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Rationale: Intense exercise in elite athletes is associated with increased left ventricular (LV) and right ventricular (RV) mass and volumes. However, the effect of physical activity on the RV in an older community-based population is unknown. Objectives: We studied the association between levels of physical activity in adults and RV mass and volumes. Methods: The Multi-Ethnic Study of Atherosclerosis (MESA) performed cardiac magnetic resonance imaging on community-based participants without clinical cardiovascular disease. RV volumes were determined from manually contoured endocardial margins. RV mass was determined from the difference between epicardial and endocardial volumes multiplied by the specific gravity of myocardium. Metabolic equivalent-minutes/day were calculated from the selfreported frequency, duration, and intensity of physical activity. Measurements and Main Results: The study sample (n 5 1,867) was aged 61.8 6 10 years, 48% male, 44% white, 27% African American, 20% Hispanic, and 9% Chinese. Higher levels of moderate and vigorous physical activity were linearly associated with higher RV mass (P 5 0.02) after adjusting for demographics, anthropometrics, smoking, cholesterol, diabetes mellitus, hypertension, and LV mass. Higher levels of intentional exercise (physical activity done for the sole purpose of conditioning or fitness) were nonlinearly associated with RV mass independent of LV mass (P 5 0.03). There were similar associations between higher levels of physical activity and larger RV volumes. Conclusions: Higher levels of physical activity in adults were associated with greater RV mass independent of the associations with LV mass; similar results were found for RV volumes. Exercise-associated RV remodeling may have important clinical implications.Keywords: exercise; pulmonary heart disease; pulmonary hypertension; magnetic resonance imaging Physical activity has many physiologic effects on the cardiovascular system, both acutely and chronically. Exercise acutely raises cardiac output through tachycardia, augmented stroke volume, and increased ejection fraction (1). Systemic and pulmonary arterial pressures increase and vascular resistances decrease. Long-term high-intensity physical activity is associated with increased left ventricle (LV) mass, volume, and wall thickness (2-6), a constellation of changes known as the ''athlete's heart.'' Most studies of the cardiac effects of physical activity focus on LV morphology in small cohorts of young male endurance athletes.The substantial differences in embryology, morphology, perfusion, workload, and downstream vascular beds (and the diseases which affect them) make extrapolation of findings from the LV to the right ventricle (RV) difficult. The small number of studies performed have shown significant effects of intense exercise on RV mass and volumes (3-6). However, because RV structure and function are difficult to measure with standard transthoracic echocardiography, little is known about the relationship between physical activity and RV str...

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Background/Introduction Cross-sectional studies are inconsistent on the potential independent adverse effects of human immunodeficiency virus (HIV)-infection on coronary artery disease (CAD). Furthermore, there is no information on the potential effects of HIV-infection on plaque volumes. Also, only the independent effects of HIV-infection on CAD have been investigated. Purpose In a prospective longitudinal observational cohort, we wished to assess whether HIV-infection accelerates CAD independently, or by acting in synergistic fashion with conventional and nonconventional cardiovascular risk factors to accelerate disease progression as assessed by clinical and volumetric parameters of CAD on coronary CT angiography (CCTA). Methods Overall, 300 asymptomatic individuals without cardiovascular symptoms but with CCTA-confirmed coronary plaques (210 males, age: 48.0±7.2 years) with or without HIV (226 HIV-infected) prospectively underwent CCTA at two time points (mean follow-up: 4.0±2.3 years). Agatston-score, number of coronary plaques, segment stenosis score were calculated, and we also segmented the coronary plaques to enumerate total, noncalcified (−100–350HU) and calcified (≥351HU) plaque volumes. Linear mixed models were used to assess the effects of HIV-infection, atherosclerotic cardiovascular disease (ASCVD) risk, years of cocaine use and high-sensitivity C-reactive protein on CCTA markers of CAD. Results In univariate analysis, there was no significant difference in CAD characteristics between HIV-infected and -uninfected, neither at baseline nor at follow-up (p>0.05 for all). Furthermore, there was no significant difference in annual progression rates between the two groups (p>0.05 for all). By multivariate analysis, HIV was not associated with any CAD parameter (p>0.05 for all). However, among HIV-infected individuals, each year of cocaine use significantly increased all CAD parameters (p<0.05 for all), while ASCVD risk score was significantly associated with CAD parameters except for Agatston-score (p<0.05). These associations were only present among HIV-infected individuals. Conclusion(s) Instead of directly worsening CAD, HIV may promote CAD through increased susceptibility to conventional and nonconventional cardiovascular risk factors. Therefore, aggressive management of both conventional and nonconventional cardiovascular risk factors is needed to reduce cardiovascular burden of HIV-infection. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Institutes of Health, National Institute on Drug Abuse

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