Kari Oakes

BALTIMORE – Distinct patterns of blood pressure changes in midlife are associated with varying degrees of risk for cardiovascular disease and death, according to a multisite study.

These patterns of change contributed to risk for both CVD and mortality, separate from the known association of absolute elevation of systolic blood pressure with CVD and death. Natalia Petruski-Ivleva of the University of North Carolina, Chapel Hill, and colleagues identified SBP patterns emerging from the biracial, multisite Atherosclerosis Risk in Communities (ARIC) study and presented the results at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

©crossstudio/ThinkStock

The study included 9,882 patients from the ARIC population who had recorded BPs at four study visits between 1987 and 1998, and whose outcomes were tracked over the period from 1987 to 2011. Median follow-up after the last study visit was 13.2 years. Participants were grouped by patterns of change in SBP over time using a latent class growth model; this analytic model allowed for the discovery of similar groups of cases within the data.

Results were adjusted for age and demographic characteristics, as well as for self-reported hypertension medication use. In addition to all-cause mortality, outcomes included coronary heart disease, heart failure, and stroke.

In all, six distinct patterns emerged of change in SBP over the study visit period, with three groups having SBPs consistently below the threshold of 140 mm Hg, and three other groups showing varying patterns of elevation. About 84% of participants fell into one of the three groups that showed parallel patterns of SBP change, with pressures slowly rising over time, but never exceeding 140 mm Hg. The remainder of participants were grouped into three other patterns. One showed a steep increase over time from an initial SBP just under 140 mm Hg to a final reading just over 160 mm Hg; a second showed high and sustained SBPs of more than 160 mm Hg at all study visits. Finally, some participants had initially elevated SBPs that fell to the normal range by the end of the study.

Overall, analysis showed a gradient of risk, with lower SBP associated with lower risk of CVD and death. This was true even for those participants in the first three groups, whose SBPs stayed below 140 mm Hg throughout. Notably, the pattern of steep increase of already elevated SBP, as well as that of sustained elevated blood pressures, were both associated with the highest all-cause mortality. Reducing SBP to less than 140 mm Hg was not associated with reduced risk of CHD in the final group.

The three higher-risk groups were more likely to be obese, black, on hypertension medication, and have diabetes. They were also older on average than participants with the three nonelevated patterns.

These patterns of change, said Ms. Petruski-Ivleva, “contribute varying amounts of risk of CVD and mortality in addition to the risk imparted by the absolute SBP level.” Though the clinical significance of these patterns of blood pressure change needs more examination, she said that the results underscore the cumulative impact of elevated SBP through midlife.

BALTIMORE – Distinct patterns of blood pressure changes in midlife are associated with varying degrees of risk for cardiovascular disease and death, according to a multisite study.

These patterns of change contributed to risk for both CVD and mortality, separate from the known association of absolute elevation of systolic blood pressure with CVD and death. Natalia Petruski-Ivleva of the University of North Carolina, Chapel Hill, and colleagues identified SBP patterns emerging from the biracial, multisite Atherosclerosis Risk in Communities (ARIC) study and presented the results at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

©crossstudio/ThinkStock

The study included 9,882 patients from the ARIC population who had recorded BPs at four study visits between 1987 and 1998, and whose outcomes were tracked over the period from 1987 to 2011. Median follow-up after the last study visit was 13.2 years. Participants were grouped by patterns of change in SBP over time using a latent class growth model; this analytic model allowed for the discovery of similar groups of cases within the data.

Results were adjusted for age and demographic characteristics, as well as for self-reported hypertension medication use. In addition to all-cause mortality, outcomes included coronary heart disease, heart failure, and stroke.

In all, six distinct patterns emerged of change in SBP over the study visit period, with three groups having SBPs consistently below the threshold of 140 mm Hg, and three other groups showing varying patterns of elevation. About 84% of participants fell into one of the three groups that showed parallel patterns of SBP change, with pressures slowly rising over time, but never exceeding 140 mm Hg. The remainder of participants were grouped into three other patterns. One showed a steep increase over time from an initial SBP just under 140 mm Hg to a final reading just over 160 mm Hg; a second showed high and sustained SBPs of more than 160 mm Hg at all study visits. Finally, some participants had initially elevated SBPs that fell to the normal range by the end of the study.

Overall, analysis showed a gradient of risk, with lower SBP associated with lower risk of CVD and death. This was true even for those participants in the first three groups, whose SBPs stayed below 140 mm Hg throughout. Notably, the pattern of steep increase of already elevated SBP, as well as that of sustained elevated blood pressures, were both associated with the highest all-cause mortality. Reducing SBP to less than 140 mm Hg was not associated with reduced risk of CHD in the final group.

The three higher-risk groups were more likely to be obese, black, on hypertension medication, and have diabetes. They were also older on average than participants with the three nonelevated patterns.

These patterns of change, said Ms. Petruski-Ivleva, “contribute varying amounts of risk of CVD and mortality in addition to the risk imparted by the absolute SBP level.” Though the clinical significance of these patterns of blood pressure change needs more examination, she said that the results underscore the cumulative impact of elevated SBP through midlife.

BALTIMORE – Distinct patterns of blood pressure changes in midlife are associated with varying degrees of risk for cardiovascular disease and death, according to a multisite study.

These patterns of change contributed to risk for both CVD and mortality, separate from the known association of absolute elevation of systolic blood pressure with CVD and death. Natalia Petruski-Ivleva of the University of North Carolina, Chapel Hill, and colleagues identified SBP patterns emerging from the biracial, multisite Atherosclerosis Risk in Communities (ARIC) study and presented the results at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

©crossstudio/ThinkStock

The study included 9,882 patients from the ARIC population who had recorded BPs at four study visits between 1987 and 1998, and whose outcomes were tracked over the period from 1987 to 2011. Median follow-up after the last study visit was 13.2 years. Participants were grouped by patterns of change in SBP over time using a latent class growth model; this analytic model allowed for the discovery of similar groups of cases within the data.

Results were adjusted for age and demographic characteristics, as well as for self-reported hypertension medication use. In addition to all-cause mortality, outcomes included coronary heart disease, heart failure, and stroke.

In all, six distinct patterns emerged of change in SBP over the study visit period, with three groups having SBPs consistently below the threshold of 140 mm Hg, and three other groups showing varying patterns of elevation. About 84% of participants fell into one of the three groups that showed parallel patterns of SBP change, with pressures slowly rising over time, but never exceeding 140 mm Hg. The remainder of participants were grouped into three other patterns. One showed a steep increase over time from an initial SBP just under 140 mm Hg to a final reading just over 160 mm Hg; a second showed high and sustained SBPs of more than 160 mm Hg at all study visits. Finally, some participants had initially elevated SBPs that fell to the normal range by the end of the study.

Overall, analysis showed a gradient of risk, with lower SBP associated with lower risk of CVD and death. This was true even for those participants in the first three groups, whose SBPs stayed below 140 mm Hg throughout. Notably, the pattern of steep increase of already elevated SBP, as well as that of sustained elevated blood pressures, were both associated with the highest all-cause mortality. Reducing SBP to less than 140 mm Hg was not associated with reduced risk of CHD in the final group.

The three higher-risk groups were more likely to be obese, black, on hypertension medication, and have diabetes. They were also older on average than participants with the three nonelevated patterns.

These patterns of change, said Ms. Petruski-Ivleva, “contribute varying amounts of risk of CVD and mortality in addition to the risk imparted by the absolute SBP level.” Though the clinical significance of these patterns of blood pressure change needs more examination, she said that the results underscore the cumulative impact of elevated SBP through midlife.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

Continue for the second trial >>

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

Continue for the second trial >>

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

Continue for the second trial >>

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

For women in midlife, an earlier age of onset of vasomotor symptoms – hot flashes and night sweats – was linked to impaired endothelial function, a very early marker for cardiovascular disease.

In the first of two related studies, an earlier age of onset for vasomotor symptoms (VMS) was associated with increased endothelial dysfunction as measured by brachial artery ultrasound. Greater frequency of hot flashes was associated with endothelial dysfunction for younger but not older participants in the second study.

Though more than 70% of women experience VMS during perimenopause and menopause, these symptoms largely have been viewed as a quality of life issue. However, this emerging research might mean that early onset of of hot flashes might serve a potential marker for increased risk for cardiovascular disease, said Rebecca C. Thurston, Ph.D., associate professor of psychiatry, psychology, and epidemiology at the University of Pittsburgh. Her work was presented in a briefing in advance of the annual meeting of the American College of Cardiology in San Diego.

Dr. Thurston and her colleagues drew from the Women’s Ischemia Syndrome Evaluation (WISE) study to evaluate 104 women at four study sites. Participants were postmenopausal and at least 50 years old, could not be on hormone replacement therapy, and had their ovaries. Women with any signs or symptoms of ischemia were excluded, and multiple potential confounders were assessed in the study’s extensive evaluation. Women were stratified by onset of VMS by self-report into three groups: those who never had VMS, those whose VMS began at age 42 or earlier, and those whose VMS began after the age of 42.

Women in the WISE study underwent brachial artery ultrasound to assess brachial artery flow mediated dilation (FMD), a known preclinical disease marker that has been linked to clinical outcomes. Lower FMD scores indicate poorer endothelial function. Women in the group with the earliest onset of VMS had significantly lower FMD values (P = 0.038), indicating poorer endothelial dysfunction. The effect persisted even after controlling for potentially confounding factors.

The second trial, the MSHeart Study, enrolled 189 women aged 40-60. All were nonsmokers with no history of CVD. All of the women had intact uteri and ovaries, and enrollees could not be using hormones or other medications that could affect vascular function (beta-blockers, calcium channel blockers, insulin, or selective serotonin reuptake inhibitors/selective norepinephrine reuptake inhibitors). Participants again underwent extensive evaluation.

Women in the MSHeart Study received a full 24 hours of objective physiologic hot flash monitoring via an external monitoring system as well as FMD evaluation by brachial artery ultrasound. Women were stratified by age into three groups: younger than 53, 53-56, and greater than age 56.

For the youngest group of women in the second study, increased frequency of objectively verified hot flashes was associated with lower FMD and poorer endothelial dysfunction (P < 0.05). The association was not significant for either of the older two groups when taken separately; however, when pooled data for participants of all ages were considered, the interaction between age and hot flash frequency was associated with reduced FMD (P = 0.02). These associations held true after adjusting for the covariates of age, race, BMI, blood vessel diameter, menopausal stage, and any prior hormone use.

These two studies, said Dr. Thurston, “may point to subgroups of women that need targeted cardiovascular prevention” by identifying early VMS as a mechanistic pathway for endothelial dysfunction. Dr. Richard Chazal, ACC vice president and session moderator, noted that the MSHeart Study in particular succeeded in “leveraging physiologic symptoms and markers, as well as the flow mediated functional dilation that we all would expect.”

The studies were sponsored by the National Heart, Lung, and Blood Institute of the National Institutes of Health.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Purestock/Thinkstock.com

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Purestock/Thinkstock.com

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

Sedentary individuals have a significant increase in a marker of subclinical heart disease, according to a recent study. Each additional hour spent seated per day was associated with a 14% increase in the amount of coronary artery calcification seen on CT imaging.

Even for those who exercise vigorously but also spend many hours sitting, prolonged sedentary activity was independently associated with greater CAC. The effect held true even after adjustment for other known cardiac risk factors, according to Dr. Jacquelyn Kulinski of the Medical College of Wisconsin, Milwaukee, and colleagues at Dallas’ University of Texas Southwestern Medical Center. The results were released in advance of their presentation on March 15 at the annual meeting of the American College of Cardiology in San Diego.

Purestock/Thinkstock.com

Using data from wrist accelerometers in the Dallas Heart Study, a multi-ethnic, population-based sample of adults residing in Dallas, Tex., Dr. Kulinski and colleagues assessed the activity of 2,031 participants without known cardiovascular disease. The median age was 50, about 62% were female, and about half of the participants were black.

The accelerometer, worn on the nondominant hand, captured 7 consecutive days of minute-by-minute activity, and could differentiate between sedentary behavior (sitting or reclining during waking hours), nonexercise activity (such as light movement around the house or a workplace), and more vigorous, purposeful exercise. CAC was assessed via two cardiac CT scans and a standardized scoring system.

Overall, participants had an average 5 hours of sedentary time per day, with a range of 2-12 hours. Higher amounts of sedentary time were associated with being older, having a higher body mass index, and having diabetes or hypertension.

The multivariate analysis included adjustments for patient demographics, clinical characteristics, and the amount to which participants participated in moderate to vigorous physical activity. The researchers found that each additional hour of sedentary time during the day was associated with a statistically significant, 14% increase in CAC. Somewhat surprisingly, Dr. Kulinski noted, there was no association between the amount of moderate to vigorous physical activity and the amount of CAC detected.

Sedentary behavior, sometimes called “sitting disease,” has previously been identified as an independent risk factor for heart disease. These findings, she said, further bolster the concept that “lack of exercise and too much sitting are independent risk factors for CAD and death.”

Dr. Kulinski noted that although fitness is one of the strongest predictors of cardiac health and longevity, there has not been a clear demonstration that increased amounts of exercise are associated with less CAC. This has been true although CAC is an established marker of early formation of the plaque that can lead to coronary artery blockage. The present study suggests that sedentary behaviors, rather than lack of vigorous exercise, may contribute more to the development of CAC than had previously been known.

ACC Vice President Richard Chazal of Lee Memorial Health System, Fort Myers, Fla., remarked in a press briefing before the meeting that this information should be reassuring to patients. “Sometimes just moving around some, even short of a vigorous exercise program, is important,” said Dr. Chazal. “Regular exercise further reduces risk, and it may do so by a mechanism distinct from coronary artery calcification.”

“On a positive note,” Dr. Kulinski said, “reducing daily sitting time by even 1-2 hours could have a significant and positive impact on future cardiovascular health, and this should really be investigated in future studies.”

Dr. James de Lemos disclosed ties with Amgen, DiaDexus, Novo Nordisk, St. Jude Medical, Abbott Diagnostics, and Siemen’s Diagnostics. Dr. Jarrett Berry reports ties with Nihon and Merck. The remaining authors have no disclosures.

BALTIMORE – Higher levels of fitness were associated with markedly reduced overall health care costs for a large group of service veterans, with annualized age-adjusted costs over a third lower when compared with the least-fit quartile.

Fitness was a stronger predictor of overall costs than any other variable assessed in the Veterans Exercise Testing Study (VETS), Dr. Jonathan Myers of the VA Palo Alto Health Care System and Stanford (Calif.) University reported at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

© AHA/Todd Buchanan

“Fitness,” Dr. Myers noted, “is a powerful predictor of risk, but few data exist that have associated health costs with objective measures of fitness.” To address this gap in the literature, Dr. Myers and his colleagues captured maximal exercise test results from the VETS cohort and capitalized on the availability of cost data from the VA Allocation Resource Center for VETS participants.

The 9,945 study participants, all of whom had clinical indications for maximal exercise testing, were almost entirely male (98%), with a mean age of 58 years. The population had a mean body mass index of 29.0 kg/m², just under the cutoff for obesity. Nearly half (43%) had a history of cardiovascular disease, 27% had hypertension, 19% had diabetes, and only 1% had heart failure. Mean follow-up time was 10.7 years.

Participants’ results on maximal exercise testing were expressed as a percentage of the age-predicted peak metabolic equivalents (METS) achieved and stratified into quartiles of <60%, 60%-80%, 80%-100%, and >100% of age-expected peak METs. Multiple regression techniques were used to assess the contribution of exercise test results and clinical characteristics to overall health care costs.

The investigators also examined costs in a variety of ways: total aggregated cost over the study period, cost per patient per study year, and median annualized cost. For all analyses, a highly significant correlation (P <.0001) existed between level of fitness and health care costs. Each additional MET achieved on exercise testing, the investigators calculated, saved $1,592.

Health care costs generally maintained the inverse relationship with fitness across the gradient from most to least fit. Median age-adjusted annualized costs from most- to least-fit quartile, for example, were $10,600, $11,900, $11,300, and $12,600.

Study limitations included the study’s overwhelmingly male makeup, though Dr. Myers noted that there would be no reason to expect different results in women. Additionally, investigators could only obtain data for overall costs, without a breakdown of inpatient vs. outpatient expenditures. In analysis, models were not fully adjusted for comorbidities, either at baseline or during the study course.

In response to a question from the audience about the relative benefits of statin use when compared with enhanced physical fitness, Dr. Myers responded, “It’s been shown that fitness trumps statins for outcomes in the VA data.”

The results presented in this study “provide objective economic-based evidence for employers, health care professionals, and professional organizations to promote physical activity” not only as a means of enhancing well-being, but as a common-sense way to hold down health care costs, Dr. Myers concluded.

The study was funded by the Veterans Affairs Health Care System. No authors reported financial disclosures.

BALTIMORE – Higher levels of fitness were associated with markedly reduced overall health care costs for a large group of service veterans, with annualized age-adjusted costs over a third lower when compared with the least-fit quartile.

Fitness was a stronger predictor of overall costs than any other variable assessed in the Veterans Exercise Testing Study (VETS), Dr. Jonathan Myers of the VA Palo Alto Health Care System and Stanford (Calif.) University reported at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

© AHA/Todd Buchanan

“Fitness,” Dr. Myers noted, “is a powerful predictor of risk, but few data exist that have associated health costs with objective measures of fitness.” To address this gap in the literature, Dr. Myers and his colleagues captured maximal exercise test results from the VETS cohort and capitalized on the availability of cost data from the VA Allocation Resource Center for VETS participants.

The 9,945 study participants, all of whom had clinical indications for maximal exercise testing, were almost entirely male (98%), with a mean age of 58 years. The population had a mean body mass index of 29.0 kg/m², just under the cutoff for obesity. Nearly half (43%) had a history of cardiovascular disease, 27% had hypertension, 19% had diabetes, and only 1% had heart failure. Mean follow-up time was 10.7 years.

Participants’ results on maximal exercise testing were expressed as a percentage of the age-predicted peak metabolic equivalents (METS) achieved and stratified into quartiles of <60%, 60%-80%, 80%-100%, and >100% of age-expected peak METs. Multiple regression techniques were used to assess the contribution of exercise test results and clinical characteristics to overall health care costs.

The investigators also examined costs in a variety of ways: total aggregated cost over the study period, cost per patient per study year, and median annualized cost. For all analyses, a highly significant correlation (P <.0001) existed between level of fitness and health care costs. Each additional MET achieved on exercise testing, the investigators calculated, saved $1,592.

Health care costs generally maintained the inverse relationship with fitness across the gradient from most to least fit. Median age-adjusted annualized costs from most- to least-fit quartile, for example, were $10,600, $11,900, $11,300, and $12,600.

Study limitations included the study’s overwhelmingly male makeup, though Dr. Myers noted that there would be no reason to expect different results in women. Additionally, investigators could only obtain data for overall costs, without a breakdown of inpatient vs. outpatient expenditures. In analysis, models were not fully adjusted for comorbidities, either at baseline or during the study course.

In response to a question from the audience about the relative benefits of statin use when compared with enhanced physical fitness, Dr. Myers responded, “It’s been shown that fitness trumps statins for outcomes in the VA data.”

The results presented in this study “provide objective economic-based evidence for employers, health care professionals, and professional organizations to promote physical activity” not only as a means of enhancing well-being, but as a common-sense way to hold down health care costs, Dr. Myers concluded.

The study was funded by the Veterans Affairs Health Care System. No authors reported financial disclosures.

BALTIMORE – Higher levels of fitness were associated with markedly reduced overall health care costs for a large group of service veterans, with annualized age-adjusted costs over a third lower when compared with the least-fit quartile.

Fitness was a stronger predictor of overall costs than any other variable assessed in the Veterans Exercise Testing Study (VETS), Dr. Jonathan Myers of the VA Palo Alto Health Care System and Stanford (Calif.) University reported at the American Heart Association Epidemiology and Prevention, Lifestyle and Cardiometabolic Health 2015 Scientific Sessions.

© AHA/Todd Buchanan

“Fitness,” Dr. Myers noted, “is a powerful predictor of risk, but few data exist that have associated health costs with objective measures of fitness.” To address this gap in the literature, Dr. Myers and his colleagues captured maximal exercise test results from the VETS cohort and capitalized on the availability of cost data from the VA Allocation Resource Center for VETS participants.

The 9,945 study participants, all of whom had clinical indications for maximal exercise testing, were almost entirely male (98%), with a mean age of 58 years. The population had a mean body mass index of 29.0 kg/m², just under the cutoff for obesity. Nearly half (43%) had a history of cardiovascular disease, 27% had hypertension, 19% had diabetes, and only 1% had heart failure. Mean follow-up time was 10.7 years.

Participants’ results on maximal exercise testing were expressed as a percentage of the age-predicted peak metabolic equivalents (METS) achieved and stratified into quartiles of <60%, 60%-80%, 80%-100%, and >100% of age-expected peak METs. Multiple regression techniques were used to assess the contribution of exercise test results and clinical characteristics to overall health care costs.

The investigators also examined costs in a variety of ways: total aggregated cost over the study period, cost per patient per study year, and median annualized cost. For all analyses, a highly significant correlation (P <.0001) existed between level of fitness and health care costs. Each additional MET achieved on exercise testing, the investigators calculated, saved $1,592.

Health care costs generally maintained the inverse relationship with fitness across the gradient from most to least fit. Median age-adjusted annualized costs from most- to least-fit quartile, for example, were $10,600, $11,900, $11,300, and $12,600.

Study limitations included the study’s overwhelmingly male makeup, though Dr. Myers noted that there would be no reason to expect different results in women. Additionally, investigators could only obtain data for overall costs, without a breakdown of inpatient vs. outpatient expenditures. In analysis, models were not fully adjusted for comorbidities, either at baseline or during the study course.

In response to a question from the audience about the relative benefits of statin use when compared with enhanced physical fitness, Dr. Myers responded, “It’s been shown that fitness trumps statins for outcomes in the VA data.”

The results presented in this study “provide objective economic-based evidence for employers, health care professionals, and professional organizations to promote physical activity” not only as a means of enhancing well-being, but as a common-sense way to hold down health care costs, Dr. Myers concluded.

The study was funded by the Veterans Affairs Health Care System. No authors reported financial disclosures.

Though 31 states now require prior authorization for prescribing atypical antipsychotic medications to Medicaid-insured youth, age limits and how the medications are regulated vary widely.

Requirements for physician peer review, an important consideration for a medication class with potentially negative cardiometabolic impact, also vary by state, Julie M. Zito, Ph.D., of the University of Maryland’s department of pharmaceutical health services research, and her associates reported in a research letter to JAMA (2015 March 3 [doi:10.1001/JAMA.2015.0763]) Dr. Zito and her colleagues noted that pediatric outpatient antipsychotic prescribing has sharply increased over the past 2 decades, and that a child on Medicaid is five times more likely to be prescribed an antipsychotic than a privately insured youth. Clear guidelines are lacking for antipsychotic prescribing, especially for the youngest patients, the study found.

Many states have instituted policies to gain greater oversight of pediatric psychotropic medication prescribing. To characterize nationwide practice, Dr. Zito and her colleagues collected information about prior authorization requirements for atypical antipsychotic prescribing for all 50 states and the District of Columbia. Information was collected by visiting webpages and supplemented by individual e-mail exchanges with state Medicaid authorities when necessary.

In all, 31 states’ Medicaid agencies had policies requiring prior authorization before atypical antipsychotics can be prescribed to Medicaid-insured children. Only seven states required prior authorization for all youth 18 and younger, while most others curtailed the requirement after ages 5, 6, or 7. A separate set of seven states had prior authorization requirements that varied by drug.

The prior authorization process also varied widely between states. Fifteen of the 31 states with prior authorization requirements had mandatory peer review by physicians – often psychiatrists – or had clinical pharmacists perform initial review with physicians available for consultation. By contrast, the other 16 states’ review processes were performed by nonphysician reviewers or were automated.

Dr. Zito and her colleagues said that the study compiled only limited data regarding each state’s policies. The authors recommended further study aimed at tracking unintended consequences of prescribing restrictions, as well as examining whether prior authorization with peer review improves quality of care. All in all, Dr. Zito said in an interview, “we need a much more comprehensive and holistic picture of this complex problem.”

Though 31 states now require prior authorization for prescribing atypical antipsychotic medications to Medicaid-insured youth, age limits and how the medications are regulated vary widely.

Requirements for physician peer review, an important consideration for a medication class with potentially negative cardiometabolic impact, also vary by state, Julie M. Zito, Ph.D., of the University of Maryland’s department of pharmaceutical health services research, and her associates reported in a research letter to JAMA (2015 March 3 [doi:10.1001/JAMA.2015.0763]) Dr. Zito and her colleagues noted that pediatric outpatient antipsychotic prescribing has sharply increased over the past 2 decades, and that a child on Medicaid is five times more likely to be prescribed an antipsychotic than a privately insured youth. Clear guidelines are lacking for antipsychotic prescribing, especially for the youngest patients, the study found.

Many states have instituted policies to gain greater oversight of pediatric psychotropic medication prescribing. To characterize nationwide practice, Dr. Zito and her colleagues collected information about prior authorization requirements for atypical antipsychotic prescribing for all 50 states and the District of Columbia. Information was collected by visiting webpages and supplemented by individual e-mail exchanges with state Medicaid authorities when necessary.

In all, 31 states’ Medicaid agencies had policies requiring prior authorization before atypical antipsychotics can be prescribed to Medicaid-insured children. Only seven states required prior authorization for all youth 18 and younger, while most others curtailed the requirement after ages 5, 6, or 7. A separate set of seven states had prior authorization requirements that varied by drug.

The prior authorization process also varied widely between states. Fifteen of the 31 states with prior authorization requirements had mandatory peer review by physicians – often psychiatrists – or had clinical pharmacists perform initial review with physicians available for consultation. By contrast, the other 16 states’ review processes were performed by nonphysician reviewers or were automated.

Dr. Zito and her colleagues said that the study compiled only limited data regarding each state’s policies. The authors recommended further study aimed at tracking unintended consequences of prescribing restrictions, as well as examining whether prior authorization with peer review improves quality of care. All in all, Dr. Zito said in an interview, “we need a much more comprehensive and holistic picture of this complex problem.”

Though 31 states now require prior authorization for prescribing atypical antipsychotic medications to Medicaid-insured youth, age limits and how the medications are regulated vary widely.

Requirements for physician peer review, an important consideration for a medication class with potentially negative cardiometabolic impact, also vary by state, Julie M. Zito, Ph.D., of the University of Maryland’s department of pharmaceutical health services research, and her associates reported in a research letter to JAMA (2015 March 3 [doi:10.1001/JAMA.2015.0763]) Dr. Zito and her colleagues noted that pediatric outpatient antipsychotic prescribing has sharply increased over the past 2 decades, and that a child on Medicaid is five times more likely to be prescribed an antipsychotic than a privately insured youth. Clear guidelines are lacking for antipsychotic prescribing, especially for the youngest patients, the study found.

Many states have instituted policies to gain greater oversight of pediatric psychotropic medication prescribing. To characterize nationwide practice, Dr. Zito and her colleagues collected information about prior authorization requirements for atypical antipsychotic prescribing for all 50 states and the District of Columbia. Information was collected by visiting webpages and supplemented by individual e-mail exchanges with state Medicaid authorities when necessary.

In all, 31 states’ Medicaid agencies had policies requiring prior authorization before atypical antipsychotics can be prescribed to Medicaid-insured children. Only seven states required prior authorization for all youth 18 and younger, while most others curtailed the requirement after ages 5, 6, or 7. A separate set of seven states had prior authorization requirements that varied by drug.

The prior authorization process also varied widely between states. Fifteen of the 31 states with prior authorization requirements had mandatory peer review by physicians – often psychiatrists – or had clinical pharmacists perform initial review with physicians available for consultation. By contrast, the other 16 states’ review processes were performed by nonphysician reviewers or were automated.

Dr. Zito and her colleagues said that the study compiled only limited data regarding each state’s policies. The authors recommended further study aimed at tracking unintended consequences of prescribing restrictions, as well as examining whether prior authorization with peer review improves quality of care. All in all, Dr. Zito said in an interview, “we need a much more comprehensive and holistic picture of this complex problem.”