gave his thoughts on the topic in an interview.

“Carrying excess weight can give considerable risks for conditions such as heart failure or respiratory disease in ways (not yet fully understood) that are not captured by metabolic health factors,” he said.

“This means that even if someone were to be labeled as living with metabolically healthy obesity, losing weight may still benefit that individual in many ways and reduce their risk of several other important health outcomes. They may also feel better.” 

Furthermore, he added: “Our Glasgow team has therefore strongly cautioned on the use of the term metabolically healthy obesity, and these new data do not change our view.”

Dr. Fauchier has acted as a speaker or consultant for AstraZeneca, Bayer, Bristol Myers Squibb Pfizer, Boehringer Ingelheim, Medtronic, Novartis, and XO. Dr. Ho had no relevant conflicts of interest. Dr. Sattar has received grants and personal fees from Boehringer Ingelheim, and personal fees from Amgen, AstraZeneca, Eli Lilly, Merck Sharp & Dohme, Novartis, Novo Nordisk, Pfizer, and Sanofi.

Carrying excess weight is associated with an increased risk for certain heart problems even when there are no metabolic disturbances, data from a large French longitudinal study have shown.

In an analysis of almost 3 million people with no prior heart issues, there was a 34% increased risk for developing heart failure and a 33% increased risk for developing atrial fibrillation, it was reported at the annual meeting of the European Association for the Study of Diabetes.

There appeared to be no increase in the risk for heart attacks, ischemic stroke, or cardiovascular death, but the study’s 5-year follow-up period may have been too short to see such differences.

“Our findings highlight the importance of preventing poor metabolic health,” study investigator Laurent Fauchier, MD, PhD, of Centre Hospitalier Universitaire Trousseau (France), observed in a press release that highlighted his EASD presentation.

“Encouraging weight loss in people with obesity, regardless of whether or not they are ‘metabolically healthy,’ will help prevent atrial fibrillation and heart failure,” he suggested.
 

‘Metabolically healthy obesity’ – a misnomer?

‘Metabolically healthy obesity’, or MHO, has been suggested as a term to describe those who have a body mass index greater than 30 mg/m² but no obvious metabolic abnormalities, such as hypertension, dyslipidemia, or diabetes. It’s a term that could cover around a third of people with obesity, but it’s one that not everyone agrees with.

“I don’t feel the label ‘MHO’ is useful,” Frederick Ho, PhD, who is part of team at the University of Glasgow (Scotland) that has done similar research in a U.K. population, said in an interview.

Courtesy Dr. Ho

“Even if – and this is a big if– [people with obesity] are at no higher risk of heart attack or stroke, they are still at higher risk of many other diseases, including heart failure and respiratory diseases. The term ‘healthy’ is sometimes interpreted as no additional health risk at all, which is not true,” Dr. Ho, a research fellow in public health, qualified.
 

Hospital discharge records checked

For their analysis Dr. Fauchier and coinvestigators obtained the medical records of all patients who had been discharged from French hospitals in 2013 and who had at least 5 years’ worth of follow-up data. For inclusion, there had to be no prior history of major cardiovascular events (MACE), which included myocardial infarction (MI), heart failure, and ischemic stroke. Patients who were underweight or malnourished were excluded.

In all, around 2.8 million patients were included for the analysis, of whom 9.5% (n = 272,838) were classified as being obese and the remainder as ‘nonobese’ (n = 2,600,201). Patients were then subdivided according to whether they had diabetes, hypertension, and hyperlipidemia, with those who did not have any of these conditions being classified as ‘metabolically healthy’ and those who had all three as ‘metabolically unhealthy.’

The results, published in Diabetes, Obesity and Metabolism, showed that just under a third (32.8%) of the obese patients were ‘metabolically healthy,’ compared with 72.7% of those who were not obese.

The adjusted hazard ratio (aHR) for experiencing MACE with heart failure was 1.22 comparing those who were obese and ‘metabolically healthy’ with those who were not obese and had no metabolic abnormalities (95% confidence interval, 1.19-1.24). Corresponding aHRs for new-onset heart failure and new-onset atrial fibrillation were 1.34 (CI, 1.31-1.37) and 1.33 (CI, 1.30-1.37). For MI, ischemic stroke, and cardiovascular death aHRs were a respective 0.92 (CI, 0.87-0.98), 0.93 (CI, 0.88-0.98), and 0.99 (CI, 0.93-1.0).
 

Findings consistent with UK Biobank data

While these are observational associations that do not show cause and effect, they do agree with other recently published data from the UK Biobank as Dr. Ho pointed out. These data are “quite interesting and partly consistent with what we found previously, e.g., a higher heart failure risk,” he said.

“We’d expect people with ‘metabolically healthy’ obesity to develop heart attack and stroke a little later than those who were initially metabolically unhealthy,” Dr. Ho noted, observing that the study was very large, but it does has a relatively short period of follow up.

“This is partly because quite a few of those with ‘MHO’ would become metabolically unhealthy after a few years,” Dr. Ho added.

Importantly, he noted, “this study has omitted several important confounders, such as physical activity and diet, which are both strong predictors of MHO and cardiovascular outcomes.”

Naveed Sattar, FMedSci, FRCPath, FRCPGlas, FRSE, professor and honorary consultant in cardiovascular and medical sciences at the University of Glasgow, with whom Dr. Ho has collaborated, gave his thoughts on the topic in an interview.

“Carrying excess weight can give considerable risks for conditions such as heart failure or respiratory disease in ways (not yet fully understood) that are not captured by metabolic health factors,” he said.

“This means that even if someone were to be labeled as living with metabolically healthy obesity, losing weight may still benefit that individual in many ways and reduce their risk of several other important health outcomes. They may also feel better.” 

Furthermore, he added: “Our Glasgow team has therefore strongly cautioned on the use of the term metabolically healthy obesity, and these new data do not change our view.”

Dr. Fauchier has acted as a speaker or consultant for AstraZeneca, Bayer, Bristol Myers Squibb Pfizer, Boehringer Ingelheim, Medtronic, Novartis, and XO. Dr. Ho had no relevant conflicts of interest. Dr. Sattar has received grants and personal fees from Boehringer Ingelheim, and personal fees from Amgen, AstraZeneca, Eli Lilly, Merck Sharp & Dohme, Novartis, Novo Nordisk, Pfizer, and Sanofi.

Among those with type 2 diabetes, women receive some cardioprotective treatments less often than men, according to a post hoc analysis of data from the REWIND trial, conducted in nearly 10,000 adults from 24 countries.

At study entry, significantly fewer women received a statin, at 73%, or daily aspirin, at 44%, compared with men, who had treatment rates of 81% and 58%, respectively, Giulia Ferrannini, MD, reported at the annual meeting of the European Association for the Study of Diabetes.

The data also show that significantly fewer women received treatment with an ACE inhibitor or angiotensin-receptor blocker (ARB), at 80%, than men, at 83%, although the absolute between-group difference was modest. Rates of a fourth metric of appropriate treatment, receipt of antihypertensive medications if systolic blood pressure was at least 130 mm Hg, were nearly identical among women and men.
 

Cardiovascular risk in women “less well managed”

“This is confirmation that women are less well managed than men when it comes to cardiovascular risk, especially if they have [type 2] diabetes,” Dr. Ferrannini said in an interview.

Similar observations have been documented before, including in a report in 2019.

The treatment disparity by sex among the 9901 women and men with type 2 diabetes enrolled in REWIND is particularly striking because in clinical trials “patients are generally better managed than in the real world,” Dr. Ferrannini noted. “Despite this, the pattern of disadvantage to women was still evident,” she added.

“In cardiovascular protection the gender issue is preponderant. Women are less well treated,” she said.

REWIND is the cardiovascular outcomes trial for the once-weekly injectable glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity, Lilly) in patients with type 2 diabetes.

The primary results, reported at the 2019 scientific sessions of the American Diabetes Association and simultaneously published in The Lancet, showed dulaglutide significantly reduced major adverse cardiovascular events (MACE) by 12%, compared with placebo. The study ran at about 300 centers worldwide, including many U.S. and Canadian sites, and 46% of enrolled patients were women.

But despite undertreatment, women had significantly better outcomes in terms of MACE, the primary endpoint, during a median 5.4 years of follow-up compared with men. After adjustment for sex, other baseline characteristics, and study-treatment assignment, women had a significant 27% lower composite rate of nonfatal MI, nonfatal stroke, or death from either cardiovascular or unknown causes, compared with men, said Dr. Ferrannini, a researcher at the Karolinska Institute in Stockholm.

The analysis by sex also showed that women had a significant outcome advantage, compared with men, for three of the four components of the combined MACE outcome: nonfatal MI, cardiovascular death, and all-cause death, as well as for the outcome of hospitalization for heart failure, which was not part of the composite MACE outcome. The only MACE outcome component that showed no significant between-group difference was nonfatal stroke, which had roughly equal incidence rates among women and men.
 

Women had half the prevalence of CVD at baseline

The results also showed that the women with type 2 diabetes enrolled in REWIND had a prevalence of existing cardiovascular disease of 20%, which was half the rate of men at study entry, at 41%. However, the between-sex differences in the primary outcome, as well as each of the individual cardiovascular disease outcomes, didn’t change based on whether or not patients had a history of cardiovascular disease at baseline.

Only one outcome showed a between-sex difference linked to prevalent cardiovascular disease at study entry, the rate of all-cause mortality, which was not significantly different between men and women with a history of cardiovascular disease, but was 39% lower in women compared with men without such a history.

“The good news is that, at baseline and after 2 years, the majority of participants were meeting the relevant treatment targets regardless of sex,” commented Peter Novodvorsky, MUDr, a diabetes researcher at the University of Sheffield (England), who chaired the session during which Dr. Ferrannini presented her findings.
 

A role for geography, or selection bias?

The new analyses did not examine whether the overall pattern of undertreatment of women differed among each of the 24 participating countries, or by region of the world.

“We have to assume that these results reflect current [routine] practice” in the 24 countries that contributed patients to the trial, noted Dr. Novodvorsky.

There is also “the well-known issue of selection bias” in randomized trials. The current findings raise the question of whether the women willing to take part in the trial somehow differed from the men, he suggested.

Dr. Ferrannini added: “Even if we do observe a gender difference in management, if the majority of women with type 2 diabetes are appropriately treated, this ‘restores’ their cardiovascular risk advantage, compared with men, with the exception of stroke.”

The main hypothesis generated by the post hoc analysis of REWIND is that “women with diabetes have better outcomes than men if they are treated properly,” she stressed, noting that this “would have to be tested in a trial designed to ascertain gender differences.”

REWIND was sponsored by Eli Lilly. Dr. Ferrannini has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Among those with type 2 diabetes, women receive some cardioprotective treatments less often than men, according to a post hoc analysis of data from the REWIND trial, conducted in nearly 10,000 adults from 24 countries.

At study entry, significantly fewer women received a statin, at 73%, or daily aspirin, at 44%, compared with men, who had treatment rates of 81% and 58%, respectively, Giulia Ferrannini, MD, reported at the annual meeting of the European Association for the Study of Diabetes.

The data also show that significantly fewer women received treatment with an ACE inhibitor or angiotensin-receptor blocker (ARB), at 80%, than men, at 83%, although the absolute between-group difference was modest. Rates of a fourth metric of appropriate treatment, receipt of antihypertensive medications if systolic blood pressure was at least 130 mm Hg, were nearly identical among women and men.
 

Cardiovascular risk in women “less well managed”

“This is confirmation that women are less well managed than men when it comes to cardiovascular risk, especially if they have [type 2] diabetes,” Dr. Ferrannini said in an interview.

Similar observations have been documented before, including in a report in 2019.

The treatment disparity by sex among the 9901 women and men with type 2 diabetes enrolled in REWIND is particularly striking because in clinical trials “patients are generally better managed than in the real world,” Dr. Ferrannini noted. “Despite this, the pattern of disadvantage to women was still evident,” she added.

“In cardiovascular protection the gender issue is preponderant. Women are less well treated,” she said.

REWIND is the cardiovascular outcomes trial for the once-weekly injectable glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity, Lilly) in patients with type 2 diabetes.

The primary results, reported at the 2019 scientific sessions of the American Diabetes Association and simultaneously published in The Lancet, showed dulaglutide significantly reduced major adverse cardiovascular events (MACE) by 12%, compared with placebo. The study ran at about 300 centers worldwide, including many U.S. and Canadian sites, and 46% of enrolled patients were women.

But despite undertreatment, women had significantly better outcomes in terms of MACE, the primary endpoint, during a median 5.4 years of follow-up compared with men. After adjustment for sex, other baseline characteristics, and study-treatment assignment, women had a significant 27% lower composite rate of nonfatal MI, nonfatal stroke, or death from either cardiovascular or unknown causes, compared with men, said Dr. Ferrannini, a researcher at the Karolinska Institute in Stockholm.

The analysis by sex also showed that women had a significant outcome advantage, compared with men, for three of the four components of the combined MACE outcome: nonfatal MI, cardiovascular death, and all-cause death, as well as for the outcome of hospitalization for heart failure, which was not part of the composite MACE outcome. The only MACE outcome component that showed no significant between-group difference was nonfatal stroke, which had roughly equal incidence rates among women and men.
 

Women had half the prevalence of CVD at baseline

The results also showed that the women with type 2 diabetes enrolled in REWIND had a prevalence of existing cardiovascular disease of 20%, which was half the rate of men at study entry, at 41%. However, the between-sex differences in the primary outcome, as well as each of the individual cardiovascular disease outcomes, didn’t change based on whether or not patients had a history of cardiovascular disease at baseline.

Only one outcome showed a between-sex difference linked to prevalent cardiovascular disease at study entry, the rate of all-cause mortality, which was not significantly different between men and women with a history of cardiovascular disease, but was 39% lower in women compared with men without such a history.

“The good news is that, at baseline and after 2 years, the majority of participants were meeting the relevant treatment targets regardless of sex,” commented Peter Novodvorsky, MUDr, a diabetes researcher at the University of Sheffield (England), who chaired the session during which Dr. Ferrannini presented her findings.
 

A role for geography, or selection bias?

The new analyses did not examine whether the overall pattern of undertreatment of women differed among each of the 24 participating countries, or by region of the world.

“We have to assume that these results reflect current [routine] practice” in the 24 countries that contributed patients to the trial, noted Dr. Novodvorsky.

There is also “the well-known issue of selection bias” in randomized trials. The current findings raise the question of whether the women willing to take part in the trial somehow differed from the men, he suggested.

Dr. Ferrannini added: “Even if we do observe a gender difference in management, if the majority of women with type 2 diabetes are appropriately treated, this ‘restores’ their cardiovascular risk advantage, compared with men, with the exception of stroke.”

The main hypothesis generated by the post hoc analysis of REWIND is that “women with diabetes have better outcomes than men if they are treated properly,” she stressed, noting that this “would have to be tested in a trial designed to ascertain gender differences.”

REWIND was sponsored by Eli Lilly. Dr. Ferrannini has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

Among those with type 2 diabetes, women receive some cardioprotective treatments less often than men, according to a post hoc analysis of data from the REWIND trial, conducted in nearly 10,000 adults from 24 countries.

At study entry, significantly fewer women received a statin, at 73%, or daily aspirin, at 44%, compared with men, who had treatment rates of 81% and 58%, respectively, Giulia Ferrannini, MD, reported at the annual meeting of the European Association for the Study of Diabetes.

The data also show that significantly fewer women received treatment with an ACE inhibitor or angiotensin-receptor blocker (ARB), at 80%, than men, at 83%, although the absolute between-group difference was modest. Rates of a fourth metric of appropriate treatment, receipt of antihypertensive medications if systolic blood pressure was at least 130 mm Hg, were nearly identical among women and men.
 

Cardiovascular risk in women “less well managed”

“This is confirmation that women are less well managed than men when it comes to cardiovascular risk, especially if they have [type 2] diabetes,” Dr. Ferrannini said in an interview.

Similar observations have been documented before, including in a report in 2019.

The treatment disparity by sex among the 9901 women and men with type 2 diabetes enrolled in REWIND is particularly striking because in clinical trials “patients are generally better managed than in the real world,” Dr. Ferrannini noted. “Despite this, the pattern of disadvantage to women was still evident,” she added.

“In cardiovascular protection the gender issue is preponderant. Women are less well treated,” she said.

REWIND is the cardiovascular outcomes trial for the once-weekly injectable glucagonlike peptide–1 receptor agonist dulaglutide (Trulicity, Lilly) in patients with type 2 diabetes.

The primary results, reported at the 2019 scientific sessions of the American Diabetes Association and simultaneously published in The Lancet, showed dulaglutide significantly reduced major adverse cardiovascular events (MACE) by 12%, compared with placebo. The study ran at about 300 centers worldwide, including many U.S. and Canadian sites, and 46% of enrolled patients were women.

But despite undertreatment, women had significantly better outcomes in terms of MACE, the primary endpoint, during a median 5.4 years of follow-up compared with men. After adjustment for sex, other baseline characteristics, and study-treatment assignment, women had a significant 27% lower composite rate of nonfatal MI, nonfatal stroke, or death from either cardiovascular or unknown causes, compared with men, said Dr. Ferrannini, a researcher at the Karolinska Institute in Stockholm.

The analysis by sex also showed that women had a significant outcome advantage, compared with men, for three of the four components of the combined MACE outcome: nonfatal MI, cardiovascular death, and all-cause death, as well as for the outcome of hospitalization for heart failure, which was not part of the composite MACE outcome. The only MACE outcome component that showed no significant between-group difference was nonfatal stroke, which had roughly equal incidence rates among women and men.
 

Women had half the prevalence of CVD at baseline

The results also showed that the women with type 2 diabetes enrolled in REWIND had a prevalence of existing cardiovascular disease of 20%, which was half the rate of men at study entry, at 41%. However, the between-sex differences in the primary outcome, as well as each of the individual cardiovascular disease outcomes, didn’t change based on whether or not patients had a history of cardiovascular disease at baseline.

Only one outcome showed a between-sex difference linked to prevalent cardiovascular disease at study entry, the rate of all-cause mortality, which was not significantly different between men and women with a history of cardiovascular disease, but was 39% lower in women compared with men without such a history.

“The good news is that, at baseline and after 2 years, the majority of participants were meeting the relevant treatment targets regardless of sex,” commented Peter Novodvorsky, MUDr, a diabetes researcher at the University of Sheffield (England), who chaired the session during which Dr. Ferrannini presented her findings.
 

A role for geography, or selection bias?

The new analyses did not examine whether the overall pattern of undertreatment of women differed among each of the 24 participating countries, or by region of the world.

“We have to assume that these results reflect current [routine] practice” in the 24 countries that contributed patients to the trial, noted Dr. Novodvorsky.

There is also “the well-known issue of selection bias” in randomized trials. The current findings raise the question of whether the women willing to take part in the trial somehow differed from the men, he suggested.

Dr. Ferrannini added: “Even if we do observe a gender difference in management, if the majority of women with type 2 diabetes are appropriately treated, this ‘restores’ their cardiovascular risk advantage, compared with men, with the exception of stroke.”

The main hypothesis generated by the post hoc analysis of REWIND is that “women with diabetes have better outcomes than men if they are treated properly,” she stressed, noting that this “would have to be tested in a trial designed to ascertain gender differences.”

REWIND was sponsored by Eli Lilly. Dr. Ferrannini has reported no relevant financial relationships.

A version of this article first appeared on Medscape.com.

When it comes to protecting diabetic hearts, sodium-glucose cotransporter-2 (SGLT2) inhibitors may have a slight edge over glucagonlike peptide-1 receptor agonists (GLP-1 RAs) according to the results of large, population-based, observational cohort study.

Around a 30% reduction in the risk for being hospitalized for heart failure was achieved in people with type 2 diabetes who were treated with a SGLT2 inhibitor over a GLP-1 RA regardless of whether the patients had a preexisting heart condition.

The findings, published in the Annals of Internal Medicine, also showed a 10% lower risk for myocardial infarction or stroke among those treated with a SGLT2 inhibitor who had preexisting cardiovascular disease (CVD), although there was no difference in risk between the two classes of drugs in those without preexisting CVD.

“These findings are important as they suggest that SGLT2 [inhibitors] and GLP-1 RA offer similar benefits in preventing myocardial infarction and stroke in patients with diabetes,” said study investigator Elisabetta Patorno, MD, DrPH, of Brigham and Women’s Hospital and Harvard Medical School in Boston, in an interview.

They also show “that SGLT2 [inhibitors] offer greater efficacy in preventing heart failure, which supports the existing guidelines,” she added.

Paul S. Jellinger, MD, MACE, of the Center for Diabetes and Endocrine Care in Hollywood, Fla., said these data were likely to be “additive to guidelines but not transformative.” The overall analysis results were “not surprising.” It was not unexpected that SGLT2 inhibitors provided a robust chronic heart failure (CHF) benefit, particularly in individuals with history of CVD, he said.

Dr. Jellinger, a clinical endocrinologist and professor of clinical medicine on the voluntary faculty at the University of Miami, observed, however, that “the similar CVD benefit in both drug classes in patients without known CVD adds to our knowledge in this somewhat controversial area and may be useful to the clinician in evaluating therapy in a diabetic individual without evidence of or at high risk for CHF.”

Furthermore, “the study also reminds us that, as demonstrated in published meta-analysis, there is also a modest CHF benefit associated with GLP-1 RA treatment particularly in patients with a history of CVD.”
 

Addressing the knowledge gap

Thanks to the results of many large-scale, prospective, cardiovascular outcomes studies, both SGLT2 inhibitors and GLP1 RA have been recommended as treatment for people with diabetes who have established CVD. But with no direct head-to-head trials having been conducted, there is a gap in knowledge and there is currently little guidance for physicians on which drug class to choose for an individual patient.

To try to clarify things, Dr. Patorno and associates looked at data from more than 370,000 people with type 2 diabetes who had been treated between April 2013 and December 2017 with either a SGLT2 inhibitor (canagliflozin, dapagliflozin, or empagliflozin) or GLP-1 RA (albiglutide, dulaglutide, exenatide, or liraglutide).

One-to-one propensity score matching was used to create the study groups: participants were first grouped according to their history of CVD, and then by the class of drug they had been prescribed. The primary outcomes were hospitalization for MI, stroke, or heart failure.

Comparing the initiation of a SGLT2 inhibitor with GLP-1 RA therapy, the hazard ratios (HRs) for MI or stroke in patients with and without a history of CVD were a respective 0.90 (95% CI, 0.82 to 0.98) and 1.07 (0.97 to 1.18).

The corresponding hazard ratios for heart failure hospitalizations were 0.71 (0.64 to 0.79) and 0.69 (0.56 to 0.85).
 

Real-world studies are of ‘increasing value’

“As in other not-randomized studies based on real-world data, residual confounding cannot be completely ruled out,” Dr. Patorno acknowledged. She added, however that “state-of-the-art methodological strategies were implemented to minimize this possibility.”

Limitations notwithstanding, “real world studies are demonstrating increasing value,” observed Dr. Jellinger. Further large-scale cardiovascular outcomes trials that directly compare these two drug classes “are unlikely given the depth of information available now,” Dr. Jellinger suggested.

“This head-to-head retrospective study may be as close as we get and does represent the first effort at a comparison of these two classes.”

Dr. Patorno said of the potential clinical implications: “Because the two classes are equally effective for stroke and myocardial infarction, but the SGLT2 inhibitors are superior for heart failure, when considered in aggregate, SGLT2 inhibitors are likely to prevent more of these adverse cardiovascular events than GLP-1 RA.”

The study received no commercial funding and was supported by the Brigham and Women’s Hospital and Harvard Medical School Division of Pharmacoepidemiology and Pharmacoeconomics.

Dr. Patorno reported no conflicts of interest. Dr. Jellinger is on the speaker’s bureau for Astra Zeneca, Amgen, and Esperion, and has served on advisory boards for Corcept and Regeneron.

When it comes to protecting diabetic hearts, sodium-glucose cotransporter-2 (SGLT2) inhibitors may have a slight edge over glucagonlike peptide-1 receptor agonists (GLP-1 RAs) according to the results of large, population-based, observational cohort study.

Around a 30% reduction in the risk for being hospitalized for heart failure was achieved in people with type 2 diabetes who were treated with a SGLT2 inhibitor over a GLP-1 RA regardless of whether the patients had a preexisting heart condition.

The findings, published in the Annals of Internal Medicine, also showed a 10% lower risk for myocardial infarction or stroke among those treated with a SGLT2 inhibitor who had preexisting cardiovascular disease (CVD), although there was no difference in risk between the two classes of drugs in those without preexisting CVD.

“These findings are important as they suggest that SGLT2 [inhibitors] and GLP-1 RA offer similar benefits in preventing myocardial infarction and stroke in patients with diabetes,” said study investigator Elisabetta Patorno, MD, DrPH, of Brigham and Women’s Hospital and Harvard Medical School in Boston, in an interview.

They also show “that SGLT2 [inhibitors] offer greater efficacy in preventing heart failure, which supports the existing guidelines,” she added.

Paul S. Jellinger, MD, MACE, of the Center for Diabetes and Endocrine Care in Hollywood, Fla., said these data were likely to be “additive to guidelines but not transformative.” The overall analysis results were “not surprising.” It was not unexpected that SGLT2 inhibitors provided a robust chronic heart failure (CHF) benefit, particularly in individuals with history of CVD, he said.

Dr. Jellinger, a clinical endocrinologist and professor of clinical medicine on the voluntary faculty at the University of Miami, observed, however, that “the similar CVD benefit in both drug classes in patients without known CVD adds to our knowledge in this somewhat controversial area and may be useful to the clinician in evaluating therapy in a diabetic individual without evidence of or at high risk for CHF.”

Furthermore, “the study also reminds us that, as demonstrated in published meta-analysis, there is also a modest CHF benefit associated with GLP-1 RA treatment particularly in patients with a history of CVD.”
 

Addressing the knowledge gap

Thanks to the results of many large-scale, prospective, cardiovascular outcomes studies, both SGLT2 inhibitors and GLP1 RA have been recommended as treatment for people with diabetes who have established CVD. But with no direct head-to-head trials having been conducted, there is a gap in knowledge and there is currently little guidance for physicians on which drug class to choose for an individual patient.

To try to clarify things, Dr. Patorno and associates looked at data from more than 370,000 people with type 2 diabetes who had been treated between April 2013 and December 2017 with either a SGLT2 inhibitor (canagliflozin, dapagliflozin, or empagliflozin) or GLP-1 RA (albiglutide, dulaglutide, exenatide, or liraglutide).

One-to-one propensity score matching was used to create the study groups: participants were first grouped according to their history of CVD, and then by the class of drug they had been prescribed. The primary outcomes were hospitalization for MI, stroke, or heart failure.

Comparing the initiation of a SGLT2 inhibitor with GLP-1 RA therapy, the hazard ratios (HRs) for MI or stroke in patients with and without a history of CVD were a respective 0.90 (95% CI, 0.82 to 0.98) and 1.07 (0.97 to 1.18).

The corresponding hazard ratios for heart failure hospitalizations were 0.71 (0.64 to 0.79) and 0.69 (0.56 to 0.85).
 

Real-world studies are of ‘increasing value’

“As in other not-randomized studies based on real-world data, residual confounding cannot be completely ruled out,” Dr. Patorno acknowledged. She added, however that “state-of-the-art methodological strategies were implemented to minimize this possibility.”

Limitations notwithstanding, “real world studies are demonstrating increasing value,” observed Dr. Jellinger. Further large-scale cardiovascular outcomes trials that directly compare these two drug classes “are unlikely given the depth of information available now,” Dr. Jellinger suggested.

“This head-to-head retrospective study may be as close as we get and does represent the first effort at a comparison of these two classes.”

Dr. Patorno said of the potential clinical implications: “Because the two classes are equally effective for stroke and myocardial infarction, but the SGLT2 inhibitors are superior for heart failure, when considered in aggregate, SGLT2 inhibitors are likely to prevent more of these adverse cardiovascular events than GLP-1 RA.”

The study received no commercial funding and was supported by the Brigham and Women’s Hospital and Harvard Medical School Division of Pharmacoepidemiology and Pharmacoeconomics.

Dr. Patorno reported no conflicts of interest. Dr. Jellinger is on the speaker’s bureau for Astra Zeneca, Amgen, and Esperion, and has served on advisory boards for Corcept and Regeneron.

When it comes to protecting diabetic hearts, sodium-glucose cotransporter-2 (SGLT2) inhibitors may have a slight edge over glucagonlike peptide-1 receptor agonists (GLP-1 RAs) according to the results of large, population-based, observational cohort study.

Around a 30% reduction in the risk for being hospitalized for heart failure was achieved in people with type 2 diabetes who were treated with a SGLT2 inhibitor over a GLP-1 RA regardless of whether the patients had a preexisting heart condition.

The findings, published in the Annals of Internal Medicine, also showed a 10% lower risk for myocardial infarction or stroke among those treated with a SGLT2 inhibitor who had preexisting cardiovascular disease (CVD), although there was no difference in risk between the two classes of drugs in those without preexisting CVD.

“These findings are important as they suggest that SGLT2 [inhibitors] and GLP-1 RA offer similar benefits in preventing myocardial infarction and stroke in patients with diabetes,” said study investigator Elisabetta Patorno, MD, DrPH, of Brigham and Women’s Hospital and Harvard Medical School in Boston, in an interview.

They also show “that SGLT2 [inhibitors] offer greater efficacy in preventing heart failure, which supports the existing guidelines,” she added.

Paul S. Jellinger, MD, MACE, of the Center for Diabetes and Endocrine Care in Hollywood, Fla., said these data were likely to be “additive to guidelines but not transformative.” The overall analysis results were “not surprising.” It was not unexpected that SGLT2 inhibitors provided a robust chronic heart failure (CHF) benefit, particularly in individuals with history of CVD, he said.

Dr. Jellinger, a clinical endocrinologist and professor of clinical medicine on the voluntary faculty at the University of Miami, observed, however, that “the similar CVD benefit in both drug classes in patients without known CVD adds to our knowledge in this somewhat controversial area and may be useful to the clinician in evaluating therapy in a diabetic individual without evidence of or at high risk for CHF.”

Furthermore, “the study also reminds us that, as demonstrated in published meta-analysis, there is also a modest CHF benefit associated with GLP-1 RA treatment particularly in patients with a history of CVD.”
 

Addressing the knowledge gap

Thanks to the results of many large-scale, prospective, cardiovascular outcomes studies, both SGLT2 inhibitors and GLP1 RA have been recommended as treatment for people with diabetes who have established CVD. But with no direct head-to-head trials having been conducted, there is a gap in knowledge and there is currently little guidance for physicians on which drug class to choose for an individual patient.

To try to clarify things, Dr. Patorno and associates looked at data from more than 370,000 people with type 2 diabetes who had been treated between April 2013 and December 2017 with either a SGLT2 inhibitor (canagliflozin, dapagliflozin, or empagliflozin) or GLP-1 RA (albiglutide, dulaglutide, exenatide, or liraglutide).

One-to-one propensity score matching was used to create the study groups: participants were first grouped according to their history of CVD, and then by the class of drug they had been prescribed. The primary outcomes were hospitalization for MI, stroke, or heart failure.

Comparing the initiation of a SGLT2 inhibitor with GLP-1 RA therapy, the hazard ratios (HRs) for MI or stroke in patients with and without a history of CVD were a respective 0.90 (95% CI, 0.82 to 0.98) and 1.07 (0.97 to 1.18).

The corresponding hazard ratios for heart failure hospitalizations were 0.71 (0.64 to 0.79) and 0.69 (0.56 to 0.85).
 

Real-world studies are of ‘increasing value’

“As in other not-randomized studies based on real-world data, residual confounding cannot be completely ruled out,” Dr. Patorno acknowledged. She added, however that “state-of-the-art methodological strategies were implemented to minimize this possibility.”

Limitations notwithstanding, “real world studies are demonstrating increasing value,” observed Dr. Jellinger. Further large-scale cardiovascular outcomes trials that directly compare these two drug classes “are unlikely given the depth of information available now,” Dr. Jellinger suggested.

“This head-to-head retrospective study may be as close as we get and does represent the first effort at a comparison of these two classes.”

Dr. Patorno said of the potential clinical implications: “Because the two classes are equally effective for stroke and myocardial infarction, but the SGLT2 inhibitors are superior for heart failure, when considered in aggregate, SGLT2 inhibitors are likely to prevent more of these adverse cardiovascular events than GLP-1 RA.”

The study received no commercial funding and was supported by the Brigham and Women’s Hospital and Harvard Medical School Division of Pharmacoepidemiology and Pharmacoeconomics.

Dr. Patorno reported no conflicts of interest. Dr. Jellinger is on the speaker’s bureau for Astra Zeneca, Amgen, and Esperion, and has served on advisory boards for Corcept and Regeneron.

Physical activity, long recommended by health experts to reduce risk for obesity, heart disease, type 2 diabetes, high blood pressure, hypercholesterolemia, and other cardiovascular disease risk factors, is also associated with increases in the amount of calcium deposited in the coronary arteries, new observational data suggest.

In a prospective cohort study of Korean men and women 18 years and older, participants who were the most physically active had the fastest progression of their coronary artery calcium (CAC) scores at 5 years, compared with those who were the least physically active.

“People who exercise may have an increase in their coronary calcium levels, but this is not necessarily bad news. This may mean that atherosclerotic lesions in the coronary arteries are becoming more stable and less dangerous, but we need additional research to understand these changes,” Eliseo Guallar, MD, PhD, professor, Johns Hopkins Bloomberg School of Public Health, Baltimore, the study’s corresponding author, said in an interview.

This paradoxical effect notwithstanding, doctors should continue to advise their patients to follow the physical activity guidelines for Americans that were published in 2018, Dr. Guallar said.

“Physical activity is a key component of a healthy lifestyle. Our analysis can be useful, however, if someone starts exercising and sees that his or her coronary calcium score goes up,” he said.

The study is published online September 20 in Heart.

The degree of build-up of calcium deposits in the coronary arteries is used to determine future cardiovascular disease risk and to guide treatment to prevent myocardial infarction and stroke. A CAC score of at least 100 Agatston units indicates that treatment with statins is warranted, the researchers write.

In the current study, investigators — led by Ki-Chul Sung, MD, Sungkyunkwan University School of Medicine, Seoul, Korea, and Yun Soo Hong, MD, Johns Hopkins Bloomberg School of Public Health, Baltimore — explored the link between different degrees of physical activity and the progression of CAC scores in healthy adults.

“While physical activity improves a wide array of cardiovascular and metabolic biomarkers, endurance athletes were more likely to have a coronary artery calcium (CAC) score >300 Agatston units or coronary plaques compared with sedentary men with a similar risk profile. It is not clear if exercise may itself be associated with calcification of the arteries,” the authors write.

The researchers studied 25,485 participants (22,741 men and 2,744 women) who were part of the Kangbuk Samsung Health Study. All were free of cardiovascular disease at study entry and underwent comprehensive health screening exams at one of two major health centers in Seoul and Suwon, South Korea, between March 1, 2011, and December 31, 2017.

At each exam, participants filled out a questionnaire that included questions on medical and family history, smoking habits, alcohol intake, and education level.

Participants were also quizzed at baseline about their physical activity, using the Korean version of the International Physical Activity Questionnaire Short Form (IPAQ-SF).

On the basis of that, they were categorized into one of three categories: inactive; moderately active, defined as at least 3 days of vigorous-intensity activity for at least 20 min/day or at least 5 days of moderate-intensity activity or walking for at least 30 min/ day or at least 5 days of any combination of walking and moderate- or vigorous-intensity activities, attaining at least 600 MET-min/week; or health-enhancing physically active (HEPA), defined as at least 3 days of vigorous-intensity activity, attaining at least 1,500 MET-min/week or 7 days of any combination of walking or moderate- or vigorous-intensity activities, attaining at least 3000 MET-min/week.  

Of the study participants, 47% were classified as inactive, 38% as moderately active, and 15% as HEPA.

Those who were more physically active tended to be older and less likely to smoke than less physically active participants. They also had lower total cholesterol, more hypertension, and existing evidence of calcium deposits in their coronary arteries.

A graded association between physical activity level and the prevalence and progression of coronary artery calcification was seen, irrespective of CAC scores at the start of monitoring.

At baseline, the estimated adjusted average baseline CAC scores in inactive participants was 9.45 (95% CI, 8.76 - 10.14), in moderately active participants was 10.20 (95% CI, 9.40 - 11.00), and in HEPA participants was 12.04 (95% CI, 10.81 - 13.26).

Compared with the least active participants, the estimated adjusted 5-year average increases in CAC was 3.20 (95% CI, 0.72 - 5.69) in moderately active participants and 8.16 (95% CI, 4.80 - 11.53) in HEPA participants.

A higher level of physical activity was associated with faster progression of CAC scores, both in participants with CAC score of 0 at baseline and in those with prevalent CAC.

The authors note there are several limitations to consider when interpreting their findings. These include the absence of an objective assessment of physical activity, the inability to evaluate the association between physical activity and CAC levels with incident cardiovascular events because of a lack of data, and the lack of information on incident myocardial infarction, stroke, CAC density, or volume.

Physical activity might increase coronary atherosclerosis through mechanical stress and vessel wall injury of coronary arteries; physiologic responses during exercise, such as increased blood pressure; increased parathyroid hormone levels; and changes in coronary hemodynamics and inflammation. “In addition, other factors, such as diet, vitamins, and minerals, may change with physical activity,” the authors write.

“The second possibility is that physical activity may increase CAC scores without increasing cardiovascular disease risk,” they write.

“The cardiovascular benefits of physical activity are unquestionable,” the authors emphasize, adding that the national guidelines recommend at least 150 to 300 minutes per week of moderate-intensity or 75 to 150 minutes per week of vigorous-intensity aerobic physical activity.

“Patients and physicians, however, need to consider that engaging in physical activity may accelerate the progression of coronary calcium, possibly due to plaque healing, stabilization and calcification,” they conclude.

Dr. Guallar added: “We would like to link our research to clinical outcomes, so that we can really be sure that the increase in coronary calcium scores does not imply an increase in risk.”

“Do these findings mean that we should stop using coronary artery calcium scores to assess coronary artery disease?” ask Gaurav Gulsin, MD, and Alastair James Moss, MD, University of Leicester, United Kingdom, in an accompanying editorial.

The study highlights the complexity of interpreting CAC scores in patients who have implemented recommendations for physical activity or started statin therapy, they note.

“While proponents would argue that it is an effective tool to screen for subclinical atherosclerosis in asymptomatic individuals, clinicians should be cautious regarding the overuse of this test in otherwise healthy individuals. The coronary artery calcium paradox should not result in paradoxical care for our patients,” Dr. Gulsin and Dr. Moss conclude.

Dr. Sung, Dr. Hong, and the other study authors report no relevant financial relationships. The British Heart Foundation provides funding support for Dr. Gulsin and Dr. Moss.

A version of this article first appeared on Medscape.com.

Physical activity, long recommended by health experts to reduce risk for obesity, heart disease, type 2 diabetes, high blood pressure, hypercholesterolemia, and other cardiovascular disease risk factors, is also associated with increases in the amount of calcium deposited in the coronary arteries, new observational data suggest.

In a prospective cohort study of Korean men and women 18 years and older, participants who were the most physically active had the fastest progression of their coronary artery calcium (CAC) scores at 5 years, compared with those who were the least physically active.

“People who exercise may have an increase in their coronary calcium levels, but this is not necessarily bad news. This may mean that atherosclerotic lesions in the coronary arteries are becoming more stable and less dangerous, but we need additional research to understand these changes,” Eliseo Guallar, MD, PhD, professor, Johns Hopkins Bloomberg School of Public Health, Baltimore, the study’s corresponding author, said in an interview.

This paradoxical effect notwithstanding, doctors should continue to advise their patients to follow the physical activity guidelines for Americans that were published in 2018, Dr. Guallar said.

“Physical activity is a key component of a healthy lifestyle. Our analysis can be useful, however, if someone starts exercising and sees that his or her coronary calcium score goes up,” he said.

The study is published online September 20 in Heart.

The degree of build-up of calcium deposits in the coronary arteries is used to determine future cardiovascular disease risk and to guide treatment to prevent myocardial infarction and stroke. A CAC score of at least 100 Agatston units indicates that treatment with statins is warranted, the researchers write.

In the current study, investigators — led by Ki-Chul Sung, MD, Sungkyunkwan University School of Medicine, Seoul, Korea, and Yun Soo Hong, MD, Johns Hopkins Bloomberg School of Public Health, Baltimore — explored the link between different degrees of physical activity and the progression of CAC scores in healthy adults.

“While physical activity improves a wide array of cardiovascular and metabolic biomarkers, endurance athletes were more likely to have a coronary artery calcium (CAC) score >300 Agatston units or coronary plaques compared with sedentary men with a similar risk profile. It is not clear if exercise may itself be associated with calcification of the arteries,” the authors write.

The researchers studied 25,485 participants (22,741 men and 2,744 women) who were part of the Kangbuk Samsung Health Study. All were free of cardiovascular disease at study entry and underwent comprehensive health screening exams at one of two major health centers in Seoul and Suwon, South Korea, between March 1, 2011, and December 31, 2017.

At each exam, participants filled out a questionnaire that included questions on medical and family history, smoking habits, alcohol intake, and education level.

Participants were also quizzed at baseline about their physical activity, using the Korean version of the International Physical Activity Questionnaire Short Form (IPAQ-SF).

On the basis of that, they were categorized into one of three categories: inactive; moderately active, defined as at least 3 days of vigorous-intensity activity for at least 20 min/day or at least 5 days of moderate-intensity activity or walking for at least 30 min/ day or at least 5 days of any combination of walking and moderate- or vigorous-intensity activities, attaining at least 600 MET-min/week; or health-enhancing physically active (HEPA), defined as at least 3 days of vigorous-intensity activity, attaining at least 1,500 MET-min/week or 7 days of any combination of walking or moderate- or vigorous-intensity activities, attaining at least 3000 MET-min/week.  

Of the study participants, 47% were classified as inactive, 38% as moderately active, and 15% as HEPA.

Those who were more physically active tended to be older and less likely to smoke than less physically active participants. They also had lower total cholesterol, more hypertension, and existing evidence of calcium deposits in their coronary arteries.

A graded association between physical activity level and the prevalence and progression of coronary artery calcification was seen, irrespective of CAC scores at the start of monitoring.

At baseline, the estimated adjusted average baseline CAC scores in inactive participants was 9.45 (95% CI, 8.76 - 10.14), in moderately active participants was 10.20 (95% CI, 9.40 - 11.00), and in HEPA participants was 12.04 (95% CI, 10.81 - 13.26).

Compared with the least active participants, the estimated adjusted 5-year average increases in CAC was 3.20 (95% CI, 0.72 - 5.69) in moderately active participants and 8.16 (95% CI, 4.80 - 11.53) in HEPA participants.

A higher level of physical activity was associated with faster progression of CAC scores, both in participants with CAC score of 0 at baseline and in those with prevalent CAC.

The authors note there are several limitations to consider when interpreting their findings. These include the absence of an objective assessment of physical activity, the inability to evaluate the association between physical activity and CAC levels with incident cardiovascular events because of a lack of data, and the lack of information on incident myocardial infarction, stroke, CAC density, or volume.

Physical activity might increase coronary atherosclerosis through mechanical stress and vessel wall injury of coronary arteries; physiologic responses during exercise, such as increased blood pressure; increased parathyroid hormone levels; and changes in coronary hemodynamics and inflammation. “In addition, other factors, such as diet, vitamins, and minerals, may change with physical activity,” the authors write.

“The second possibility is that physical activity may increase CAC scores without increasing cardiovascular disease risk,” they write.

“The cardiovascular benefits of physical activity are unquestionable,” the authors emphasize, adding that the national guidelines recommend at least 150 to 300 minutes per week of moderate-intensity or 75 to 150 minutes per week of vigorous-intensity aerobic physical activity.

“Patients and physicians, however, need to consider that engaging in physical activity may accelerate the progression of coronary calcium, possibly due to plaque healing, stabilization and calcification,” they conclude.

Dr. Guallar added: “We would like to link our research to clinical outcomes, so that we can really be sure that the increase in coronary calcium scores does not imply an increase in risk.”

“Do these findings mean that we should stop using coronary artery calcium scores to assess coronary artery disease?” ask Gaurav Gulsin, MD, and Alastair James Moss, MD, University of Leicester, United Kingdom, in an accompanying editorial.

The study highlights the complexity of interpreting CAC scores in patients who have implemented recommendations for physical activity or started statin therapy, they note.

“While proponents would argue that it is an effective tool to screen for subclinical atherosclerosis in asymptomatic individuals, clinicians should be cautious regarding the overuse of this test in otherwise healthy individuals. The coronary artery calcium paradox should not result in paradoxical care for our patients,” Dr. Gulsin and Dr. Moss conclude.

Dr. Sung, Dr. Hong, and the other study authors report no relevant financial relationships. The British Heart Foundation provides funding support for Dr. Gulsin and Dr. Moss.

A version of this article first appeared on Medscape.com.

Physical activity, long recommended by health experts to reduce risk for obesity, heart disease, type 2 diabetes, high blood pressure, hypercholesterolemia, and other cardiovascular disease risk factors, is also associated with increases in the amount of calcium deposited in the coronary arteries, new observational data suggest.

In a prospective cohort study of Korean men and women 18 years and older, participants who were the most physically active had the fastest progression of their coronary artery calcium (CAC) scores at 5 years, compared with those who were the least physically active.

“People who exercise may have an increase in their coronary calcium levels, but this is not necessarily bad news. This may mean that atherosclerotic lesions in the coronary arteries are becoming more stable and less dangerous, but we need additional research to understand these changes,” Eliseo Guallar, MD, PhD, professor, Johns Hopkins Bloomberg School of Public Health, Baltimore, the study’s corresponding author, said in an interview.

This paradoxical effect notwithstanding, doctors should continue to advise their patients to follow the physical activity guidelines for Americans that were published in 2018, Dr. Guallar said.

“Physical activity is a key component of a healthy lifestyle. Our analysis can be useful, however, if someone starts exercising and sees that his or her coronary calcium score goes up,” he said.

The study is published online September 20 in Heart.

The degree of build-up of calcium deposits in the coronary arteries is used to determine future cardiovascular disease risk and to guide treatment to prevent myocardial infarction and stroke. A CAC score of at least 100 Agatston units indicates that treatment with statins is warranted, the researchers write.

In the current study, investigators — led by Ki-Chul Sung, MD, Sungkyunkwan University School of Medicine, Seoul, Korea, and Yun Soo Hong, MD, Johns Hopkins Bloomberg School of Public Health, Baltimore — explored the link between different degrees of physical activity and the progression of CAC scores in healthy adults.

“While physical activity improves a wide array of cardiovascular and metabolic biomarkers, endurance athletes were more likely to have a coronary artery calcium (CAC) score >300 Agatston units or coronary plaques compared with sedentary men with a similar risk profile. It is not clear if exercise may itself be associated with calcification of the arteries,” the authors write.

The researchers studied 25,485 participants (22,741 men and 2,744 women) who were part of the Kangbuk Samsung Health Study. All were free of cardiovascular disease at study entry and underwent comprehensive health screening exams at one of two major health centers in Seoul and Suwon, South Korea, between March 1, 2011, and December 31, 2017.

At each exam, participants filled out a questionnaire that included questions on medical and family history, smoking habits, alcohol intake, and education level.

Participants were also quizzed at baseline about their physical activity, using the Korean version of the International Physical Activity Questionnaire Short Form (IPAQ-SF).

On the basis of that, they were categorized into one of three categories: inactive; moderately active, defined as at least 3 days of vigorous-intensity activity for at least 20 min/day or at least 5 days of moderate-intensity activity or walking for at least 30 min/ day or at least 5 days of any combination of walking and moderate- or vigorous-intensity activities, attaining at least 600 MET-min/week; or health-enhancing physically active (HEPA), defined as at least 3 days of vigorous-intensity activity, attaining at least 1,500 MET-min/week or 7 days of any combination of walking or moderate- or vigorous-intensity activities, attaining at least 3000 MET-min/week.  

Of the study participants, 47% were classified as inactive, 38% as moderately active, and 15% as HEPA.

Those who were more physically active tended to be older and less likely to smoke than less physically active participants. They also had lower total cholesterol, more hypertension, and existing evidence of calcium deposits in their coronary arteries.

A graded association between physical activity level and the prevalence and progression of coronary artery calcification was seen, irrespective of CAC scores at the start of monitoring.

At baseline, the estimated adjusted average baseline CAC scores in inactive participants was 9.45 (95% CI, 8.76 - 10.14), in moderately active participants was 10.20 (95% CI, 9.40 - 11.00), and in HEPA participants was 12.04 (95% CI, 10.81 - 13.26).

Compared with the least active participants, the estimated adjusted 5-year average increases in CAC was 3.20 (95% CI, 0.72 - 5.69) in moderately active participants and 8.16 (95% CI, 4.80 - 11.53) in HEPA participants.

A higher level of physical activity was associated with faster progression of CAC scores, both in participants with CAC score of 0 at baseline and in those with prevalent CAC.

The authors note there are several limitations to consider when interpreting their findings. These include the absence of an objective assessment of physical activity, the inability to evaluate the association between physical activity and CAC levels with incident cardiovascular events because of a lack of data, and the lack of information on incident myocardial infarction, stroke, CAC density, or volume.

Physical activity might increase coronary atherosclerosis through mechanical stress and vessel wall injury of coronary arteries; physiologic responses during exercise, such as increased blood pressure; increased parathyroid hormone levels; and changes in coronary hemodynamics and inflammation. “In addition, other factors, such as diet, vitamins, and minerals, may change with physical activity,” the authors write.

“The second possibility is that physical activity may increase CAC scores without increasing cardiovascular disease risk,” they write.

“The cardiovascular benefits of physical activity are unquestionable,” the authors emphasize, adding that the national guidelines recommend at least 150 to 300 minutes per week of moderate-intensity or 75 to 150 minutes per week of vigorous-intensity aerobic physical activity.

“Patients and physicians, however, need to consider that engaging in physical activity may accelerate the progression of coronary calcium, possibly due to plaque healing, stabilization and calcification,” they conclude.

Dr. Guallar added: “We would like to link our research to clinical outcomes, so that we can really be sure that the increase in coronary calcium scores does not imply an increase in risk.”

“Do these findings mean that we should stop using coronary artery calcium scores to assess coronary artery disease?” ask Gaurav Gulsin, MD, and Alastair James Moss, MD, University of Leicester, United Kingdom, in an accompanying editorial.

The study highlights the complexity of interpreting CAC scores in patients who have implemented recommendations for physical activity or started statin therapy, they note.

“While proponents would argue that it is an effective tool to screen for subclinical atherosclerosis in asymptomatic individuals, clinicians should be cautious regarding the overuse of this test in otherwise healthy individuals. The coronary artery calcium paradox should not result in paradoxical care for our patients,” Dr. Gulsin and Dr. Moss conclude.

Dr. Sung, Dr. Hong, and the other study authors report no relevant financial relationships. The British Heart Foundation provides funding support for Dr. Gulsin and Dr. Moss.

A version of this article first appeared on Medscape.com.

A 4-month, structured diet and exercise intervention lowered blood pressure in adults with resistant blood pressure, according to results from a randomized, clinical trial. The program also led to improvements in baroreflex sensitivity, heart rate variability, and flow-mediated dilation, compared with individuals who received only a single education session.

The intervention included instruction from a nutritionist on how to follow the Dietary Approaches to Stop Hypertension (DASH) diet, as well as restricting calories and sodium to less than 2,300 mg/day. It included weekly, 45-minute group counseling sessions, run by a clinical psychiatrist, focusing on eating behaviors. The exercise component included 30- to 45-minute sessions at 70%-85% of initial heart rate reserve, carried out three times per week at a cardiac rehabilitation facility.

“While some individuals can make the lifestyle changes on their own, a structured program of supervised exercise and dietary modification conducted by a multidisciplinary team of physicians, psychologists, nutritionists, and physical therapists/exercise physiologists found in cardiac rehabilitation programs throughout the country is likely to be more effective. There are many cardiac rehabilitation programs throughout the country that are accessible to most patients,” said lead author James Blumenthal, PhD, the J.P. Gibbons Professor in Psychiatry and Behavioral Sciences at Duke University, Durham, N.C.

The study, called Treating Resistant Hypertension Using Lifestyle Modification to Promote Health (TRIUMPH), was published in Circulation. It is one of few that have examined lifestyle interventions in resistant hypertension, defined as systolic blood pressure ≥ 130 mm Hg or diastolic blood pressure ≥ 80 mm Hg after adherence to three or more optimally-dosed antihypertensive medications of three different classes, including one diuretic.

“This is a nice study [that] emphasizes what we often forget: Lifestyle factors, especially salt intake, are important drivers of resistant hypertension. Our own studies have shown that this is predominantly a salt retaining state, and one would expect dietary salt restriction to be particularly effective in this group of patients and that is what this study showed,” said Bryan Williams, MD, who was asked to comment on the study. Dr. Williams is chair of medicine at University College London.

The results should also be reassuring to some who worried that exercise might lead to worsened blood pressure. “This study showed that in patients with resistant hypertension, though not out of control blood pressures, exercise was not only safe, but effective in lowering their blood pressure,” said Deepak L. Bhatt, MD, MPH, who was asked to comment. He is executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, and professor of medicine at Harvard Medical School, both in Boston.

The new research isn’t unique. In August, researchers in Portugal and Brazil showed that a 12-week exercise-only intervention reduced 24-hour and daytime ambulatory systolic and diastolic blood pressure. The two studies communicate the same message. “Lifestyle changes can work for resistant hypertension. So, two independent, modest-sized studies with essentially the same, positive, actionable conclusion,” said Dr. Bhatt, adding that the next step should be a larger, multicenter trial.

In the new study, 90 patients were assigned to the diet and exercise intervention and 50 to the control group. They had a mean age of 63 years, and 48% were women. Participants attended 94% of DASH diet classes and 89% of exercise sessions, and both groups had excellent adherence to medications.

The treatment group had a greater reduction in clinic systolic BP (–12.5 versus –7.1 mm Hg; P = .005) and diastolic BP (–5.9 versus –3.7 mm Hg; P = .034), as well as 24-hour ambulatory systolic BP (–7.0 versus –0.3 mm Hg; P = .001). The treatment group also had more improvement in resting baroreflex sensitivity (2.3 versus –1.1 ms/mm Hg; P = .003), high-frequency heart rate variability (0.4 versus –0.2 ln ms²; P = .025, and flow-mediated dilation (0.3% versus –1.4%, P = .022). The two groups had similar outcomes with respect to pulse wave velocity and left ventricular mass.

“Results of the TRIUMPH study suggest that policymakers should consider resistant hypertension as a new indication for cardiac rehabilitation with appropriate coverage by governmental agencies and private insurers,” Dr. Blumenthal said.

“This is an important new, evidence-based intervention for resistant hypertension. It is safe and relatively inexpensive. It should now be something physicians routinely offer these patients. Hopefully in the future, insurers will cover cardiac rehabilitation for patients with resistant hypertension,” Dr. Bhatt said.

The study also pointed towards an effective approach for patients who may be unable to sustain lifestyle changes. “Of course, not every patient will be able to maintain a healthy diet and an exercise program on their own, thus a cardiac rehabilitation program can be an excellent way to increase the likelihood of successful lifestyle modification,” Dr. Bhatt said.

TRIUMPH was sponsored by grants from the National Heart, Lung, and Blood Institute. None of the authors had disclosures to report. Dr. Bhatt disclosed having financial relationships with more than 40 pharmaceutical companies. Dr. Williams reported having no relevant financial disclosures.
 

A 4-month, structured diet and exercise intervention lowered blood pressure in adults with resistant blood pressure, according to results from a randomized, clinical trial. The program also led to improvements in baroreflex sensitivity, heart rate variability, and flow-mediated dilation, compared with individuals who received only a single education session.

The intervention included instruction from a nutritionist on how to follow the Dietary Approaches to Stop Hypertension (DASH) diet, as well as restricting calories and sodium to less than 2,300 mg/day. It included weekly, 45-minute group counseling sessions, run by a clinical psychiatrist, focusing on eating behaviors. The exercise component included 30- to 45-minute sessions at 70%-85% of initial heart rate reserve, carried out three times per week at a cardiac rehabilitation facility.

“While some individuals can make the lifestyle changes on their own, a structured program of supervised exercise and dietary modification conducted by a multidisciplinary team of physicians, psychologists, nutritionists, and physical therapists/exercise physiologists found in cardiac rehabilitation programs throughout the country is likely to be more effective. There are many cardiac rehabilitation programs throughout the country that are accessible to most patients,” said lead author James Blumenthal, PhD, the J.P. Gibbons Professor in Psychiatry and Behavioral Sciences at Duke University, Durham, N.C.

The study, called Treating Resistant Hypertension Using Lifestyle Modification to Promote Health (TRIUMPH), was published in Circulation. It is one of few that have examined lifestyle interventions in resistant hypertension, defined as systolic blood pressure ≥ 130 mm Hg or diastolic blood pressure ≥ 80 mm Hg after adherence to three or more optimally-dosed antihypertensive medications of three different classes, including one diuretic.

“This is a nice study [that] emphasizes what we often forget: Lifestyle factors, especially salt intake, are important drivers of resistant hypertension. Our own studies have shown that this is predominantly a salt retaining state, and one would expect dietary salt restriction to be particularly effective in this group of patients and that is what this study showed,” said Bryan Williams, MD, who was asked to comment on the study. Dr. Williams is chair of medicine at University College London.

The results should also be reassuring to some who worried that exercise might lead to worsened blood pressure. “This study showed that in patients with resistant hypertension, though not out of control blood pressures, exercise was not only safe, but effective in lowering their blood pressure,” said Deepak L. Bhatt, MD, MPH, who was asked to comment. He is executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, and professor of medicine at Harvard Medical School, both in Boston.

The new research isn’t unique. In August, researchers in Portugal and Brazil showed that a 12-week exercise-only intervention reduced 24-hour and daytime ambulatory systolic and diastolic blood pressure. The two studies communicate the same message. “Lifestyle changes can work for resistant hypertension. So, two independent, modest-sized studies with essentially the same, positive, actionable conclusion,” said Dr. Bhatt, adding that the next step should be a larger, multicenter trial.

In the new study, 90 patients were assigned to the diet and exercise intervention and 50 to the control group. They had a mean age of 63 years, and 48% were women. Participants attended 94% of DASH diet classes and 89% of exercise sessions, and both groups had excellent adherence to medications.

The treatment group had a greater reduction in clinic systolic BP (–12.5 versus –7.1 mm Hg; P = .005) and diastolic BP (–5.9 versus –3.7 mm Hg; P = .034), as well as 24-hour ambulatory systolic BP (–7.0 versus –0.3 mm Hg; P = .001). The treatment group also had more improvement in resting baroreflex sensitivity (2.3 versus –1.1 ms/mm Hg; P = .003), high-frequency heart rate variability (0.4 versus –0.2 ln ms²; P = .025, and flow-mediated dilation (0.3% versus –1.4%, P = .022). The two groups had similar outcomes with respect to pulse wave velocity and left ventricular mass.

“Results of the TRIUMPH study suggest that policymakers should consider resistant hypertension as a new indication for cardiac rehabilitation with appropriate coverage by governmental agencies and private insurers,” Dr. Blumenthal said.

“This is an important new, evidence-based intervention for resistant hypertension. It is safe and relatively inexpensive. It should now be something physicians routinely offer these patients. Hopefully in the future, insurers will cover cardiac rehabilitation for patients with resistant hypertension,” Dr. Bhatt said.

The study also pointed towards an effective approach for patients who may be unable to sustain lifestyle changes. “Of course, not every patient will be able to maintain a healthy diet and an exercise program on their own, thus a cardiac rehabilitation program can be an excellent way to increase the likelihood of successful lifestyle modification,” Dr. Bhatt said.

TRIUMPH was sponsored by grants from the National Heart, Lung, and Blood Institute. None of the authors had disclosures to report. Dr. Bhatt disclosed having financial relationships with more than 40 pharmaceutical companies. Dr. Williams reported having no relevant financial disclosures.
 

A 4-month, structured diet and exercise intervention lowered blood pressure in adults with resistant blood pressure, according to results from a randomized, clinical trial. The program also led to improvements in baroreflex sensitivity, heart rate variability, and flow-mediated dilation, compared with individuals who received only a single education session.

The intervention included instruction from a nutritionist on how to follow the Dietary Approaches to Stop Hypertension (DASH) diet, as well as restricting calories and sodium to less than 2,300 mg/day. It included weekly, 45-minute group counseling sessions, run by a clinical psychiatrist, focusing on eating behaviors. The exercise component included 30- to 45-minute sessions at 70%-85% of initial heart rate reserve, carried out three times per week at a cardiac rehabilitation facility.

“While some individuals can make the lifestyle changes on their own, a structured program of supervised exercise and dietary modification conducted by a multidisciplinary team of physicians, psychologists, nutritionists, and physical therapists/exercise physiologists found in cardiac rehabilitation programs throughout the country is likely to be more effective. There are many cardiac rehabilitation programs throughout the country that are accessible to most patients,” said lead author James Blumenthal, PhD, the J.P. Gibbons Professor in Psychiatry and Behavioral Sciences at Duke University, Durham, N.C.

The study, called Treating Resistant Hypertension Using Lifestyle Modification to Promote Health (TRIUMPH), was published in Circulation. It is one of few that have examined lifestyle interventions in resistant hypertension, defined as systolic blood pressure ≥ 130 mm Hg or diastolic blood pressure ≥ 80 mm Hg after adherence to three or more optimally-dosed antihypertensive medications of three different classes, including one diuretic.

“This is a nice study [that] emphasizes what we often forget: Lifestyle factors, especially salt intake, are important drivers of resistant hypertension. Our own studies have shown that this is predominantly a salt retaining state, and one would expect dietary salt restriction to be particularly effective in this group of patients and that is what this study showed,” said Bryan Williams, MD, who was asked to comment on the study. Dr. Williams is chair of medicine at University College London.

The results should also be reassuring to some who worried that exercise might lead to worsened blood pressure. “This study showed that in patients with resistant hypertension, though not out of control blood pressures, exercise was not only safe, but effective in lowering their blood pressure,” said Deepak L. Bhatt, MD, MPH, who was asked to comment. He is executive director of interventional cardiovascular programs at Brigham and Women’s Hospital, and professor of medicine at Harvard Medical School, both in Boston.

The new research isn’t unique. In August, researchers in Portugal and Brazil showed that a 12-week exercise-only intervention reduced 24-hour and daytime ambulatory systolic and diastolic blood pressure. The two studies communicate the same message. “Lifestyle changes can work for resistant hypertension. So, two independent, modest-sized studies with essentially the same, positive, actionable conclusion,” said Dr. Bhatt, adding that the next step should be a larger, multicenter trial.

In the new study, 90 patients were assigned to the diet and exercise intervention and 50 to the control group. They had a mean age of 63 years, and 48% were women. Participants attended 94% of DASH diet classes and 89% of exercise sessions, and both groups had excellent adherence to medications.

The treatment group had a greater reduction in clinic systolic BP (–12.5 versus –7.1 mm Hg; P = .005) and diastolic BP (–5.9 versus –3.7 mm Hg; P = .034), as well as 24-hour ambulatory systolic BP (–7.0 versus –0.3 mm Hg; P = .001). The treatment group also had more improvement in resting baroreflex sensitivity (2.3 versus –1.1 ms/mm Hg; P = .003), high-frequency heart rate variability (0.4 versus –0.2 ln ms²; P = .025, and flow-mediated dilation (0.3% versus –1.4%, P = .022). The two groups had similar outcomes with respect to pulse wave velocity and left ventricular mass.

“Results of the TRIUMPH study suggest that policymakers should consider resistant hypertension as a new indication for cardiac rehabilitation with appropriate coverage by governmental agencies and private insurers,” Dr. Blumenthal said.

“This is an important new, evidence-based intervention for resistant hypertension. It is safe and relatively inexpensive. It should now be something physicians routinely offer these patients. Hopefully in the future, insurers will cover cardiac rehabilitation for patients with resistant hypertension,” Dr. Bhatt said.

The study also pointed towards an effective approach for patients who may be unable to sustain lifestyle changes. “Of course, not every patient will be able to maintain a healthy diet and an exercise program on their own, thus a cardiac rehabilitation program can be an excellent way to increase the likelihood of successful lifestyle modification,” Dr. Bhatt said.

TRIUMPH was sponsored by grants from the National Heart, Lung, and Blood Institute. None of the authors had disclosures to report. Dr. Bhatt disclosed having financial relationships with more than 40 pharmaceutical companies. Dr. Williams reported having no relevant financial disclosures.