Right ventricular function across the spectrum of health and disease

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.

Keywords: Heart Failure; Pulmonary Arterial Hypertension.

Figure 1

Example of right ventricular pressure-volume analysis derived from (A) a healthy control; (B) a patient with heart failure with reduced ejection fraction (unpublished data from senior author’s laboratory); and (C) a patient with heart failure with reduced ejection fraction supported by a continuous-flow left ventricular assist device. All data obtained from senior author’s laboratory.

Figure 2

Apical four-chamber two-dimensional echocardiogram of the heart of a 23-year-old non-athlete (left) and a 23-year-old professional cyclist. The volume load of endurance athletics results in dilatation of all four cardiac chambers. The 10 cm echocardiographic field depth is marked in red to highlight the differences in cardiac size. Reproduced with permission.

Figure 3

Example of tracings of haemodynamic response to exercise in a healthy 48-year-old man (185 cm, 92 kg) without any history of cardiovascular or pulmonary disease. Fick cardiac output and oxygen uptake (VO₂) values during exercise: Rest pre-exercise: 5.0 L/min, 3.8 mL/kg/min; 100 Watts: 10.2 L/min, 12.1 mL/kg/min;150 Watts: 14.6 L/min, 20.7 mL/kg/min; 250 Watts: 21.3 L/min, 31.1 mL/kg/min. Unpublished data from senior author’s laboratory.

Figure 4

Example of right ventricular pressure-volume analysis during supine ergometry exercise from a patient with idiopathic pulmonary arterial hypertension (IPAH), systemic sclerosis-associated PAH (SSc-PAH) and a control patient with dyspnoea not related to pulmonary hypertension (PH). Data obtained at rest (stage 0), as well as progressive increases in exercise intensity (stages 1–3). Black point represents the point of end-systolic pressure volume relationship (ESPVR). Reproduced with permission. RVP, right ventricular pressure; RVV, right ventricular volume.

Figure 5

Right ventricular (RV) end-diastolic pressure-volume relations from patients with heart failure with preserved ejection fraction (HFpEF) and controls. Solid lines indicate resting condition and dashed lines indicate response to handgrip exercise. Black curves represent end-diastolic pressure volume curves determined vena caval occlusion. Note the upward shift in the end-diastolic pressure-volume relationship during exercise among patients with HFpEF compared with that of the control patients. Reproduced with permission.

Figure 6

Echocardiographic assessment of an 83-yearl-old patient with a dilated right ventricle with systolic dysfunction. Three-dimensional echocardiography demonstrates the right ventricle during diastole (A) and systole (B). Transoesophageal echocardiography of the same patient demonstrates right ventricular structure during diastole (C) and systole (D).