Abstract
Knowledge of right ventricular (RV) structure and function has historically lagged behind that of the left ventricle (LV). However, advancements in invasive and non-invasive evaluations, combined with epidemiological analyses, have advanced the current understanding of RV (patho)physiology across the spectrum of health and disease, and reinforce the centrality of the RV in contributing to clinical outcomes. In the healthy heart, ventricular-arterial coupling is preserved during rest and in response to increased myocardial demand (eg, exercise) due to substantial RV contractile reserve. However, prolonged exposure to increased myocardial demand, such as endurance exercise, may precipitate RV dysfunction, suggesting that unlike the LV, the RV is unable to sustain high levels of contractility for extended periods of time. Emerging data increasingly indicate that both LV and RV function contribute to clinical heart failure. Reductions in quality-of-life, functional capacity and overall clinical outcomes are worsened among patients with heart failure when there is evidence of RV dysfunction. In addition, the RV is adversely impacted by pulmonary vascular disease, and among affected patients, overall RV function differs based on mechanisms of the underlying pulmonary hypertension, which may result from variations in sarcomere function within RV cardiomyocytes.