Physical Activity and Right Ventricular Structure and Function: The MESA-Right Ventricle Study.

Aaron, CP; Tandri, H; Barr, R. Graham; Johnson, C; Bagiella, E; Chahal, H; Jain, A; Kizer, J; Lima, Joao; Bluemke, DA; Kawut, S.M.

doi:10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4146

Cited by 25 publications

(30 citation statements)

References 6 publications

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“…It could be argued that all prior studies in athletic cohorts have been underpowered to assess subtle ventricular differences. This proposition is supported by the results of Aaron et al, 45 who recruited a large cohort of 1,867 nonathletes and demonstrated that the amount of strenuous activity predicted RV mass and volumes independent of LV size. Some parallel insights may be gained from animal experiments on the basis of an induced aortacaval fistula in pigs.…”

Section: Chronic Rv Remodeling In Athletessupporting

confidence: 53%

The Response of the Pulmonary Circulation and Right Ventricle to Exercise: Exercise‐Induced Right Ventricular Dysfunction and Structural Remodeling in Endurance Athletes (2013 Grover Conference Series)

2014

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There is unequivocal evidence that exercise results in considerable health benefits. These are the result of positive hormonal, metabolic, neuronal, and structural changes brought about by the intermittent physiological challenge of exercise. However, there is evolving evidence that intense exercise may place disproportionate physiological stress on the right ventricle (RV) and the pulmonary circulation. Both echocardiographic and invasive studies are consistent in demonstrating that pulmonary arterial pressures increase progressively with exercise intensity, such that the harder one exercises, the greater the load on the RV. This disproportionate load can result in fatigue or damage of the RV if the intensity and duration of exercise is sufficiently prolonged. This is distinctly different from the load imposed by exercise on the left ventricle (LV), which is moderated by a greater capacity for reductions in systemic afterload. Finally, given the increasing RV demand during exercise, it may be hypothesized that chronic exercise-induced cardiac remodeling (the so-called athlete's heart) may also disproportionately affect the RV. Indeed, there is evidence, although somewhat inconsistent, that RV volume increases may be relatively greater than those for the LV. Perhaps more importantly, there is a suggestion that chronic endurance exercise may cause electrical remodeling, predisposing some athletes to serious arrhythmias originating from the RV. Thus, a relatively consistent picture is emerging of acute stress, prolonged fatigue, and long-term remodeling, which all disproportionately affect the RV. Thus, we contend that the RV should be considered a potential Achilles' heel of the exercising heart.

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Section: Chronic Rv Remodeling In Athletessupporting

confidence: 53%

The Response of the Pulmonary Circulation and Right Ventricle to Exercise: Exercise‐Induced Right Ventricular Dysfunction and Structural Remodeling in Endurance Athletes (2013 Grover Conference Series)

2014

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“…On the other hand, epidemiologic studies suggest testosterone deficiency is associated with worse cardiovascular outcomes among men, and there is some evidence that testosterone supplementation improves functional capacity in androgen-deficient men with CHF (39,40). The association between androgens (both bioT and DHEA) and greater RV mass and volumes here may not be detrimental per se, as has been proposed with exercise-induced increases in LV mass in trained athletes and in RV mass in MESA participants (41). In fact, higher levels of both bioT (in men) and DHEA (in women) were associated with higher RVSV.…”

Section: Discussionmentioning

confidence: 80%

Sex Hormones Are Associated with Right Ventricular Structure and Function

Ventetuolo¹,

Ouyang²,

Bluemke³

et al. 2011

Am J Respir Crit Care Med

159

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Rationale: Sex hormones have effects on the left ventricle, but hormonal influences on the right ventricle (RV) are unknown. Objectives: We hypothesized that sex hormones would be associated with RV morphology in a large cohort free of cardiovascular disease. Methods: Sex hormones were measured by immunoassay and RV ejection fraction (RVEF), stroke volume (RVSV), mass, end-diastolic volume, and end-systolic volume (RVESV) were measured by cardiac magnetic resonance imaging in 1,957 men and 1,738 postmenopausal women. The relationship between each hormone and RV parameter was assessed by multivariate linear regression. Conclusions: Higher estradiol levels were associated with better RV systolic function in women using hormone therapy. Higher levels of androgens were associated with greater RV mass and volumes in both sexes.Keywords: sex; sex hormones; right ventricle Sex differences in atherosclerosis and congestive heart failure (CHF) have been well described, with women experiencing a significant lag in the onset of coronary artery disease and lower rates of CHF compared with men (1). Estrogen, testosterone, dehydroepiandrosterone (DHEA), and sex hormone-binding globulin (SHBG) have important, albeit controversial, roles in left ventricular (LV) function and systemic vascular disease, whereas the effects of sex hormones on right ventricular (RV) and pulmonary vascular function are unknown.Estrogen has protective effects on the pulmonary vasculature and improves RV contractility in animals (2-4). Testosterone has been shown to be a pulmonary vasodilator, yet has unclear effects on pulmonary endothelium (5, 6). Treatment with DHEA prevents pulmonary vascular changes and RV hypertrophy, and prolongs survival in animal models of pulmonary hypertension (PH) (7,8). SHBG is expressed in myocytes of failing human hearts and in murine fetal lung epithelium, but its role in pulmonary vascular function has not been studied (9, 10).Despite the beneficial effects of estrogen on the pulmonary vasculature, female sex is the best established clinical risk factor for idiopathic pulmonary arterial hypertension (PAH) (11). Yet, women have higher RV ejection fraction (RVEF) and improved survival compared with men with PAH (12-14). In systemic cardiovascular disease, an individual's estrogen:testosterone balance may be more predictive of disease risk than either hormone alone (15,16). Last, it is unknown how sex hormones affect the interaction of the RV with the pulmonary vasculature, particularly in individuals with no known (or subclinical) PH.We examined the cross-sectional association of serum estradiol (E2), bioavailable testosterone (bioT), DHEA, SHBG, and the E2:testosterone ratio (E2:T) with RV structure and function assessed by cardiac magnetic resonance imaging (MRI) in a large AT A GLANCE COMMENTARY Scientific Knowledge on the SubjectFemale sex is a risk factor for the development of pulmonary hypertension (PH), yet women appear to have better right ventricular (RV) function and improved survival compared to men with PH....

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“…55,56 Thus, RV wall stress exceeds that of the LV, making it more susceptible to acute injury during endurance exercise 55,[57][58][59][60][61] and, as a result, repeated small 'hits' may promote chronic remodeling of the endurance athlete's RV. 55,57,62,63 Thus, the hemodynamic stress, acute injury, and chronic remodeling all disproportionately favor the RV.…”

Section: From Cardiac Plasticity To Arrhythmogenic Remodelingmentioning

confidence: 99%