Cardiology

NEW ORLEANS – Treatment of patients with heart failure with preserved ejection fraction (HFpEF) with the SGLT2 inhibitor dapagliflozin (Farxiga) for 24 weeks produced significant and beneficial reductions in left-heart filling pressures in a mechanistic, randomized clinical study.

The findings “provide new insight into the mechanisms underlying the favorable clinical effects of dapagliflozin in patients with HFpEF,” Barry A. Borlaug, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. “Elevations in left heart filling pressures at rest and during exercise are fundamental pathophysiologic features of HFpEF,” he noted.

Results from prior studies documented the benefit of dapagliflozin for improving clinical outcomes in patients with HFpEF in the DELIVER trial, and for the related sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin (Jardiance) in the EMPEROR-Preserved trial. The new findings presented by Dr. Borlaug provide evidence from a placebo-controlled, prospective study for one way by which these SGLT2 inhibitors exert this benefit in patients with HFpEF.

The results of his single-center study showed that, in patients with HFpEF who also exhibited “severe” elevations in pulmonary capillary wedge pressure (PCWP) during exercise, 24 weeks of treatment with dapagliflozin led to a significant reduction in PCWP during exercise. The treatment produced an average 6.1–mm Hg drop from baseline compared with control patients who received placebo. A similar pattern occurred when these patients were at rest, when dapagliflozin treatment linked with a significant average reduction in PCWP from baseline of 3.5 mm Hg compared with controls.
 

Improving a ‘specific and fundamental’ feature of HFpEF

“This fantastic study looked at one of the fundamental aspects of HFpEF,” said John R. Teerlink, MD, designated discussant for the study. “You’ve shown that dapagliflozin targets a specific and fundamental” manifestation of HFpEF by lowering PCWP, said Dr. Teerlink, director of Heart Failure at the San Francisco Veterans Affairs Medical Center.

However, Dr. Teerlink added, the study did not directly address the related question of what physiologic action of dapagliflozin produces this notable drop in PCWP.

“We’re just starting to look at that,” replied Dr. Borlaug, a cardiologist and professor at the Mayo Clinic in Rochester, Minn.

He reported finding an intriguing correlate in the current study linked to the cut in PCWP with dapagliflozin treatment. The SGLT2 inhibitor at a standard daily 10-mg dose produced an average 3.5-kg drop in body weight in the dapagliflozin-treated patients that significantly linked with the changes in PCWP both at rest and during exercise. Dapagliflozin-treated patients also showed a significant reduction from their baseline plasma volume compared with placebo-treated patients, but this “poorly correlated” with the dapagliflozin-linked cuts in PCWP, Dr. Borlaug said.

“I don’t think this means weight loss is the cause of the hemodynamic benefit, but maybe it’s an indicator. When patients [with HFpEF] lose weight, they are in a metabolic state that leads to good changes in hemodynamics,” he suggested. “My guess is that there is probably a combination of many different little things [caused by dapagliflozin treatment of patients with HFpEF] that together result in the 20%-25% relative improvement we see in filling pressure.”
 

An ‘obese, cardiometabolic’ HFpEF phenotype

The study enrolled patients with HFpEF and a left ventricular ejection fraction of at least 50%, a New York Heart Association functional class of 2 or 3, and a PCWP during exercise of at least 25 mm Hg. Of the 37 evaluable patients, about two-thirds of the patients were women, more than two-thirds were in functional class 3, about 70% were obese, and their average ejection fraction was about 62%. The study excluded patients with HFpEF who also had type 1 diabetes, cardiomyopathy, pericardial disease, or other causes of dyspnea or heart failure.

Dr. Teerlink asked about the generalizability of the findings, as the study cohort seemed to differ in certain respects from the patients enrolled in the DELIVER trial, and because of the many apparently distinct patient phenotypes that exist within the scope of HFpEF.

An “obese, cardiometabolic phenotype” predominated the study cohort, Dr. Borlaug said. “The patients we enrolled look like the HFpEF patients seen in U.S. clinics.” However, he added that “in reality, many [HFpEF phenotypes] coexist in one patient. It’s not that simple,” that every patient with HFpEF can be categorized into a single HFpEF phenotype.

The researchers monitored PCWP invasively with high-fidelity micromanometer catheters.

The study was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Borlaug has received research funding from AstraZeneca, as well as from Corvia, GlaxoSmithKline, Medtronic, Mesoblast, Novo Nordisk, and Tenax. Dr. Teerlink has had financial relationships with AstraZeneca, as well as with Amgen, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cytokinetics, Medtronic, Merck, Novartis, Servier, and Windtree Therapeutics.

NEW ORLEANS – Treatment of patients with heart failure with preserved ejection fraction (HFpEF) with the SGLT2 inhibitor dapagliflozin (Farxiga) for 24 weeks produced significant and beneficial reductions in left-heart filling pressures in a mechanistic, randomized clinical study.

The findings “provide new insight into the mechanisms underlying the favorable clinical effects of dapagliflozin in patients with HFpEF,” Barry A. Borlaug, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. “Elevations in left heart filling pressures at rest and during exercise are fundamental pathophysiologic features of HFpEF,” he noted.

Results from prior studies documented the benefit of dapagliflozin for improving clinical outcomes in patients with HFpEF in the DELIVER trial, and for the related sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin (Jardiance) in the EMPEROR-Preserved trial. The new findings presented by Dr. Borlaug provide evidence from a placebo-controlled, prospective study for one way by which these SGLT2 inhibitors exert this benefit in patients with HFpEF.

The results of his single-center study showed that, in patients with HFpEF who also exhibited “severe” elevations in pulmonary capillary wedge pressure (PCWP) during exercise, 24 weeks of treatment with dapagliflozin led to a significant reduction in PCWP during exercise. The treatment produced an average 6.1–mm Hg drop from baseline compared with control patients who received placebo. A similar pattern occurred when these patients were at rest, when dapagliflozin treatment linked with a significant average reduction in PCWP from baseline of 3.5 mm Hg compared with controls.
 

Improving a ‘specific and fundamental’ feature of HFpEF

“This fantastic study looked at one of the fundamental aspects of HFpEF,” said John R. Teerlink, MD, designated discussant for the study. “You’ve shown that dapagliflozin targets a specific and fundamental” manifestation of HFpEF by lowering PCWP, said Dr. Teerlink, director of Heart Failure at the San Francisco Veterans Affairs Medical Center.

However, Dr. Teerlink added, the study did not directly address the related question of what physiologic action of dapagliflozin produces this notable drop in PCWP.

“We’re just starting to look at that,” replied Dr. Borlaug, a cardiologist and professor at the Mayo Clinic in Rochester, Minn.

He reported finding an intriguing correlate in the current study linked to the cut in PCWP with dapagliflozin treatment. The SGLT2 inhibitor at a standard daily 10-mg dose produced an average 3.5-kg drop in body weight in the dapagliflozin-treated patients that significantly linked with the changes in PCWP both at rest and during exercise. Dapagliflozin-treated patients also showed a significant reduction from their baseline plasma volume compared with placebo-treated patients, but this “poorly correlated” with the dapagliflozin-linked cuts in PCWP, Dr. Borlaug said.

“I don’t think this means weight loss is the cause of the hemodynamic benefit, but maybe it’s an indicator. When patients [with HFpEF] lose weight, they are in a metabolic state that leads to good changes in hemodynamics,” he suggested. “My guess is that there is probably a combination of many different little things [caused by dapagliflozin treatment of patients with HFpEF] that together result in the 20%-25% relative improvement we see in filling pressure.”
 

An ‘obese, cardiometabolic’ HFpEF phenotype

The study enrolled patients with HFpEF and a left ventricular ejection fraction of at least 50%, a New York Heart Association functional class of 2 or 3, and a PCWP during exercise of at least 25 mm Hg. Of the 37 evaluable patients, about two-thirds of the patients were women, more than two-thirds were in functional class 3, about 70% were obese, and their average ejection fraction was about 62%. The study excluded patients with HFpEF who also had type 1 diabetes, cardiomyopathy, pericardial disease, or other causes of dyspnea or heart failure.

Dr. Teerlink asked about the generalizability of the findings, as the study cohort seemed to differ in certain respects from the patients enrolled in the DELIVER trial, and because of the many apparently distinct patient phenotypes that exist within the scope of HFpEF.

An “obese, cardiometabolic phenotype” predominated the study cohort, Dr. Borlaug said. “The patients we enrolled look like the HFpEF patients seen in U.S. clinics.” However, he added that “in reality, many [HFpEF phenotypes] coexist in one patient. It’s not that simple,” that every patient with HFpEF can be categorized into a single HFpEF phenotype.

The researchers monitored PCWP invasively with high-fidelity micromanometer catheters.

The study was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Borlaug has received research funding from AstraZeneca, as well as from Corvia, GlaxoSmithKline, Medtronic, Mesoblast, Novo Nordisk, and Tenax. Dr. Teerlink has had financial relationships with AstraZeneca, as well as with Amgen, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cytokinetics, Medtronic, Merck, Novartis, Servier, and Windtree Therapeutics.

NEW ORLEANS – Treatment of patients with heart failure with preserved ejection fraction (HFpEF) with the SGLT2 inhibitor dapagliflozin (Farxiga) for 24 weeks produced significant and beneficial reductions in left-heart filling pressures in a mechanistic, randomized clinical study.

The findings “provide new insight into the mechanisms underlying the favorable clinical effects of dapagliflozin in patients with HFpEF,” Barry A. Borlaug, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation. “Elevations in left heart filling pressures at rest and during exercise are fundamental pathophysiologic features of HFpEF,” he noted.

Results from prior studies documented the benefit of dapagliflozin for improving clinical outcomes in patients with HFpEF in the DELIVER trial, and for the related sodium-glucose cotransporter 2 (SGLT2) inhibitor empagliflozin (Jardiance) in the EMPEROR-Preserved trial. The new findings presented by Dr. Borlaug provide evidence from a placebo-controlled, prospective study for one way by which these SGLT2 inhibitors exert this benefit in patients with HFpEF.

The results of his single-center study showed that, in patients with HFpEF who also exhibited “severe” elevations in pulmonary capillary wedge pressure (PCWP) during exercise, 24 weeks of treatment with dapagliflozin led to a significant reduction in PCWP during exercise. The treatment produced an average 6.1–mm Hg drop from baseline compared with control patients who received placebo. A similar pattern occurred when these patients were at rest, when dapagliflozin treatment linked with a significant average reduction in PCWP from baseline of 3.5 mm Hg compared with controls.
 

Improving a ‘specific and fundamental’ feature of HFpEF

“This fantastic study looked at one of the fundamental aspects of HFpEF,” said John R. Teerlink, MD, designated discussant for the study. “You’ve shown that dapagliflozin targets a specific and fundamental” manifestation of HFpEF by lowering PCWP, said Dr. Teerlink, director of Heart Failure at the San Francisco Veterans Affairs Medical Center.

However, Dr. Teerlink added, the study did not directly address the related question of what physiologic action of dapagliflozin produces this notable drop in PCWP.

“We’re just starting to look at that,” replied Dr. Borlaug, a cardiologist and professor at the Mayo Clinic in Rochester, Minn.

He reported finding an intriguing correlate in the current study linked to the cut in PCWP with dapagliflozin treatment. The SGLT2 inhibitor at a standard daily 10-mg dose produced an average 3.5-kg drop in body weight in the dapagliflozin-treated patients that significantly linked with the changes in PCWP both at rest and during exercise. Dapagliflozin-treated patients also showed a significant reduction from their baseline plasma volume compared with placebo-treated patients, but this “poorly correlated” with the dapagliflozin-linked cuts in PCWP, Dr. Borlaug said.

“I don’t think this means weight loss is the cause of the hemodynamic benefit, but maybe it’s an indicator. When patients [with HFpEF] lose weight, they are in a metabolic state that leads to good changes in hemodynamics,” he suggested. “My guess is that there is probably a combination of many different little things [caused by dapagliflozin treatment of patients with HFpEF] that together result in the 20%-25% relative improvement we see in filling pressure.”
 

An ‘obese, cardiometabolic’ HFpEF phenotype

The study enrolled patients with HFpEF and a left ventricular ejection fraction of at least 50%, a New York Heart Association functional class of 2 or 3, and a PCWP during exercise of at least 25 mm Hg. Of the 37 evaluable patients, about two-thirds of the patients were women, more than two-thirds were in functional class 3, about 70% were obese, and their average ejection fraction was about 62%. The study excluded patients with HFpEF who also had type 1 diabetes, cardiomyopathy, pericardial disease, or other causes of dyspnea or heart failure.

Dr. Teerlink asked about the generalizability of the findings, as the study cohort seemed to differ in certain respects from the patients enrolled in the DELIVER trial, and because of the many apparently distinct patient phenotypes that exist within the scope of HFpEF.

An “obese, cardiometabolic phenotype” predominated the study cohort, Dr. Borlaug said. “The patients we enrolled look like the HFpEF patients seen in U.S. clinics.” However, he added that “in reality, many [HFpEF phenotypes] coexist in one patient. It’s not that simple,” that every patient with HFpEF can be categorized into a single HFpEF phenotype.

The researchers monitored PCWP invasively with high-fidelity micromanometer catheters.

The study was sponsored by AstraZeneca, the company that markets dapagliflozin (Farxiga). Dr. Borlaug has received research funding from AstraZeneca, as well as from Corvia, GlaxoSmithKline, Medtronic, Mesoblast, Novo Nordisk, and Tenax. Dr. Teerlink has had financial relationships with AstraZeneca, as well as with Amgen, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Cytokinetics, Medtronic, Merck, Novartis, Servier, and Windtree Therapeutics.

Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.

“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”

“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”

The study was published online in the Journal of the American College of Cardiology.
 

CRF up, mortality risk down

Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.

Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.

The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.

CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.

Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.

Conversely, medication use was progressively higher among those in low CRF categories.

After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.

For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).

Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.

A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.

The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”

“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”

“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”

If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
 

CRF impact “woefully underestimated”

Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.

“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”

Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:

• Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
• At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
• Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
• Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
• Fit people who undergo elective or emergent surgical procedures have better outcomes.
• Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.

Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”

“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.

“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”

In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”

“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.

No funding or relevant financial relationships were disclosed.

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

Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.

“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”

“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”

The study was published online in the Journal of the American College of Cardiology.
 

CRF up, mortality risk down

Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.

Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.

The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.

CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.

Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.

Conversely, medication use was progressively higher among those in low CRF categories.

After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.

For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).

Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.

A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.

The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”

“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”

“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”

If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
 

CRF impact “woefully underestimated”

Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.

“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”

Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:

• Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
• At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
• Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
• Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
• Fit people who undergo elective or emergent surgical procedures have better outcomes.
• Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.

Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”

“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.

“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”

In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”

“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.

No funding or relevant financial relationships were disclosed.

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

Even relatively small changes in cardiorespiratory fitness (CRF) are associated with “considerable” impact on clinical symptoms and mortality risk among individuals with and without cardiovascular disease, new observational data in United States veterans suggest.

“We had a few surprises,” Peter Kokkinos, PhD, Robert Wood Johnson Medical School, New Brunswick, N. J., and the VA Medical Center, Washington, told this news organization. “First, the mortality risk was greatly attenuated in those who were moderate- and high-fit at baseline, despite a decline in fitness over time. In fact, in those with no CVD, the risk was not significantly elevated even when CRF declined by at least one MET [metabolic equivalent of task] for the moderate-fit and two or more METs for the high-fit group.”

“Second,” he said, “Our findings suggest that the impact of CRF on human health is not ephemeral, but rather carries a certain protection over time. Third, the changes in CRF necessary to impact mortality risk are relatively small (> 1.0 METs). This has a substantial clinical and public health significance.”

The study was published online in the Journal of the American College of Cardiology.
 

CRF up, mortality risk down

Dr. Kokkinos and colleagues analyzed data from 93,060 U.S. veterans; of these, 95% were men (mean age, 61.4 years) and 5% were women (mean age, 57.1 years). Overall, 72% of participants were White; 19.8%, African American; 5.2%, Hispanic; 1.9%, Native American, Asian, or Hawaiian; and 1.2%, unknown.

Participants were assigned to age-specific fitness quartiles based on peak METs achieved on a baseline exercise treadmill test (ETT). Each CRF quartile was stratified based on CRF changes (increase, decrease, no change) on the final ETT, with at least two ETT assessments at least 1 year apart.

The mean follow-up was 5.8 years (663,522 person-years), during which 18,302 deaths (19.7%) occurred, for an average annual mortality rate of 27.6 events per 1,000 person-years.

CRF was unchanged in 25.1% of the cohort, increased in 29.3%, and decreased in 45.6%. The trend was similar for those with and without CVD.

Significant differences were seen in all variables across CRF categories. In general, body weight, body mass index, CVD risk factors, and overall disease burden were progressively more unfavorable for those in the lowest CRF categories.

Conversely, medication use was progressively higher among those in low CRF categories.

After adjustment, higher CRF was inversely related to mortality risk for the entire cohort, with and without CVD. Cumulative survival rates across CRF categories declined progressively with increased fitness.

For patients with CVD (hazard ratio, 1.11), other significant predictors of all-cause mortality for patients were age (HR, 1.07), body mass index (HR, 0.98), chronic kidney disease (HR, 1.85), smoking (HR, 1.57), type 2 diabetes (HR, 1.42), hypertension (HR, 1.39), and cancers (HR, 1.37).

Generally, changes in CRF of at least 1.0 MET were associated with inverse and proportionate changes in mortality risk, regardless of baseline CRF status. For example, they note, a CRF decline of > 2.0 METs was associated with a 74% increased mortality risk for low-fit individuals with CVD, and a 69% increase for those without CVD.

A second analysis was done after excluding patients whose CRF declined and who died within 2 years of their last ETT, to account for the possibility that higher mortality rates and CRF declines were consequences of underlying disease (reverse causality). The association between changes in CRF and mortality risk persisted and remained similar to that observed in the entire cohort.

The authors add, “It is noteworthy that CRF increased by at least 1 MET in approximately 29% of the participants in the current study and decreased in approximately 46% of participants. This finding underscores the need to promote physical activity to maintain or increase CRF levels in middle-aged and older individuals.”

“Our findings make a persuasive argument that CRF is a strong and independent determinant of all-cause mortality risk, independent of genetic factors,” Dr. Kokkinos said. “We know that CRF is determined to some degree by genetic factors. However, improvements in aerobic capacity or CRF over time are largely the outcomes of regular engagement in aerobic activities of adequate intensity and volume.”

“Conversely,” he said, “a decline in CRF is likely the result of sedentary behavior, the onset of a chronic condition, or aging.”

If genetics were the sole contributor to mortality risk, then changes in CRF would not influence mortality risk, he concluded.
 

CRF impact “woefully underestimated”

Barry A. Franklin, PhD, past chair of both the American Heart Association’s Council on Physical Activity and Metabolism and the National Advocacy Committee, said the study substantiates previous smaller studies and is a “seminal” work.

“CRF is woefully underestimated as an index of health outcomes and survival,” said Dr. Franklin, director of preventive cardiology and cardiac rehabilitation at Beaumont Health in Royal Oak, Mich. “Moderate to vigorous physical activity should be regularly promoted by the medical community.”

Dr. Franklin’s recent review, published in Mayo Clinic Proceedings, provides evidence for other exercise benefits that clinicians may not be aware of, he noted. These include:

• Each 1 MET increase in CRF is generally associated with approximately 16% reduction in mortality.
• At any given risk factor profile or coronary calcium score, unfit people have 2-3 times the mortality as their fit counterparts.
• Fitness is inversely related to annual health care costs (each 1 MET increase in CRF is associated with approximately 6% lower annual health care costs).
• Physically active people hospitalized with acute coronary syndromes have better short-term outcomes (likely because of a phenomenon called ‘exercise preconditioning’).
• Fit people who undergo elective or emergent surgical procedures have better outcomes.
• Regular physical activity is a common characteristic in population subsets who routinely live into their 90s and to 100+.

Dr. Franklin had this advice for clinicians seeking to promote CRF increases of 1 MET or more among patients: “Sedentary people who embark on a walking program, who over time increase their walking speed to 3 mph or faster, invariably show at least a 1 MET increase in CRF during subsequent peak or symptom-limited treadmill testing.”

“Another general rule is that if an exercise program decreases heart rate at a given or fixed workload by about 10 beats per minute [bpm], the same treadmill workload that initially was accomplished at a heart rate of 120 bpm is now being accomplished at a heart rate of 110 bpm,” likely resulting in about a 1 MET increase in fitness.

“Accordingly,” he added, “a 20-bpm decrease would suggest a 2 MET increase in fitness!”

In a related editorial, Leonard A. Kaminsky, Ball State University, Muncie, Ind. and colleagues, write, “We agree with and believe the conclusion, reached by Kokkinos et al., bears repeating. We (again) call on both clinicians and public health professionals to adopt CRF as a key health indicator.”

“This should be done by coupling routine assessments of CRF with continued advocacy for promoting physical activity as an essential healthy lifestyle behavior,” they write.

No funding or relevant financial relationships were disclosed.

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

Sports-related sudden cardiac arrest (Sr-SCA) appears to be extremely rare in women, compared with men, despite similar characteristics and circumstances of occurrence, data from three European population-based registries suggest.

“Our study shows that cardiac arrest during sports activities is up to 13 times less frequent in women, which means that the risk of sports-related cardiac arrest is substantially lower in women than in men. This tighter risk is consistent across all age subgroups and registries,” Orianne Weizman, MD, MPH, Université Paris Cité, said in an interview.

“Even if it is a nonconsensual suggestion, the question of risk-adapted screening in women must be asked,” Dr. Weizman and colleagues propose.

Their study was published online  in the Journal of the American College of Cardiology.
 

Annual incidence

Among 34,826 cases of SCA in the registries that occurred in adults between 2006 and 2017, 760 (2.2%) were related to sports, and the vast majority occurred in men (706, 92.9%). Only 54 (7.1%) occurred in women.

Viktor Cap/Thinkstock

Overall, the average annual incidence of Sr-SCA in women was 0.19 per million, compared with 2.63 per million in men (P < .0001).

When extrapolating to the total European population and accounting for age and sex, this translates into 98 expected cases of Sr-SCA each year in women versus 1,350 cases annually in men.

The average age of Sr-SCA was similar in women and men (59 years). Most cases occurred during moderate-vigorous physical activity, although data on the types of sports and time spent on sports per week or month were not defined.

However, the investigators note that women with Sr-SCA were more likely than men to be engaged in light or moderate physical activity at the time of arrest (17.5% vs. 4.2%) – suggesting a potential higher propensity for women to present with SCA at moderate workloads.

The incidence of Sr-SCA increased only slightly in postmenopausal women, while there was an 8-fold increase in men aged 60-74 years, relative to peers younger than 40 years.

History of heart disease was relatively uncommon in both men and women. Previous myocardial infarction was the most frequent preexisting condition in men (26.8%), whereas nonischemic heart disease (cardiomyopathy and valvular heart disease) was more frequent among women (29.0%).

Cardiovascular risk factors were frequently present in both men and women, with at least one factor present in two-thirds of the patients, regardless of sex.

Pulseless electrical activity and asystole were more common in women than in men (40.7% vs. 19.1%), as has been shown in previous studies of resuscitation from SCA in the general population. Ventricular tachycardia or fibrillation was the initial rhythm in 80.9% of men and 59.3% of women.

The cause of SCA was MI in 31.4% of women and 29.0% of men. Other cases were related to dilated cardiomyopathy (5.6% in women, 1.8% in men) or hypertrophic cardiomyopathy (1.9% in women, 1.3% in men). Electrical heart disease was found in two women (3.7%) and 15 men (2.1%).

In most cases (86%), one or more witnesses were present and assisted after the collapse. There was no significant difference between men and women in bystander response, time to defibrillation, and survival, which approached 60% at hospital discharge with early bystander cardiorespiratory resuscitation and automatic external defibrillator use.

A limitation of the study is a predominantly White European population, meaning that the findings may not be extrapolated to other populations.
 

Tailored screening?

“These findings raise questions about the causes of this extremely low risk, which are not yet clear, and the extent to which we should revise our pre-sport screening methods,” Dr. Weizman told this news organization.

“We suggest that extensive, routinely conducted screening in women would not be cost-effective because of the extremely rare incidence of serious events,” Dr. Weizman said.

What’s lacking, however, is sport-specific data on whether specific activities (endurance or resistance) would be more risky for women. Further information, particularly on the sports at highest risk for Sr-SCA in women, is needed to propose tailor-made screening algorithms, Dr. Weizman noted.

The value of preparticipation screening for occult heart disease beyond the history and physical examination has been debated, with some organizations recommending electrocardiogram in addition to baseline assessments.

But this can lead to false-positives, “with the anxiety and cost associated with additional testing,” Anne Curtis, MD, State University of New York at Buffalo, Buffalo General Medical Center, and Jan Tijssen, PhD, University of Amsterdam, write in a linked editorial.

Currently, the American Heart Association recommends screening before sports participation, with a focused personal and family history and physical examination.

Dr. Curtis told this news organization that the U.S. guidelines “should stay as they are, but if one were to change them, it would be important to recognize that male athletes are much more likely to suffer arrhythmic events during sports than female athletes.”

“That to me means that female athletes in particular should not need to have ECGs prior to sports participation unless the history and physical examination detects a potential problem that needs further investigation,” Dr. Curtis said.

“Both women and men should be screened for cardiovascular risk factors during routine primary care, with appropriate interventions for hypertension, hyperlipidemia, smoking, and other risk factors,” Dr. Curtis and Dr. Tijssen advise in their editorial.

“In asymptomatic individuals who wish to become more active, in most cases they should be given the green light to proceed, starting slow and increasing intensity/duration over time, without specific additional testing. This advice is particularly relevant for women, given the findings of the current and prior studies,” they add.

This research was funded by Horizon 2020 and COST Action PARQ, supported by the European Cooperation in Science and Technology. Additional support was provided by INSERM, University of Paris, Assistance Publique-Hôpitaux de Paris, Fondation Coeur et Artères, Global Heart Watch, Fédération Française de Cardiologie, Société Française de Cardiologie, Fondation Recherche Medicale, as well as unrestricted grants from industrial partners. The authors and Dr. Tijssen have declared no relevant financial relationships. Dr. Curtis has disclosed relationships with Janssen several pharmaceutical companies.

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

Sports-related sudden cardiac arrest (Sr-SCA) appears to be extremely rare in women, compared with men, despite similar characteristics and circumstances of occurrence, data from three European population-based registries suggest.

“Our study shows that cardiac arrest during sports activities is up to 13 times less frequent in women, which means that the risk of sports-related cardiac arrest is substantially lower in women than in men. This tighter risk is consistent across all age subgroups and registries,” Orianne Weizman, MD, MPH, Université Paris Cité, said in an interview.

“Even if it is a nonconsensual suggestion, the question of risk-adapted screening in women must be asked,” Dr. Weizman and colleagues propose.

Their study was published online  in the Journal of the American College of Cardiology.
 

Annual incidence

Among 34,826 cases of SCA in the registries that occurred in adults between 2006 and 2017, 760 (2.2%) were related to sports, and the vast majority occurred in men (706, 92.9%). Only 54 (7.1%) occurred in women.

Viktor Cap/Thinkstock

Overall, the average annual incidence of Sr-SCA in women was 0.19 per million, compared with 2.63 per million in men (P < .0001).

When extrapolating to the total European population and accounting for age and sex, this translates into 98 expected cases of Sr-SCA each year in women versus 1,350 cases annually in men.

The average age of Sr-SCA was similar in women and men (59 years). Most cases occurred during moderate-vigorous physical activity, although data on the types of sports and time spent on sports per week or month were not defined.

However, the investigators note that women with Sr-SCA were more likely than men to be engaged in light or moderate physical activity at the time of arrest (17.5% vs. 4.2%) – suggesting a potential higher propensity for women to present with SCA at moderate workloads.

The incidence of Sr-SCA increased only slightly in postmenopausal women, while there was an 8-fold increase in men aged 60-74 years, relative to peers younger than 40 years.

History of heart disease was relatively uncommon in both men and women. Previous myocardial infarction was the most frequent preexisting condition in men (26.8%), whereas nonischemic heart disease (cardiomyopathy and valvular heart disease) was more frequent among women (29.0%).

Cardiovascular risk factors were frequently present in both men and women, with at least one factor present in two-thirds of the patients, regardless of sex.

Pulseless electrical activity and asystole were more common in women than in men (40.7% vs. 19.1%), as has been shown in previous studies of resuscitation from SCA in the general population. Ventricular tachycardia or fibrillation was the initial rhythm in 80.9% of men and 59.3% of women.

The cause of SCA was MI in 31.4% of women and 29.0% of men. Other cases were related to dilated cardiomyopathy (5.6% in women, 1.8% in men) or hypertrophic cardiomyopathy (1.9% in women, 1.3% in men). Electrical heart disease was found in two women (3.7%) and 15 men (2.1%).

In most cases (86%), one or more witnesses were present and assisted after the collapse. There was no significant difference between men and women in bystander response, time to defibrillation, and survival, which approached 60% at hospital discharge with early bystander cardiorespiratory resuscitation and automatic external defibrillator use.

A limitation of the study is a predominantly White European population, meaning that the findings may not be extrapolated to other populations.
 

Tailored screening?

“These findings raise questions about the causes of this extremely low risk, which are not yet clear, and the extent to which we should revise our pre-sport screening methods,” Dr. Weizman told this news organization.

“We suggest that extensive, routinely conducted screening in women would not be cost-effective because of the extremely rare incidence of serious events,” Dr. Weizman said.

What’s lacking, however, is sport-specific data on whether specific activities (endurance or resistance) would be more risky for women. Further information, particularly on the sports at highest risk for Sr-SCA in women, is needed to propose tailor-made screening algorithms, Dr. Weizman noted.

The value of preparticipation screening for occult heart disease beyond the history and physical examination has been debated, with some organizations recommending electrocardiogram in addition to baseline assessments.

But this can lead to false-positives, “with the anxiety and cost associated with additional testing,” Anne Curtis, MD, State University of New York at Buffalo, Buffalo General Medical Center, and Jan Tijssen, PhD, University of Amsterdam, write in a linked editorial.

Currently, the American Heart Association recommends screening before sports participation, with a focused personal and family history and physical examination.

Dr. Curtis told this news organization that the U.S. guidelines “should stay as they are, but if one were to change them, it would be important to recognize that male athletes are much more likely to suffer arrhythmic events during sports than female athletes.”

“That to me means that female athletes in particular should not need to have ECGs prior to sports participation unless the history and physical examination detects a potential problem that needs further investigation,” Dr. Curtis said.

“Both women and men should be screened for cardiovascular risk factors during routine primary care, with appropriate interventions for hypertension, hyperlipidemia, smoking, and other risk factors,” Dr. Curtis and Dr. Tijssen advise in their editorial.

“In asymptomatic individuals who wish to become more active, in most cases they should be given the green light to proceed, starting slow and increasing intensity/duration over time, without specific additional testing. This advice is particularly relevant for women, given the findings of the current and prior studies,” they add.

This research was funded by Horizon 2020 and COST Action PARQ, supported by the European Cooperation in Science and Technology. Additional support was provided by INSERM, University of Paris, Assistance Publique-Hôpitaux de Paris, Fondation Coeur et Artères, Global Heart Watch, Fédération Française de Cardiologie, Société Française de Cardiologie, Fondation Recherche Medicale, as well as unrestricted grants from industrial partners. The authors and Dr. Tijssen have declared no relevant financial relationships. Dr. Curtis has disclosed relationships with Janssen several pharmaceutical companies.

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

Sports-related sudden cardiac arrest (Sr-SCA) appears to be extremely rare in women, compared with men, despite similar characteristics and circumstances of occurrence, data from three European population-based registries suggest.

“Our study shows that cardiac arrest during sports activities is up to 13 times less frequent in women, which means that the risk of sports-related cardiac arrest is substantially lower in women than in men. This tighter risk is consistent across all age subgroups and registries,” Orianne Weizman, MD, MPH, Université Paris Cité, said in an interview.

“Even if it is a nonconsensual suggestion, the question of risk-adapted screening in women must be asked,” Dr. Weizman and colleagues propose.

Their study was published online  in the Journal of the American College of Cardiology.
 

Annual incidence

Among 34,826 cases of SCA in the registries that occurred in adults between 2006 and 2017, 760 (2.2%) were related to sports, and the vast majority occurred in men (706, 92.9%). Only 54 (7.1%) occurred in women.

Viktor Cap/Thinkstock

Overall, the average annual incidence of Sr-SCA in women was 0.19 per million, compared with 2.63 per million in men (P < .0001).

When extrapolating to the total European population and accounting for age and sex, this translates into 98 expected cases of Sr-SCA each year in women versus 1,350 cases annually in men.

The average age of Sr-SCA was similar in women and men (59 years). Most cases occurred during moderate-vigorous physical activity, although data on the types of sports and time spent on sports per week or month were not defined.

However, the investigators note that women with Sr-SCA were more likely than men to be engaged in light or moderate physical activity at the time of arrest (17.5% vs. 4.2%) – suggesting a potential higher propensity for women to present with SCA at moderate workloads.

The incidence of Sr-SCA increased only slightly in postmenopausal women, while there was an 8-fold increase in men aged 60-74 years, relative to peers younger than 40 years.

History of heart disease was relatively uncommon in both men and women. Previous myocardial infarction was the most frequent preexisting condition in men (26.8%), whereas nonischemic heart disease (cardiomyopathy and valvular heart disease) was more frequent among women (29.0%).

Cardiovascular risk factors were frequently present in both men and women, with at least one factor present in two-thirds of the patients, regardless of sex.

Pulseless electrical activity and asystole were more common in women than in men (40.7% vs. 19.1%), as has been shown in previous studies of resuscitation from SCA in the general population. Ventricular tachycardia or fibrillation was the initial rhythm in 80.9% of men and 59.3% of women.

The cause of SCA was MI in 31.4% of women and 29.0% of men. Other cases were related to dilated cardiomyopathy (5.6% in women, 1.8% in men) or hypertrophic cardiomyopathy (1.9% in women, 1.3% in men). Electrical heart disease was found in two women (3.7%) and 15 men (2.1%).

In most cases (86%), one or more witnesses were present and assisted after the collapse. There was no significant difference between men and women in bystander response, time to defibrillation, and survival, which approached 60% at hospital discharge with early bystander cardiorespiratory resuscitation and automatic external defibrillator use.

A limitation of the study is a predominantly White European population, meaning that the findings may not be extrapolated to other populations.
 

Tailored screening?

“These findings raise questions about the causes of this extremely low risk, which are not yet clear, and the extent to which we should revise our pre-sport screening methods,” Dr. Weizman told this news organization.

“We suggest that extensive, routinely conducted screening in women would not be cost-effective because of the extremely rare incidence of serious events,” Dr. Weizman said.

What’s lacking, however, is sport-specific data on whether specific activities (endurance or resistance) would be more risky for women. Further information, particularly on the sports at highest risk for Sr-SCA in women, is needed to propose tailor-made screening algorithms, Dr. Weizman noted.

The value of preparticipation screening for occult heart disease beyond the history and physical examination has been debated, with some organizations recommending electrocardiogram in addition to baseline assessments.

But this can lead to false-positives, “with the anxiety and cost associated with additional testing,” Anne Curtis, MD, State University of New York at Buffalo, Buffalo General Medical Center, and Jan Tijssen, PhD, University of Amsterdam, write in a linked editorial.

Currently, the American Heart Association recommends screening before sports participation, with a focused personal and family history and physical examination.

Dr. Curtis told this news organization that the U.S. guidelines “should stay as they are, but if one were to change them, it would be important to recognize that male athletes are much more likely to suffer arrhythmic events during sports than female athletes.”

“That to me means that female athletes in particular should not need to have ECGs prior to sports participation unless the history and physical examination detects a potential problem that needs further investigation,” Dr. Curtis said.

“Both women and men should be screened for cardiovascular risk factors during routine primary care, with appropriate interventions for hypertension, hyperlipidemia, smoking, and other risk factors,” Dr. Curtis and Dr. Tijssen advise in their editorial.

“In asymptomatic individuals who wish to become more active, in most cases they should be given the green light to proceed, starting slow and increasing intensity/duration over time, without specific additional testing. This advice is particularly relevant for women, given the findings of the current and prior studies,” they add.

This research was funded by Horizon 2020 and COST Action PARQ, supported by the European Cooperation in Science and Technology. Additional support was provided by INSERM, University of Paris, Assistance Publique-Hôpitaux de Paris, Fondation Coeur et Artères, Global Heart Watch, Fédération Française de Cardiologie, Société Française de Cardiologie, Fondation Recherche Medicale, as well as unrestricted grants from industrial partners. The authors and Dr. Tijssen have declared no relevant financial relationships. Dr. Curtis has disclosed relationships with Janssen several pharmaceutical companies.

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

The U.S. Food and Drug Administration has expanded the indicated age range for evinacumab-dgnb (Evkeeza, Regeneron Pharmaceuticals), which was approved 2 years ago as an adjunct to other lipid-lowering therapies for homozygous familial hypercholesterolemia (HoFH) in patients aged 12 and older.

Olivier Le Moal/Getty Images

The antibody-based agent’s indication now also covers patients aged 5-11 years with the rare genetic disorder, Regeneron announced. It blocks angiopoietin-like 3 (ANGPTL3), inhibiting lipoprotein lipase and endothelial lipase, thereby cutting LDL-cholesterol levels by mechanisms not directly involving the LDL receptor.

The expanded indication is based on a study that saw a 48% drop in LDL-cholesterol levels over 24 weeks, the primary endpoint, across 20 HoFH patients aged 5-11 years who received evinacumab-dgnb on top of maximally tolerated standard lipid-modifying therapy, the company reports.

Levels of apolipoprotein B, non-HDL cholesterol, and total cholesterol also fell significantly in the trial, which was completed in January.

The drug’s efficacy and safety resembled those of a previously reported larger study of patients with HoFH aged 12 years and older (mean age about 40 years) that led to its initial approval.

“The safety and effectiveness of Evkeeza have not been established in patients with other causes of hypercholesterolemia, including those with heterozygous familial hypercholesterolemia,” the company states. Nor is it known whether the drug affects clinical outcomes.

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

The U.S. Food and Drug Administration has expanded the indicated age range for evinacumab-dgnb (Evkeeza, Regeneron Pharmaceuticals), which was approved 2 years ago as an adjunct to other lipid-lowering therapies for homozygous familial hypercholesterolemia (HoFH) in patients aged 12 and older.

Olivier Le Moal/Getty Images

The antibody-based agent’s indication now also covers patients aged 5-11 years with the rare genetic disorder, Regeneron announced. It blocks angiopoietin-like 3 (ANGPTL3), inhibiting lipoprotein lipase and endothelial lipase, thereby cutting LDL-cholesterol levels by mechanisms not directly involving the LDL receptor.

The expanded indication is based on a study that saw a 48% drop in LDL-cholesterol levels over 24 weeks, the primary endpoint, across 20 HoFH patients aged 5-11 years who received evinacumab-dgnb on top of maximally tolerated standard lipid-modifying therapy, the company reports.

Levels of apolipoprotein B, non-HDL cholesterol, and total cholesterol also fell significantly in the trial, which was completed in January.

The drug’s efficacy and safety resembled those of a previously reported larger study of patients with HoFH aged 12 years and older (mean age about 40 years) that led to its initial approval.

“The safety and effectiveness of Evkeeza have not been established in patients with other causes of hypercholesterolemia, including those with heterozygous familial hypercholesterolemia,” the company states. Nor is it known whether the drug affects clinical outcomes.

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

The U.S. Food and Drug Administration has expanded the indicated age range for evinacumab-dgnb (Evkeeza, Regeneron Pharmaceuticals), which was approved 2 years ago as an adjunct to other lipid-lowering therapies for homozygous familial hypercholesterolemia (HoFH) in patients aged 12 and older.

Olivier Le Moal/Getty Images

The antibody-based agent’s indication now also covers patients aged 5-11 years with the rare genetic disorder, Regeneron announced. It blocks angiopoietin-like 3 (ANGPTL3), inhibiting lipoprotein lipase and endothelial lipase, thereby cutting LDL-cholesterol levels by mechanisms not directly involving the LDL receptor.

The expanded indication is based on a study that saw a 48% drop in LDL-cholesterol levels over 24 weeks, the primary endpoint, across 20 HoFH patients aged 5-11 years who received evinacumab-dgnb on top of maximally tolerated standard lipid-modifying therapy, the company reports.

Levels of apolipoprotein B, non-HDL cholesterol, and total cholesterol also fell significantly in the trial, which was completed in January.

The drug’s efficacy and safety resembled those of a previously reported larger study of patients with HoFH aged 12 years and older (mean age about 40 years) that led to its initial approval.

“The safety and effectiveness of Evkeeza have not been established in patients with other causes of hypercholesterolemia, including those with heterozygous familial hypercholesterolemia,” the company states. Nor is it known whether the drug affects clinical outcomes.

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

“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. The recommended amount of weekly physical activity is 2.5 hours (150 minutes), but less than half of adults over 18 meet the guidelines for aerobic exercise, according to recent data from the Centers for Disease Control and Prevention.

Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.

Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.

Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
 

Tip 1: ‘[Clinician], heal thyself’

Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.

If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.

What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.

Now that self-reflection has been addressed, let’s get to patient counseling.
 

Tip 2: Motivate, don’t berate

Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”

Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.

Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.

I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.

Tip 3: Set SMARTER goals

After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.

For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”

Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
 

Tip 4: Use accountability tools

Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.

Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
 

Tip 5: Prepare and PLAN for setbacks

Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.

Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.

While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.

We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
 

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

“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. The recommended amount of weekly physical activity is 2.5 hours (150 minutes), but less than half of adults over 18 meet the guidelines for aerobic exercise, according to recent data from the Centers for Disease Control and Prevention.

Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.

Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.

Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
 

Tip 1: ‘[Clinician], heal thyself’

Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.

If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.

What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.

Now that self-reflection has been addressed, let’s get to patient counseling.
 

Tip 2: Motivate, don’t berate

Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”

Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.

Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.

I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.

Tip 3: Set SMARTER goals

After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.

For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”

Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
 

Tip 4: Use accountability tools

Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.

Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
 

Tip 5: Prepare and PLAN for setbacks

Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.

Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.

While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.

We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
 

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

“Just Do It” is a cute marketing slogan. But let’s face it: Clinically, it doesn’t work well. Most people just don’t exercise. The recommended amount of weekly physical activity is 2.5 hours (150 minutes), but less than half of adults over 18 meet the guidelines for aerobic exercise, according to recent data from the Centers for Disease Control and Prevention.

Furthermore, when surveyed about aerobic exercise and strength training, only 24.6% meet these weekly recommendations. These low rates of physical activity are alarming, given the immense benefits of exercise in improving mental and physical health and well-being.

Many people know that exercise is good for them but struggle to go workout consistently. I know firsthand how challenging this can be. In addition to being an integrative obesity specialist, I have gone from 0 minutes of physical activity in 2014 to becoming a fitness enthusiast who’s run more than 5,300 miles over 8 years. I know that as doctors and clinicians, we can profoundly influence our patients’ exercise journey.

Here are five tips to help motivate your patients make the change from “I Won’t Do It” to “I’m Doing It.”
 

Tip 1: ‘[Clinician], heal thyself’

Data don’t lie. Doctors who move more are more likely to counsel patients on exercise. I’ve been the doctor on both sides of the exercise spectrum. At my heaviest weight and lowest physical activity level, I felt hypocritical counseling patients on exercise.

If and when I counseled my patients on exercise, it was very directive and impersonal. When I started running consistently, I went to the opposite end of the spectrum. In my running zeal, it took a while for me to understand that not everyone wants to run dozens of miles a week. Shocking! Some people can’t handle intense workouts. The “I did it so you can too” perspective wasn’t helpful for long-term change in most patients.

What has been beneficial is recalling the obstacles and emotions I had (and still have) with staying consistent with physical activity. When physicians and clinicians move regularly, we’re more equipped to give our patients genuine counseling based on practicality rather than theory.

Now that self-reflection has been addressed, let’s get to patient counseling.
 

Tip 2: Motivate, don’t berate

Lectures on why patients should exercise are less helpful than asking, “Why aren›t you able to exercise more often?”

Asking open-ended questions is essential in motivational interviewing. Motivational interviewing promotes behavioral change through collaborative conversation.

Instead of telling the patient what to do, motivational interviewing seeks to establish a person’s why and create an effective plan based on their motivation. Asking open-ended questions is also helpful in determining any challenges to regular exercise, rather than calling these challenges “excuses,” which can be counterproductive.

I encourage patients to embrace challenges as opportunities for improvement. If they say: “I can’t find time to work out,” I suggest that they create time to work out by walking 10-15 minutes during lunch or after dinner. The information gleaned from open-ended questions helps set practical SMARTER goals, which we will discuss next.

Tip 3: Set SMARTER goals

After assessing the patient’s motivation and barriers, use this information to transform their desire to change into an actionable plan through a SMARTER goal. SMARTER stands for Specific, Measurable, Attainable, Relevant, Time-Sensitive, Enjoyable, and Rewarding. Practical goals have each of these components. That’s why “Just Do It” or even “Exercise 150 minutes a week” isn’t a clear path for actionable change. SMARTER goals go beyond what to do and help people personalize how to change.

For example, the SMARTER version of “exercise 150 minutes a week” for a busy person who works 50 hours a week may look like this: “My goal is to incorporate 150 minutes of physical activity through 60 minutes of aerobic exercise Monday through Friday (20-minute lunch walks) and 90 minutes of combination resistance training on the weekend (two 45-minute sessions) while listening to my favorite music. To meet my goal, I will reward myself by calling a friend to catch up or buy myself a new workout outfit.”

Exercise prescriptions are another helpful way to empower patients with a realistic exercise strategy. In my practice, I developed my own exercise prescription which focuses on overcoming time barriers to exercise and finding personally enjoyable exercises. To enhance self-directed physical activity, I›ve found it useful to have patients complete part of the “exercise prescription” on their own before or after their visit.
 

Tip 4: Use accountability tools

Making a SMARTER goal is one thing, but sticking with it takes regular reinforcement. Even with the best plan, once patients leave the office, there are many distractions from their goals. Accountability is the secret sauce to cultivating consistency. Fitness trackers are an affordable form of accountability. Studies show that wearing a fitness tracker can help people get up to 40 minutes of extra walking, compared with people who don’t wear trackers.

Additionally, clinicians can use different ways to offer exercise accountability. For example, more frequent check-ins, individually or in groups, can be helpful. The increase in telehealth has made interval visits easier. Reimbursement and time can limit clinician-level accountability, however. Other options are referring patients to online support groups or programs sponsored by the government or organizations. For years, I coled a Walk With a Doc chapter in Richmond, Va. There are chapters throughout the country.
 

Tip 5: Prepare and PLAN for setbacks

Breaking news: Most plans don’t go quite as envisioned. Accounting for the potential of setbacks early on helps patients set realistic expectations. As physicians and clinicians, we can help our patients anticipate a few likely obstacles. This may lessen the impact when a setback occurs. Also, it’s helpful to have the patient prepare for a setback with a PLAN for recovering quickly. PLAN stands for Ponder what happened; Learn from it; Adjust the original goal; Now get back on track. Getting back on track as soon as possible is important to keep patients motivated and prevent muscle deconditioning.

Exercise is medicine. Physical inactivity is a leading contributor to many preventable diseases. Although the physical activity statistics are disappointing, improvement is possible. Many systemic changes are needed to increase physical activity on a population level.

While waiting for more extensive changes, we have the power to equip patients with personalized, actionable tools for improving and maintaining physical activity.

We can transform one person at a time through our clinical encounters. Let’s use effective tools to help patients shift from “I Won’t Do It” to “I’m Doing It.”

Sylvia Gonsahn-Bollie, MD, DipABOM, is an integrative obesity specialist focused on individualized solutions for emotional and biological overeating. Her bestselling book, “Embrace You: Your Guide to Transforming Weight Loss Misconceptions Into Lifelong Wellness,” was Healthline.com’s Best Overall Weight Loss Book of 2022 and one of Livestrong.com’s 8 Best Weight-Loss Books to Read in 2022. She reported no conflicts of interest.
 

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

Datascope/Getinge is recalling certain Cardiosave Hybrid and Cardiosave Rescue Intra-Aortic Balloon Pumps (IABPs) because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The U.S. Food and Drug Administration has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.

The FDA warns that an unexpected pump shutdown and any interruption to therapy that occurs can lead to hemodynamic instability, organ damage, and/or death, especially in patients who are critically ill and most likely to receive therapy using these devices.

Wikimedia Commons/FitzColinGerald/Creative Commons License

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

Datascope/Getinge is recalling certain Cardiosave Hybrid and Cardiosave Rescue Intra-Aortic Balloon Pumps (IABPs) because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The U.S. Food and Drug Administration has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.

The FDA warns that an unexpected pump shutdown and any interruption to therapy that occurs can lead to hemodynamic instability, organ damage, and/or death, especially in patients who are critically ill and most likely to receive therapy using these devices.

Wikimedia Commons/FitzColinGerald/Creative Commons License

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

Datascope/Getinge is recalling certain Cardiosave Hybrid and Cardiosave Rescue Intra-Aortic Balloon Pumps (IABPs) because the coiled cable connecting the display and base on some units may fail, causing an unexpected shutdown without warnings or alarms to alert the user.

The U.S. Food and Drug Administration has identified this as a class I recall, the most serious type of recall, because of the risk for serious injury or death.

The FDA warns that an unexpected pump shutdown and any interruption to therapy that occurs can lead to hemodynamic instability, organ damage, and/or death, especially in patients who are critically ill and most likely to receive therapy using these devices.

Wikimedia Commons/FitzColinGerald/Creative Commons License

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

Overall risk for venous thromboembolism (VTE) in nonhospitalized COVID-19 patients is low, but some of those patients may have factors that increase the risk and warrant more surveillance, according to a new retrospective cohort study.

Though VTE risk is well studied and significant in those hospitalized with COVID, little is known about the risk in the outpatient setting, said the authors of the new research published online in JAMA Network Open.

The study was conducted at two integrated health care delivery systems in northern and southern California. Data were gathered from the Kaiser Permanente Virtual Data Warehouse and electronic health records.
 

Nearly 400,000 patients studied

Researchers, led by Margaret Fang, MD, with the division of hospital medicine, University of California, San Francisco, identified 398,530 outpatients with COVID-19 from Jan. 1, 2020, through Jan. 31, 2021.

VTE risk was low overall for ambulatory COVID patients.

“It is a reassuring study,” Dr. Fang said in an interview.

The researchers found that the risk is highest in the first 30 days after COVID-19 diagnosis (unadjusted rate, 0.58; 95% confidence interval, 0.51-0.67 per 100 person-years vs. 0.09; 95% CI, 0.08-0.11 per 100 person-years after 30 days).
 

Factors linked with high VTE risk

They also found that several factors were linked with a higher risk of blood clots in the study population, including being at least 55 years old; being male; having a history of blood clots or thrombophilia; and a body mass index (BMI) of at least 30 kg/m².

The authors write, “These findings may help identify subsets of patients with COVID-19 who could benefit from VTE preventive strategies and more intensive short-term surveillance.”
 

Are routine anticoagulants justified?

Previously, randomized clinical trials have found that hospitalized patients with moderate COVID-19 may benefit from therapeutically dosed heparin anticoagulants but that therapeutic anticoagulation had no net benefit – and perhaps could even harm – patients who were critically ill with COVID.

“[M]uch less is known about the optimal thromboprophylaxis strategy for people with milder presentations of COVID-19 who do not require hospitalization,” they write.
 

Mild COVID VTE risk similar to general population

The authors note that rates of blood clots linked with COVID-19 are not much higher than the average blood clot rate in the general population, which is about 0.1-0.2 per 100 person-years.

Therefore, the results don’t justify routine administration of anticoagulation given the costs, inconvenience, and bleeding risks, they acknowledge.

Dr. Fang told this publication that it’s hard to know what to tell patients, given the overall low VTE risk. She said their study wasn’t designed to advise when to give prophylaxis.
 

Physicians should inform patients of their higher risk

“We should tell our patients who fall into these risk categories that blood clot is a concern after the development of COVID, especially in those first 30 days. And some people might benefit from increased surveillance,” Dr. Fang said.

”I think this study would support ongoing studies that look at whether selected patients benefit from VTE prophylaxis, for example low-dose anticoagulants,” she said.

Dr. Fang said the subgroup factors they found increased risk of blood clots for all patients, not just COVID-19 patients. It’s not clear why factors such as being male may increase blood clot risk, though that is consistent with previous literature, but higher risk with higher BMI might be related to a combination of inflammation or decreased mobility, she said.
 

Unanswered questions

Robert H. Hopkins Jr., MD, says the study helps answer a couple of important questions – that the VTE risk in nonhospitalized COVID-19 patients is low and when and for which patients risk may be highest.

However, there are several unanswered questions that argue against routine initiation of anticoagulants, notes the professor of internal medicine and pediatrics chief, division of general internal medicine, at University of Arkansas for Medical Sciences, Little Rock.

One is the change in the COVID variant landscape.

“We do not know whether rates of VTE are same or lower or higher with current circulating variants,” Dr. Hopkins said.

The authors acknowledge this as a limitation. Study data predate Omicron and subvariants, which appear to lower clinical severity, so it’s unclear whether VTE risk is different in this Omicron era.

Dr. Hopkins added another unknown: “We do not know whether vaccination affects rates of VTE in ambulatory breakthrough infection.”

Dr. Hopkins and the authors also note the lack of a control group in the study, to better compare risk.

Coauthor Dr. Prasad reports consultant fees from EpiExcellence LLC outside the submitted work. Coauthor Dr. Go reports grants paid to the division of research, Kaiser Permanente Northern California, from CSL Behring, Novartis, Bristol Meyers Squibb/Pfizer Alliance, and Janssen outside the submitted work.

The research was funded through Patient-Centered Outcomes Research Institute.

Dr. Hopkins reports no relevant financial relationships.

Overall risk for venous thromboembolism (VTE) in nonhospitalized COVID-19 patients is low, but some of those patients may have factors that increase the risk and warrant more surveillance, according to a new retrospective cohort study.

Though VTE risk is well studied and significant in those hospitalized with COVID, little is known about the risk in the outpatient setting, said the authors of the new research published online in JAMA Network Open.

The study was conducted at two integrated health care delivery systems in northern and southern California. Data were gathered from the Kaiser Permanente Virtual Data Warehouse and electronic health records.
 

Nearly 400,000 patients studied

Researchers, led by Margaret Fang, MD, with the division of hospital medicine, University of California, San Francisco, identified 398,530 outpatients with COVID-19 from Jan. 1, 2020, through Jan. 31, 2021.

VTE risk was low overall for ambulatory COVID patients.

“It is a reassuring study,” Dr. Fang said in an interview.

The researchers found that the risk is highest in the first 30 days after COVID-19 diagnosis (unadjusted rate, 0.58; 95% confidence interval, 0.51-0.67 per 100 person-years vs. 0.09; 95% CI, 0.08-0.11 per 100 person-years after 30 days).
 

Factors linked with high VTE risk

They also found that several factors were linked with a higher risk of blood clots in the study population, including being at least 55 years old; being male; having a history of blood clots or thrombophilia; and a body mass index (BMI) of at least 30 kg/m².

The authors write, “These findings may help identify subsets of patients with COVID-19 who could benefit from VTE preventive strategies and more intensive short-term surveillance.”
 

Are routine anticoagulants justified?

Previously, randomized clinical trials have found that hospitalized patients with moderate COVID-19 may benefit from therapeutically dosed heparin anticoagulants but that therapeutic anticoagulation had no net benefit – and perhaps could even harm – patients who were critically ill with COVID.

“[M]uch less is known about the optimal thromboprophylaxis strategy for people with milder presentations of COVID-19 who do not require hospitalization,” they write.
 

Mild COVID VTE risk similar to general population

The authors note that rates of blood clots linked with COVID-19 are not much higher than the average blood clot rate in the general population, which is about 0.1-0.2 per 100 person-years.

Therefore, the results don’t justify routine administration of anticoagulation given the costs, inconvenience, and bleeding risks, they acknowledge.

Dr. Fang told this publication that it’s hard to know what to tell patients, given the overall low VTE risk. She said their study wasn’t designed to advise when to give prophylaxis.
 

Physicians should inform patients of their higher risk

“We should tell our patients who fall into these risk categories that blood clot is a concern after the development of COVID, especially in those first 30 days. And some people might benefit from increased surveillance,” Dr. Fang said.

”I think this study would support ongoing studies that look at whether selected patients benefit from VTE prophylaxis, for example low-dose anticoagulants,” she said.

Dr. Fang said the subgroup factors they found increased risk of blood clots for all patients, not just COVID-19 patients. It’s not clear why factors such as being male may increase blood clot risk, though that is consistent with previous literature, but higher risk with higher BMI might be related to a combination of inflammation or decreased mobility, she said.
 

Unanswered questions

Robert H. Hopkins Jr., MD, says the study helps answer a couple of important questions – that the VTE risk in nonhospitalized COVID-19 patients is low and when and for which patients risk may be highest.

However, there are several unanswered questions that argue against routine initiation of anticoagulants, notes the professor of internal medicine and pediatrics chief, division of general internal medicine, at University of Arkansas for Medical Sciences, Little Rock.

One is the change in the COVID variant landscape.

“We do not know whether rates of VTE are same or lower or higher with current circulating variants,” Dr. Hopkins said.

The authors acknowledge this as a limitation. Study data predate Omicron and subvariants, which appear to lower clinical severity, so it’s unclear whether VTE risk is different in this Omicron era.

Dr. Hopkins added another unknown: “We do not know whether vaccination affects rates of VTE in ambulatory breakthrough infection.”

Dr. Hopkins and the authors also note the lack of a control group in the study, to better compare risk.

Coauthor Dr. Prasad reports consultant fees from EpiExcellence LLC outside the submitted work. Coauthor Dr. Go reports grants paid to the division of research, Kaiser Permanente Northern California, from CSL Behring, Novartis, Bristol Meyers Squibb/Pfizer Alliance, and Janssen outside the submitted work.

The research was funded through Patient-Centered Outcomes Research Institute.

Dr. Hopkins reports no relevant financial relationships.

Overall risk for venous thromboembolism (VTE) in nonhospitalized COVID-19 patients is low, but some of those patients may have factors that increase the risk and warrant more surveillance, according to a new retrospective cohort study.

Though VTE risk is well studied and significant in those hospitalized with COVID, little is known about the risk in the outpatient setting, said the authors of the new research published online in JAMA Network Open.

The study was conducted at two integrated health care delivery systems in northern and southern California. Data were gathered from the Kaiser Permanente Virtual Data Warehouse and electronic health records.
 

Nearly 400,000 patients studied

Researchers, led by Margaret Fang, MD, with the division of hospital medicine, University of California, San Francisco, identified 398,530 outpatients with COVID-19 from Jan. 1, 2020, through Jan. 31, 2021.

VTE risk was low overall for ambulatory COVID patients.

“It is a reassuring study,” Dr. Fang said in an interview.

The researchers found that the risk is highest in the first 30 days after COVID-19 diagnosis (unadjusted rate, 0.58; 95% confidence interval, 0.51-0.67 per 100 person-years vs. 0.09; 95% CI, 0.08-0.11 per 100 person-years after 30 days).
 

Factors linked with high VTE risk

They also found that several factors were linked with a higher risk of blood clots in the study population, including being at least 55 years old; being male; having a history of blood clots or thrombophilia; and a body mass index (BMI) of at least 30 kg/m².

The authors write, “These findings may help identify subsets of patients with COVID-19 who could benefit from VTE preventive strategies and more intensive short-term surveillance.”
 

Are routine anticoagulants justified?

Previously, randomized clinical trials have found that hospitalized patients with moderate COVID-19 may benefit from therapeutically dosed heparin anticoagulants but that therapeutic anticoagulation had no net benefit – and perhaps could even harm – patients who were critically ill with COVID.

“[M]uch less is known about the optimal thromboprophylaxis strategy for people with milder presentations of COVID-19 who do not require hospitalization,” they write.
 

Mild COVID VTE risk similar to general population

The authors note that rates of blood clots linked with COVID-19 are not much higher than the average blood clot rate in the general population, which is about 0.1-0.2 per 100 person-years.

Therefore, the results don’t justify routine administration of anticoagulation given the costs, inconvenience, and bleeding risks, they acknowledge.

Dr. Fang told this publication that it’s hard to know what to tell patients, given the overall low VTE risk. She said their study wasn’t designed to advise when to give prophylaxis.
 

Physicians should inform patients of their higher risk

“We should tell our patients who fall into these risk categories that blood clot is a concern after the development of COVID, especially in those first 30 days. And some people might benefit from increased surveillance,” Dr. Fang said.

”I think this study would support ongoing studies that look at whether selected patients benefit from VTE prophylaxis, for example low-dose anticoagulants,” she said.

Dr. Fang said the subgroup factors they found increased risk of blood clots for all patients, not just COVID-19 patients. It’s not clear why factors such as being male may increase blood clot risk, though that is consistent with previous literature, but higher risk with higher BMI might be related to a combination of inflammation or decreased mobility, she said.
 

Unanswered questions

Robert H. Hopkins Jr., MD, says the study helps answer a couple of important questions – that the VTE risk in nonhospitalized COVID-19 patients is low and when and for which patients risk may be highest.

However, there are several unanswered questions that argue against routine initiation of anticoagulants, notes the professor of internal medicine and pediatrics chief, division of general internal medicine, at University of Arkansas for Medical Sciences, Little Rock.

One is the change in the COVID variant landscape.

“We do not know whether rates of VTE are same or lower or higher with current circulating variants,” Dr. Hopkins said.

The authors acknowledge this as a limitation. Study data predate Omicron and subvariants, which appear to lower clinical severity, so it’s unclear whether VTE risk is different in this Omicron era.

Dr. Hopkins added another unknown: “We do not know whether vaccination affects rates of VTE in ambulatory breakthrough infection.”

Dr. Hopkins and the authors also note the lack of a control group in the study, to better compare risk.

Coauthor Dr. Prasad reports consultant fees from EpiExcellence LLC outside the submitted work. Coauthor Dr. Go reports grants paid to the division of research, Kaiser Permanente Northern California, from CSL Behring, Novartis, Bristol Meyers Squibb/Pfizer Alliance, and Janssen outside the submitted work.

The research was funded through Patient-Centered Outcomes Research Institute.

Dr. Hopkins reports no relevant financial relationships.

Providing care for individuals with both cardiovascular disease (CVD) and obesity necessitates addressing both conditions at the same time, say the authors of a new state-of-the-art review.

“CVD and obesity are common conditions that frequently coexist. We cannot treat one of these conditions while ignoring the other,” Rosana G. Bianchettin, MD, of the division of cardiovascular diseases, Mayo Clinic, Rochester, Minn., and colleagues wrote in their review, recently published in the Journal of the American College of Cardiology.

The review outlines, for example, how obesity can impair common imaging tests used to diagnose heart disease, potentially reducing their accuracy.

And cardiac procedures such as percutaneous coronary intervention, open heart surgery, and revascularization all involve greater risk in the setting of obesity, while procedures such as valve replacement and heart transplantation carry a greater likelihood of failure.

Obesity can also alter drug pharmacokinetics and pharmacodynamics.

Weight reduction is an important part of the management of patients with cardiovascular disease and obesity, and “cardiac rehabilitation programs represent a potential opportunity for structured interventions,” the authors noted. However, “when other measures are insufficient, bariatric surgery can improve outcomes.”

They also advised against relying solely on body mass index (BMI) to assess adiposity: “It is prudent to investigate a range of complementary ... parameters alongside standard BMI calculations (accounting for age, race, and sex), including measures of central obesity, such as waist circumference, waist-to-hip ratio, and weight-to-height ratio.”
 

Excess fat acts as filter and can skew diagnostic results

“Obesity affects nearly all the diagnostic tests used in cardiology, such as ECG, CT scan, MRI, and echocardiogram,” senior author Francisco Lopez-Jimenez, MD, director of preventive cardiology at Mayo Clinic, explained in a statement.

The review includes a detailed table of these key obesity-related challenges. With electrocardiograms, for example, obesity can cause displacement of the heart, increased cardiac workload, and widening of the distance between the heart and the recording electrodes.

Obesity also lowers the sensitivity of exercise echocardiography, and use of CT coronary angiogram is completely precluded in people with a BMI above 40 kg/m². In interventional radiology, there may be poor visualization of target areas.

“Excess fat acts as a kind of filter and can skew test readings to under- or overdiagnosis,” noted Dr. Lopez-Jimenez.
 

Therapeutic challenges: Drugs may work differently

A longer table in the review summarizes the therapeutic challenges involved in lifestyle modification, pharmacology, cardiac procedures, and other therapeutic measures for people with the two conditions.

Obesity can limit a person’s ability to exercise, for example, and smoking cessation may promote overeating and further weight gain.

Moreover, “tailoring pharmacotherapy is difficult because of unique pharmacokinetic and pharmacodynamic factors in people with obesity that alter distribution, metabolism, and elimination of drugs. Each drug also has special properties that must be considered when it is administrated,” the authors wrote.

Examples include the higher volume of distribution of lipophilic drugs in those with increased fat mass, alterations in liver metabolism, and difficulties with anticoagulant dosing.
 

Cardiac rehabilitation is an intervention opportunity

Although cardiac rehabilitation is “a cornerstone in secondary prevention” for people who have experienced a cardiac event, only 8% of such programs include formal in-house behavioral weight-loss programs.

But that could be remedied and expanded with the use of options such as home-based rehabilitation and telephone counseling, particularly in rural communities, Dr. Bianchettin and colleagues said.

“Motivated individuals will benefit from multicomponent approaches and should be encouraged to set specific, proximal, shared goals with their health care professional. A multitude of tools are available to support self-monitoring (e.g., smartphone applications, food diaries), and scheduled regular follow-up and feedback on progress can help to maintain motivation,” they wrote.

The bottom line, said Dr. Lopez-Jimenez: “Obesity is an important risk factor to address in patients with heart disease and it requires us to do something. ... The patient needs to know that their clinician can help them lose weight. Overall, weight-loss solutions come down to finding the right therapy for the patient.”

Dr. Bianchettin reported no relevant financial relationships. Dr. Lopez-Jimenez has reported conducting research related to 3D body assessment with Select Research, Mayo Clinic, and may benefit in the future if the technology is commercialized; he has not received any relevant monetary, financial, or other type of compensation to date, in relationship to this arrangement. He is a member of the scientific advisory board for Novo Nordisk.

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

Providing care for individuals with both cardiovascular disease (CVD) and obesity necessitates addressing both conditions at the same time, say the authors of a new state-of-the-art review.

“CVD and obesity are common conditions that frequently coexist. We cannot treat one of these conditions while ignoring the other,” Rosana G. Bianchettin, MD, of the division of cardiovascular diseases, Mayo Clinic, Rochester, Minn., and colleagues wrote in their review, recently published in the Journal of the American College of Cardiology.

The review outlines, for example, how obesity can impair common imaging tests used to diagnose heart disease, potentially reducing their accuracy.

And cardiac procedures such as percutaneous coronary intervention, open heart surgery, and revascularization all involve greater risk in the setting of obesity, while procedures such as valve replacement and heart transplantation carry a greater likelihood of failure.

Obesity can also alter drug pharmacokinetics and pharmacodynamics.

Weight reduction is an important part of the management of patients with cardiovascular disease and obesity, and “cardiac rehabilitation programs represent a potential opportunity for structured interventions,” the authors noted. However, “when other measures are insufficient, bariatric surgery can improve outcomes.”

They also advised against relying solely on body mass index (BMI) to assess adiposity: “It is prudent to investigate a range of complementary ... parameters alongside standard BMI calculations (accounting for age, race, and sex), including measures of central obesity, such as waist circumference, waist-to-hip ratio, and weight-to-height ratio.”
 

Excess fat acts as filter and can skew diagnostic results

“Obesity affects nearly all the diagnostic tests used in cardiology, such as ECG, CT scan, MRI, and echocardiogram,” senior author Francisco Lopez-Jimenez, MD, director of preventive cardiology at Mayo Clinic, explained in a statement.

The review includes a detailed table of these key obesity-related challenges. With electrocardiograms, for example, obesity can cause displacement of the heart, increased cardiac workload, and widening of the distance between the heart and the recording electrodes.

Obesity also lowers the sensitivity of exercise echocardiography, and use of CT coronary angiogram is completely precluded in people with a BMI above 40 kg/m². In interventional radiology, there may be poor visualization of target areas.

“Excess fat acts as a kind of filter and can skew test readings to under- or overdiagnosis,” noted Dr. Lopez-Jimenez.
 

Therapeutic challenges: Drugs may work differently

A longer table in the review summarizes the therapeutic challenges involved in lifestyle modification, pharmacology, cardiac procedures, and other therapeutic measures for people with the two conditions.

Obesity can limit a person’s ability to exercise, for example, and smoking cessation may promote overeating and further weight gain.

Moreover, “tailoring pharmacotherapy is difficult because of unique pharmacokinetic and pharmacodynamic factors in people with obesity that alter distribution, metabolism, and elimination of drugs. Each drug also has special properties that must be considered when it is administrated,” the authors wrote.

Examples include the higher volume of distribution of lipophilic drugs in those with increased fat mass, alterations in liver metabolism, and difficulties with anticoagulant dosing.
 

Cardiac rehabilitation is an intervention opportunity

Although cardiac rehabilitation is “a cornerstone in secondary prevention” for people who have experienced a cardiac event, only 8% of such programs include formal in-house behavioral weight-loss programs.

But that could be remedied and expanded with the use of options such as home-based rehabilitation and telephone counseling, particularly in rural communities, Dr. Bianchettin and colleagues said.

“Motivated individuals will benefit from multicomponent approaches and should be encouraged to set specific, proximal, shared goals with their health care professional. A multitude of tools are available to support self-monitoring (e.g., smartphone applications, food diaries), and scheduled regular follow-up and feedback on progress can help to maintain motivation,” they wrote.

The bottom line, said Dr. Lopez-Jimenez: “Obesity is an important risk factor to address in patients with heart disease and it requires us to do something. ... The patient needs to know that their clinician can help them lose weight. Overall, weight-loss solutions come down to finding the right therapy for the patient.”

Dr. Bianchettin reported no relevant financial relationships. Dr. Lopez-Jimenez has reported conducting research related to 3D body assessment with Select Research, Mayo Clinic, and may benefit in the future if the technology is commercialized; he has not received any relevant monetary, financial, or other type of compensation to date, in relationship to this arrangement. He is a member of the scientific advisory board for Novo Nordisk.

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

Providing care for individuals with both cardiovascular disease (CVD) and obesity necessitates addressing both conditions at the same time, say the authors of a new state-of-the-art review.

“CVD and obesity are common conditions that frequently coexist. We cannot treat one of these conditions while ignoring the other,” Rosana G. Bianchettin, MD, of the division of cardiovascular diseases, Mayo Clinic, Rochester, Minn., and colleagues wrote in their review, recently published in the Journal of the American College of Cardiology.

The review outlines, for example, how obesity can impair common imaging tests used to diagnose heart disease, potentially reducing their accuracy.

And cardiac procedures such as percutaneous coronary intervention, open heart surgery, and revascularization all involve greater risk in the setting of obesity, while procedures such as valve replacement and heart transplantation carry a greater likelihood of failure.

Obesity can also alter drug pharmacokinetics and pharmacodynamics.

Weight reduction is an important part of the management of patients with cardiovascular disease and obesity, and “cardiac rehabilitation programs represent a potential opportunity for structured interventions,” the authors noted. However, “when other measures are insufficient, bariatric surgery can improve outcomes.”

They also advised against relying solely on body mass index (BMI) to assess adiposity: “It is prudent to investigate a range of complementary ... parameters alongside standard BMI calculations (accounting for age, race, and sex), including measures of central obesity, such as waist circumference, waist-to-hip ratio, and weight-to-height ratio.”
 

Excess fat acts as filter and can skew diagnostic results

“Obesity affects nearly all the diagnostic tests used in cardiology, such as ECG, CT scan, MRI, and echocardiogram,” senior author Francisco Lopez-Jimenez, MD, director of preventive cardiology at Mayo Clinic, explained in a statement.

The review includes a detailed table of these key obesity-related challenges. With electrocardiograms, for example, obesity can cause displacement of the heart, increased cardiac workload, and widening of the distance between the heart and the recording electrodes.

Obesity also lowers the sensitivity of exercise echocardiography, and use of CT coronary angiogram is completely precluded in people with a BMI above 40 kg/m². In interventional radiology, there may be poor visualization of target areas.

“Excess fat acts as a kind of filter and can skew test readings to under- or overdiagnosis,” noted Dr. Lopez-Jimenez.
 

Therapeutic challenges: Drugs may work differently

A longer table in the review summarizes the therapeutic challenges involved in lifestyle modification, pharmacology, cardiac procedures, and other therapeutic measures for people with the two conditions.

Obesity can limit a person’s ability to exercise, for example, and smoking cessation may promote overeating and further weight gain.

Moreover, “tailoring pharmacotherapy is difficult because of unique pharmacokinetic and pharmacodynamic factors in people with obesity that alter distribution, metabolism, and elimination of drugs. Each drug also has special properties that must be considered when it is administrated,” the authors wrote.

Examples include the higher volume of distribution of lipophilic drugs in those with increased fat mass, alterations in liver metabolism, and difficulties with anticoagulant dosing.
 

Cardiac rehabilitation is an intervention opportunity

Although cardiac rehabilitation is “a cornerstone in secondary prevention” for people who have experienced a cardiac event, only 8% of such programs include formal in-house behavioral weight-loss programs.

But that could be remedied and expanded with the use of options such as home-based rehabilitation and telephone counseling, particularly in rural communities, Dr. Bianchettin and colleagues said.

“Motivated individuals will benefit from multicomponent approaches and should be encouraged to set specific, proximal, shared goals with their health care professional. A multitude of tools are available to support self-monitoring (e.g., smartphone applications, food diaries), and scheduled regular follow-up and feedback on progress can help to maintain motivation,” they wrote.

The bottom line, said Dr. Lopez-Jimenez: “Obesity is an important risk factor to address in patients with heart disease and it requires us to do something. ... The patient needs to know that their clinician can help them lose weight. Overall, weight-loss solutions come down to finding the right therapy for the patient.”

Dr. Bianchettin reported no relevant financial relationships. Dr. Lopez-Jimenez has reported conducting research related to 3D body assessment with Select Research, Mayo Clinic, and may benefit in the future if the technology is commercialized; he has not received any relevant monetary, financial, or other type of compensation to date, in relationship to this arrangement. He is a member of the scientific advisory board for Novo Nordisk.

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

NEW ORLEANS – An investigational, first-in class agent that delivers a completely new type of intervention to patients with pulmonary arterial hypertension (PAH) scored a clear win in the STELLAR trial, the first to complete among three phase 3 trials that are testing this agent.

Sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved from baseline average 6-minute walk distance (6MWD) by a significant and clinically meaningful 40.8 meters, compared with placebo, for the trial’s primary efficacy endpoint (P < .001). The treatment also “delivered broad clinical benefit across multiple domains including hemodynamics, World Health Organization functional class, disease biomarkers, risk scores and patient-reported outcomes,” Marius M. Hoeper, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation.

Mitchel L. Zoler/MDedge News

“These results establish the clinical utility of sotatercept, administered in combination with approved PAH therapies, as a new treatment for PAH,” added Dr. Hoeper, professor and deputy director of the department of respiratory medicine at Hannover (Germany) Medical School,

“The most important aspect was the hemodynamic improvement,” with sotatercept treatment, which led to an average 235 dyn/sec per cm⁻⁵ reduction in pulmonary vascular resistance from baseline and an average cut in pulmonary artery pressure of 13.9 mm Hg from baseline, compared with placebo, a result that’s “unheard of,” Dr. Hoeper said in a press conference during the meeting.

“With other tested agents we usually see very little improvement in pulmonary artery pressure. This is a signal that we achieved some reversing of the pathological changes in the pulmonary vessels that lead to” PAH, he added.

Simultaneously with his report the findings also appeared online in the New England Journal of Medicine.
 

‘A new hope’ for patients with PAH

Based on the reported findings, sotatercept is a “very exciting boutique molecule” that will “offer patients with PAH a very exciting new treatment,” commented Rhonda Cooper-DeHoff, PharmD, a designated discussant and a researcher at the University of Florida, Gainesville.

Mitchel L. Zoler/MDedge News

“This study is a new hope for patients with PAH. Until now, they’ve had really bad outcomes, but [in this study] we see significant differences in 6MWD, hemodynamics, and risk factors. Overall, I think the benefit is greater than the risk” it may pose to patients through potential adverse effects, commented Julia Grapsa, MD, PhD, a cardiologist at St. Thomas Hospital in London, and another discussant at the meeting.

“The results are impressive” and “encouraging,” and “suggest that sotatercept may represent a new and clinically consequential addition to current medications for PAH,” wrote three clinicians from Canyons Region Intermountain Medical Center in Murray, Utah, in an editorial that accompanied the published report.

But the authors of the editorial also raised several cautions and concerns. They questioned the generalizability of the findings, noting that the patients with PAH enrolled in the study were all adults who were clinically stable and an average of more than 8 years out from their initial PAH diagnosis, and more than 90% were on stable treatment for PAH with two or three agents specific for treating the disorder. The study cohort also had a disproportionately high enrollment of patients with idiopathic (59%) or heritable (18%) forms of PAH, and the 15% of patients in the trial with connective tissue disease represented a disproportionately low prevalence of this PAH subtype.

The editorialists also called for “ongoing vigilance” for adverse effects from sotatercept treatment, although they acknowledged that the adverse effects reported to date from sotatercept are “largely reassuring.”
 

Death or clinical worsening cut by 84%

STELLAR randomized 323 patients at 91 sites in 21 countries with WHO Group 1 PAH and with WHO functional class II or III disease to receive either sotatercept or placebo for 24 weeks, with an option for treatment to continue beyond that until the last patient in the study reached 24 weeks on treatment, resulting in an overall median treatment duration of nearly 33 weeks.

In addition to the significant result for the primary endpoint, the 163 patients who received sotatercept had significant improvements, compared with 160 placebo-treated patients, for eight of nine secondary endpoints. The only secondary endpoint with a neutral result was for a measure of cognitive and emotional wellbeing, a parameter that was already at a normal level at baseline in most enrolled patients, Dr. Hoeper explained.

The incidence of either death or an event indicative of clinical worsening during the overall median follow-up of almost 33 weeks was 26.3% among the control patients and 5.5% among those who received sotatercept. This translated into a significant reduction for this endpoint of 84% with sotatercept treatment, compared with placebo.

The rates of treatment-emergent adverse events leading to discontinuation were roughly the same in the control and sotatercept arms, and the incidence of severe or serious treatment-emergent adverse events was higher among the control patients.

The most common adverse event on sotatercept was bleeding events, which occurred in 32% of those on sotatercept and in 16% of the control patients, but the events in the sotatercept arm were “mostly mild,” said Dr. Hoeper. The next most frequent adverse event during sotatercept treatment was appearance of telangiectasias, which occurred in 14% of those on sotatercept and in 4% of control patients.

“It’s an uncommon adverse event profile, but not unexpected for a drug with its mechanism of action,” he said.

Drug binds activin, a pathologic driver of PAH

Sotatercept is an engineered molecule that combines a section of a human immunoglobulin G molecule with a portion of the receptor for activin. This structure allows sotatercept to bind free activin molecules in a patient’s blood, thereby removing a key driver of the pulmonary vascular wall remodeling that is at the pathologic root of PAH.

“Hyperproliferation of blood vessel–wall cells” caused by activin signaling “is perhaps the most important driver of PAH,” Dr. Hoeper said. “Sotatercept allows us for the first time to target the underlying mechanism behind PAH.”

Still ongoing are the HYPERION and ZENITH phase 3 trials of sotatercept. HYPERION is enrolling patients with newly diagnosed or high-risk PAH and is expected to complete in 2028. ZENITH is enrolling patients with more advanced PAH and a higher mortality risk, with results expected in 2026.

Sotatercept has received “Breakthrough Therapy” designation and “Orphan Drug” designation by the Food and Drug Administration, and “Priority Medicines” designation and “Orphan Drug” designation by the European Medicines Agency for the treatment of PAH. One recent review estimated a worldwide PAH prevalence of about 3-4 cases/100,000, which for the United States translates into a total prevalence of perhaps 10,000-15,000 affected people.

STELLAR was funded by Acceleron Pharma, a subsidiary of Merck. Dr. Hoeper is a consultant to Acceleron. Dr. Cooper-DeHoff, Dr. Grapsa, and the authors of the editorial on STELLAR have no relevant disclosures.

NEW ORLEANS – An investigational, first-in class agent that delivers a completely new type of intervention to patients with pulmonary arterial hypertension (PAH) scored a clear win in the STELLAR trial, the first to complete among three phase 3 trials that are testing this agent.

Sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved from baseline average 6-minute walk distance (6MWD) by a significant and clinically meaningful 40.8 meters, compared with placebo, for the trial’s primary efficacy endpoint (P < .001). The treatment also “delivered broad clinical benefit across multiple domains including hemodynamics, World Health Organization functional class, disease biomarkers, risk scores and patient-reported outcomes,” Marius M. Hoeper, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation.

Mitchel L. Zoler/MDedge News

“These results establish the clinical utility of sotatercept, administered in combination with approved PAH therapies, as a new treatment for PAH,” added Dr. Hoeper, professor and deputy director of the department of respiratory medicine at Hannover (Germany) Medical School,

“The most important aspect was the hemodynamic improvement,” with sotatercept treatment, which led to an average 235 dyn/sec per cm⁻⁵ reduction in pulmonary vascular resistance from baseline and an average cut in pulmonary artery pressure of 13.9 mm Hg from baseline, compared with placebo, a result that’s “unheard of,” Dr. Hoeper said in a press conference during the meeting.

“With other tested agents we usually see very little improvement in pulmonary artery pressure. This is a signal that we achieved some reversing of the pathological changes in the pulmonary vessels that lead to” PAH, he added.

Simultaneously with his report the findings also appeared online in the New England Journal of Medicine.
 

‘A new hope’ for patients with PAH

Based on the reported findings, sotatercept is a “very exciting boutique molecule” that will “offer patients with PAH a very exciting new treatment,” commented Rhonda Cooper-DeHoff, PharmD, a designated discussant and a researcher at the University of Florida, Gainesville.

Mitchel L. Zoler/MDedge News

“This study is a new hope for patients with PAH. Until now, they’ve had really bad outcomes, but [in this study] we see significant differences in 6MWD, hemodynamics, and risk factors. Overall, I think the benefit is greater than the risk” it may pose to patients through potential adverse effects, commented Julia Grapsa, MD, PhD, a cardiologist at St. Thomas Hospital in London, and another discussant at the meeting.

“The results are impressive” and “encouraging,” and “suggest that sotatercept may represent a new and clinically consequential addition to current medications for PAH,” wrote three clinicians from Canyons Region Intermountain Medical Center in Murray, Utah, in an editorial that accompanied the published report.

But the authors of the editorial also raised several cautions and concerns. They questioned the generalizability of the findings, noting that the patients with PAH enrolled in the study were all adults who were clinically stable and an average of more than 8 years out from their initial PAH diagnosis, and more than 90% were on stable treatment for PAH with two or three agents specific for treating the disorder. The study cohort also had a disproportionately high enrollment of patients with idiopathic (59%) or heritable (18%) forms of PAH, and the 15% of patients in the trial with connective tissue disease represented a disproportionately low prevalence of this PAH subtype.

The editorialists also called for “ongoing vigilance” for adverse effects from sotatercept treatment, although they acknowledged that the adverse effects reported to date from sotatercept are “largely reassuring.”
 

Death or clinical worsening cut by 84%

STELLAR randomized 323 patients at 91 sites in 21 countries with WHO Group 1 PAH and with WHO functional class II or III disease to receive either sotatercept or placebo for 24 weeks, with an option for treatment to continue beyond that until the last patient in the study reached 24 weeks on treatment, resulting in an overall median treatment duration of nearly 33 weeks.

In addition to the significant result for the primary endpoint, the 163 patients who received sotatercept had significant improvements, compared with 160 placebo-treated patients, for eight of nine secondary endpoints. The only secondary endpoint with a neutral result was for a measure of cognitive and emotional wellbeing, a parameter that was already at a normal level at baseline in most enrolled patients, Dr. Hoeper explained.

The incidence of either death or an event indicative of clinical worsening during the overall median follow-up of almost 33 weeks was 26.3% among the control patients and 5.5% among those who received sotatercept. This translated into a significant reduction for this endpoint of 84% with sotatercept treatment, compared with placebo.

The rates of treatment-emergent adverse events leading to discontinuation were roughly the same in the control and sotatercept arms, and the incidence of severe or serious treatment-emergent adverse events was higher among the control patients.

The most common adverse event on sotatercept was bleeding events, which occurred in 32% of those on sotatercept and in 16% of the control patients, but the events in the sotatercept arm were “mostly mild,” said Dr. Hoeper. The next most frequent adverse event during sotatercept treatment was appearance of telangiectasias, which occurred in 14% of those on sotatercept and in 4% of control patients.

“It’s an uncommon adverse event profile, but not unexpected for a drug with its mechanism of action,” he said.

Drug binds activin, a pathologic driver of PAH

Sotatercept is an engineered molecule that combines a section of a human immunoglobulin G molecule with a portion of the receptor for activin. This structure allows sotatercept to bind free activin molecules in a patient’s blood, thereby removing a key driver of the pulmonary vascular wall remodeling that is at the pathologic root of PAH.

“Hyperproliferation of blood vessel–wall cells” caused by activin signaling “is perhaps the most important driver of PAH,” Dr. Hoeper said. “Sotatercept allows us for the first time to target the underlying mechanism behind PAH.”

Still ongoing are the HYPERION and ZENITH phase 3 trials of sotatercept. HYPERION is enrolling patients with newly diagnosed or high-risk PAH and is expected to complete in 2028. ZENITH is enrolling patients with more advanced PAH and a higher mortality risk, with results expected in 2026.

Sotatercept has received “Breakthrough Therapy” designation and “Orphan Drug” designation by the Food and Drug Administration, and “Priority Medicines” designation and “Orphan Drug” designation by the European Medicines Agency for the treatment of PAH. One recent review estimated a worldwide PAH prevalence of about 3-4 cases/100,000, which for the United States translates into a total prevalence of perhaps 10,000-15,000 affected people.

STELLAR was funded by Acceleron Pharma, a subsidiary of Merck. Dr. Hoeper is a consultant to Acceleron. Dr. Cooper-DeHoff, Dr. Grapsa, and the authors of the editorial on STELLAR have no relevant disclosures.

NEW ORLEANS – An investigational, first-in class agent that delivers a completely new type of intervention to patients with pulmonary arterial hypertension (PAH) scored a clear win in the STELLAR trial, the first to complete among three phase 3 trials that are testing this agent.

Sotatercept, administered subcutaneously every 3 weeks for 24 weeks, improved from baseline average 6-minute walk distance (6MWD) by a significant and clinically meaningful 40.8 meters, compared with placebo, for the trial’s primary efficacy endpoint (P < .001). The treatment also “delivered broad clinical benefit across multiple domains including hemodynamics, World Health Organization functional class, disease biomarkers, risk scores and patient-reported outcomes,” Marius M. Hoeper, MD, said at the joint scientific sessions of the American College of Cardiology and the World Heart Federation.

Mitchel L. Zoler/MDedge News

“These results establish the clinical utility of sotatercept, administered in combination with approved PAH therapies, as a new treatment for PAH,” added Dr. Hoeper, professor and deputy director of the department of respiratory medicine at Hannover (Germany) Medical School,

“The most important aspect was the hemodynamic improvement,” with sotatercept treatment, which led to an average 235 dyn/sec per cm⁻⁵ reduction in pulmonary vascular resistance from baseline and an average cut in pulmonary artery pressure of 13.9 mm Hg from baseline, compared with placebo, a result that’s “unheard of,” Dr. Hoeper said in a press conference during the meeting.

“With other tested agents we usually see very little improvement in pulmonary artery pressure. This is a signal that we achieved some reversing of the pathological changes in the pulmonary vessels that lead to” PAH, he added.

Simultaneously with his report the findings also appeared online in the New England Journal of Medicine.
 

‘A new hope’ for patients with PAH

Based on the reported findings, sotatercept is a “very exciting boutique molecule” that will “offer patients with PAH a very exciting new treatment,” commented Rhonda Cooper-DeHoff, PharmD, a designated discussant and a researcher at the University of Florida, Gainesville.

Mitchel L. Zoler/MDedge News

“This study is a new hope for patients with PAH. Until now, they’ve had really bad outcomes, but [in this study] we see significant differences in 6MWD, hemodynamics, and risk factors. Overall, I think the benefit is greater than the risk” it may pose to patients through potential adverse effects, commented Julia Grapsa, MD, PhD, a cardiologist at St. Thomas Hospital in London, and another discussant at the meeting.

“The results are impressive” and “encouraging,” and “suggest that sotatercept may represent a new and clinically consequential addition to current medications for PAH,” wrote three clinicians from Canyons Region Intermountain Medical Center in Murray, Utah, in an editorial that accompanied the published report.

But the authors of the editorial also raised several cautions and concerns. They questioned the generalizability of the findings, noting that the patients with PAH enrolled in the study were all adults who were clinically stable and an average of more than 8 years out from their initial PAH diagnosis, and more than 90% were on stable treatment for PAH with two or three agents specific for treating the disorder. The study cohort also had a disproportionately high enrollment of patients with idiopathic (59%) or heritable (18%) forms of PAH, and the 15% of patients in the trial with connective tissue disease represented a disproportionately low prevalence of this PAH subtype.

The editorialists also called for “ongoing vigilance” for adverse effects from sotatercept treatment, although they acknowledged that the adverse effects reported to date from sotatercept are “largely reassuring.”
 

Death or clinical worsening cut by 84%

STELLAR randomized 323 patients at 91 sites in 21 countries with WHO Group 1 PAH and with WHO functional class II or III disease to receive either sotatercept or placebo for 24 weeks, with an option for treatment to continue beyond that until the last patient in the study reached 24 weeks on treatment, resulting in an overall median treatment duration of nearly 33 weeks.

In addition to the significant result for the primary endpoint, the 163 patients who received sotatercept had significant improvements, compared with 160 placebo-treated patients, for eight of nine secondary endpoints. The only secondary endpoint with a neutral result was for a measure of cognitive and emotional wellbeing, a parameter that was already at a normal level at baseline in most enrolled patients, Dr. Hoeper explained.

The incidence of either death or an event indicative of clinical worsening during the overall median follow-up of almost 33 weeks was 26.3% among the control patients and 5.5% among those who received sotatercept. This translated into a significant reduction for this endpoint of 84% with sotatercept treatment, compared with placebo.

The rates of treatment-emergent adverse events leading to discontinuation were roughly the same in the control and sotatercept arms, and the incidence of severe or serious treatment-emergent adverse events was higher among the control patients.

The most common adverse event on sotatercept was bleeding events, which occurred in 32% of those on sotatercept and in 16% of the control patients, but the events in the sotatercept arm were “mostly mild,” said Dr. Hoeper. The next most frequent adverse event during sotatercept treatment was appearance of telangiectasias, which occurred in 14% of those on sotatercept and in 4% of control patients.

“It’s an uncommon adverse event profile, but not unexpected for a drug with its mechanism of action,” he said.

Drug binds activin, a pathologic driver of PAH

Sotatercept is an engineered molecule that combines a section of a human immunoglobulin G molecule with a portion of the receptor for activin. This structure allows sotatercept to bind free activin molecules in a patient’s blood, thereby removing a key driver of the pulmonary vascular wall remodeling that is at the pathologic root of PAH.

“Hyperproliferation of blood vessel–wall cells” caused by activin signaling “is perhaps the most important driver of PAH,” Dr. Hoeper said. “Sotatercept allows us for the first time to target the underlying mechanism behind PAH.”

Still ongoing are the HYPERION and ZENITH phase 3 trials of sotatercept. HYPERION is enrolling patients with newly diagnosed or high-risk PAH and is expected to complete in 2028. ZENITH is enrolling patients with more advanced PAH and a higher mortality risk, with results expected in 2026.

Sotatercept has received “Breakthrough Therapy” designation and “Orphan Drug” designation by the Food and Drug Administration, and “Priority Medicines” designation and “Orphan Drug” designation by the European Medicines Agency for the treatment of PAH. One recent review estimated a worldwide PAH prevalence of about 3-4 cases/100,000, which for the United States translates into a total prevalence of perhaps 10,000-15,000 affected people.

STELLAR was funded by Acceleron Pharma, a subsidiary of Merck. Dr. Hoeper is a consultant to Acceleron. Dr. Cooper-DeHoff, Dr. Grapsa, and the authors of the editorial on STELLAR have no relevant disclosures.

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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

As a lifeguard during college and then a physician assistant in emergency medicine for almost 3 decades, people often ask how I deal with emergency situations. I tell them the emotions turn off; skills and training take over. That is exactly what happened one day while I was surfing.

There’s a famous surf spot called Old Man’s on San Onofre beach in north San Diego County. It has nice, gentle waves that people say are similar to Waikiki in Hawaii. Since the waves are so forgiving, a lot of older people surf there. I taught my boys and some friends how to surf there. Everyone enjoys the water. It’s just a really fun vibe.

In September of 2008, I was at Old Man’s surfing with friends. After a while, I told them I was going to catch the next wave in. When I rode the wave to the beach, I saw an older guy waving his arms above his head, trying to get the lifeguard’s attention. His friend was lying on the sand at the water’s edge, unconscious. The lifeguards were about 200 yards away in their truck. Since it was off-season, they weren’t in the nearby towers.

I threw my board down on the sand and ran over. The guy was blue in the face and had some secretions around his mouth. He wasn’t breathing and had no pulse. I told his friend to get the lifeguards.

I gave two rescue breaths, and then started CPR. The waves were still lapping against his feet. I could sense people gathering around, so I said, “Okay, we’re going to be hooking him up to electricity, let’s get him out of the water.” I didn’t want him in contact with the water that could potentially transmit that electricity to anyone else.

Many hands reached in and we dragged him up to dry sand. When we pulled down his wetsuit, I saw an old midline sternotomy incision on his chest and I thought: “Oh man, he’s got a cardiac history.” I said, “I need a towel,” and suddenly there was a towel in my hand. I dried him off and continued doing CPR.

The lifeguard truck pulled up and in my peripheral vision I saw two lifeguards running over with their first aid kit. While doing compressions, I yelled over my shoulder: “Bring your AED! Get your oxygen!” They ran back to the truck.

At that point, a young woman came up and said: “I’m a nuclear medicine tech. What can I do?” I asked her to help me keep his airway open. I positioned her at his head, and she did a chin lift.

The two lifeguards came running back. One was very experienced, and he started getting the AED ready and putting the pads on. The other lifeguard was younger. He was nervous and shaking, trying to figure out how to turn on the oxygen tank. I told him: “Buddy, you better figure that out real fast.”

The AED said there was a shockable rhythm so it delivered a shock. I started compressions again. The younger lifeguard finally figured out how to turn on the oxygen tank. Now we had oxygen, a bag valve mask, and an AED. We let our training take over and quickly melded together as an efficient team.

Two minutes later the AED analyzed the rhythm and administered another shock. More compressions. Then another shock and compressions. I had so much adrenaline going through my body that I wasn’t even getting tired.

By then I had been doing compressions for a good 10 minutes. Finally, I asked: “Hey, when are the paramedics going to get here?” And the lifeguard said: “They’re on their way.” But we were all the way down on a very remote section of beach.

We did CPR on him for what seemed like eternity, probably only 15-20 minutes. Sometimes he would get a pulse back and pink up, and we could stop and get a break. But then I would see him become cyanotic. His pulse would become thready, so I would start again.

The paramedics finally arrived and loaded him into the ambulance. He was still blue in the face, and I honestly thought he would probably not survive. I said a quick prayer for him as they drove off.

For the next week, I wondered what happened to him. The next time I was at the beach, I approached some older guys and said: “Hey, I was doing CPR on a guy here last week. Do you know what happened to him?” They gave me a thumbs up sign and said: “He’s doing great!” I was amazed!

While at the beach, I saw the nuclear med tech who helped with the airway and oxygen. She told me she’d called her hospital after the incident and asked if they had received a full arrest from the beach. They said: “Yes, he was sitting up, awake and talking when he came through the door.”

A few weeks later, the local paper called and wanted to do an interview and get some photos on the beach. We set up a time to meet, and I told the reporter that if he ever found out who the guy was, I would love to meet him. I had two reasons: First, because I had done mouth-to-mouth on him and I wanted to make sure he didn’t have any communicable diseases. Second, and this is a little weirder, I wanted to find out if he had an out-of-body experience. They fascinate me.

The reporter called back a few minutes later and said: “You’ll never believe this – while I was talking to you, my phone beeped with another call. The person left a message, and it was the guy. He wants to meet you.” I was amazed at the coincidence that he would call at exactly the same time.

Later that day, we all met at the beach. I gave him a big hug and told him he looked a lot better than the last time I saw him. He now had a pacemaker/defibrillator. I found out he was married and had three teenage boys (who still have a father). He told me on the day of the incident he developed chest pain, weakness, and shortness of breath while surfing, so he came in and sat down at the water’s edge to catch his breath. That was the last thing he remembered. 

When I told him I did mouth-to-mouth on him, he laughed and reassured me that he didn’t have any contagious diseases. Then I asked him about an out-of-body experience, like hovering above his body and watching the CPR. “Did you see us doing that?” I asked. He said: “No, nothing but black. The next thing I remember is waking up in the back of the ambulance, and the paramedic asked me, ‘how does it feel to come back from the dead?’ ” He answered: “I think I have to throw up.”

He was cleared to surf 6 weeks later, and I thought it would be fun to surf with him. But when he started paddling out, he said his defibrillator went off, so he has now retired to golf.

I’ve been a PA in the emergency room for 28 years. I’ve done CPR for so long it’s instinctive for me. It really saves lives, especially with the AED. When people say: “You saved his life,” I say: “No, I didn’t. I just kept him alive and let the AED do its job.”

Ms. Westbrook-May is an emergency medicine physician assistant in Newport Beach, Calif.

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