ACC 2015

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.

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.