The following are key points to remember from this review on the anatomy, function, and dysfunction of the right ventricle (RV):

1. The RV is a thin-walled, crescent-shaped structure with three distinct anatomical sections: 1) inlet comprised of the tricuspid valve, chords, and papillary muscles; 2) trabeculated apex; and 3) outlet, which supports the pulmonary valve leaflets.
2. The RV is morphologically and functionally distinct from the left ventricle (LV). The RV has coarse trabeculations, trileaflet atrioventricular valve with apical displacement, and presence of multiple papillary muscles. However, the RV and LV are closely inter-related in function through the septum, a common pericardial space, and epicardial circumferential myocytes, leading to systolic and diastolic interdependence.
3. Structurally, RV cardiomyocytes are 15% smaller than LV myocytes and hence the RV has more collagen. However, gene expression and protein composition are similar. Yet, metabolism differs, making the RV more resistant to ischemia. Contributing factors include more oxidative metabolism than anaerobic glycolysis and higher oxygen extraction compared to the LV. Furthermore, coronary flow to the RV occurs in both systole and diastole.
4. Normal RV contracts in a peristalsis like motion with the inlet playing an active role; the apex plays a passive role and the outlet acts as a buffer. The interventricular septum is an important contributor, with the LV contributing to 20-40% of RV stroke volume. Measuring RV function is complex. Contractility can be measured with elastance, defined as a change in pressure for a given change in volume. The most accurate measure of RV contractility is RV end-systolic elastance calculated from invasive pressure volume loops as RV end-systolic pressure (or mean pulmonary artery pressure) divided by end-systolic volume.
5. The most common cause for RV pressure overload is pulmonary hypertension, leading to RV hypertrophy and dilatation. Pressure overload is associated with RV myocyte hypertrophy, and disarray and hypertrophy of circumferential myocytes in the septoparietal band may lead to muscular subpulmonic stenosis. As the adaptive remodeling with concentric hypertrophy transitions in maladaptive remodeling with eccentric hypertrophy and dyssynchrony, the filling pressures increase, leading to clinical decompensation. However, fibrotic changes in the RV are lesser than the LV, so most patients with pulmonary hypertension recover function after lung transplantation.
6. RV volume overload is associated with RV dilatation and hypertrophy with diastolic leftward shift of the septum affecting the LV function due to geometric changes. Due to its morphology, the RV tolerates volume overload better and RV contractility remains preserved for a long time. Chronic volume overload leads to RV systolic dysfunction and increases morbidity and mortality in the presence of RV pressure overload and RV dilatation. Hence, corrective interventions should be performed prior to significant RV dilatation.
7. Patterns of contractility in different regions of the RV differ based on the underlying disease, causing RV volume overload. In patients with atrial septal defect, proximal contractility is preserved, but apical strain is supranormal. In pulmonary insufficiency, the apical region is most affected, with more contractility in the proximal segments.
8. Up to 50% of patients with acute myocardial infarction at postmortem show RV involvement. RV injury is more common in inferior infarcts, but also seen in anterior infarcts. After the acute ischemic event, the RV function tends to recover with a low prevalence of chronic scars. Post-infarct RV dysfunction is multifactorial and related to LV-RV interaction, increased afterload, ischemia, and mitral regurgitation.
9. In arrhythmogenic cardiomyopathy, newer studies show preferential involvement of the RV basal inferior and anterior segments in early disease with the LV basal inferolateral segment. Furthermore, microstructural abnormalities precede the electrical phase of the disease, challenging the conventional notion of electrical disease preceding structural disease.
10. In other nonischemic cardiomyopathies, RV dysfunction (EF ≤45%) is present in 35-40% of patients. RV scarring is usually absent. In hypertrophic cardiomyopathy, RV myocardial disarray and hypertrophy are seen in up to 30% of patients.
11. In cardiac amyloidosis, increased RV wall thickness and late enhancement are common. RV dysfunction is related to RV amyloid deposition and LV involvement. However, as opposed to the LV, there are no preferential areas of amyloid deposition in the RV. Light chain amyloidosis is more likely to involve the RV than transthyretin amyloidosis.
12. In acute myocarditis, approximately 20% of patients have RV free wall involvement and RV involvement signals worse outcomes. Similarly, in patients with proven extracardiac sarcoidosis, 15-20% show RV free wall or interventricular septum involvement. RV involvement in sarcoidosis is associated with a higher risk for mortality from ventricular tachyarrhythmias.

Keywords: Amyloidosis, Blood Pressure, Cardiomyopathies, Cardiomyopathy, Hypertrophic, Constriction, Pathologic, Diastole, Dilatation, Glycolysis, Heart Septal Defects, Atrial, Heart Failure, Hypertension, Pulmonary, Hypertrophy, Right Ventricular, Lung Transplantation, Mitral Valve Insufficiency, Myocardial Infarction, Myocarditis, Myocytes, Cardiac, Oxidative Stress, Papillary Muscles, Pericardium, Peristalsis, Sarcoidosis, Stroke Volume, Systole, Tachycardia, Ventricular Dysfunction, Right, Ventricular Function, Right

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