Right ventricular hypertrophy
Right ventricular hypertrophy (RVH) is a pathologic increase in the muscle mass of the right ventricle, the lower right chamber of the heart that pumps deoxygenated blood to the lungs. It typically develops as an adaptive response to chronic pressure overload on the right ventricle.[1] This condition most commonly arises from pulmonary hypertension or other lung diseases that increase pulmonary vascular resistance, but can also result from congenital heart defects or left heart failure. If progressive and untreated, RVH may lead to right-sided heart failure and increased risk of arrhythmias or sudden death.[1] Epidemiologically, RVH is not a primary disease but a secondary finding, with prevalence varying by underlying condition and population. For example, it occurs in approximately 33.6% of out-of-hospital patients with systemic hypertension and is common in chronic pulmonary hypertension, affecting up to 50% of cases in some cohorts. In hypertrophic cardiomyopathy, extreme RVH is rare, seen in about 1.3% of patients.[1]Introduction
Definition and overview
Right ventricular hypertrophy (RVH) is a pathologic condition characterized by thickening of the right ventricular wall, typically exceeding 5 mm in thickness, due to chronic pressure overload that results in increased myocardial mass.[1][2] This enlargement represents an abnormal adaptation of the right ventricle, the chamber responsible for pumping deoxygenated blood to the lungs, in response to sustained elevations in pulmonary arterial pressure.[1] The condition was first described in 1891 by German physician Ernst von Romberg, who identified right ventricular hypertrophy coexisting with sclerotic changes in the pulmonary arteries during an autopsy, marking an early recognition of its association with pulmonary vascular pathology.[3] In the normal heart, the right ventricular wall is relatively thin, measuring 3 to 5 mm, to accommodate the low-resistance pulmonary circulation.[1] In contrast to left ventricular hypertrophy, which often stems from systemic hypertension burdening the high-pressure left ventricle, RVH affects the lower-pressure right ventricle and is predominantly a consequence of pulmonary or lung-related stressors.[4][5] RVH initially functions as an adaptive mechanism to preserve cardiac output and right ventricular function against increased afterload; however, prolonged stress can lead to maladaptive remodeling, including fibrosis and dilation, which heighten the risk of right heart failure.[6][1]Epidemiology
Right ventricular hypertrophy (RVH) is a significant finding in patients with chronic lung diseases, affecting approximately 20-30% of those with moderate to severe chronic obstructive pulmonary disease (COPD), where right ventricular enlargement and hypertrophy develop as adaptive responses to hypoxic pulmonary vasoconstriction and vascular remodeling. In cohorts with pulmonary hypertension (PH), particularly group 3 PH due to lung diseases, the prevalence of RVH rises substantially, often exceeding 50% in advanced cases and approaching 80% in severe pulmonary arterial hypertension subsets, reflecting the direct impact of elevated pulmonary pressures on right ventricular remodeling.[7][1][8] In the general adult population, the prevalence of RVH via imaging studies is estimated at 1-7%, depending on diagnostic criteria and modality; for instance, the Multi-Ethnic Study of Atherosclerosis (MESA) reported a 7.3% prevalence of increased right ventricular mass in a multiethnic cohort without overt cardiovascular disease, while electrocardiography detects it in only 0.1-2% due to lower sensitivity. Incidence rates are low in asymptomatic individuals, approximately 1-2% over several years in population-based imaging follow-ups, but rise sharply with age and comorbidities like hypertension or lung disease, contributing to 10-12% of incident heart failure cases in at-risk groups.[9][10][9] Demographically, RVH is more common in older adults over 60 years, with prevalence doubling in those aged 65 and above due to cumulative exposure to risk factors such as chronic lung conditions and left heart disease. It exhibits a male predominance in certain etiologies, including COPD, where severe disease and associated PH occur more frequently in men, and in autopsy studies of hypertensives, where male sex independently correlates with RVH (prevalence ratio 1.08). Specific populations, such as individuals with congenital heart disease, show higher rates, often exceeding 30-50% depending on the defect, due to inherent pressure or volume overload. As of 2025, enhanced detection through cardiac magnetic resonance imaging and computed tomography has increased identified cases, with MESA data underscoring RVH as a predictor of cardiovascular events, independent of left ventricular metrics.[9][11][12][1][9]Anatomy and physiology
Normal right ventricle structure and function
The right ventricle (RV) is a thin-walled chamber, with a normal wall thickness of 3 to 5 mm, that occupies the anterior and inferior aspects of the heart, immediately beneath the sternum.[13] It exhibits a crescent-shaped appearance in transverse sections, wrapping around the left ventricle, and is divided into three functional regions: the inlet, trabecular (apical), and outlet portions, which facilitate efficient blood flow.[13] This structure enables the RV to receive deoxygenated blood from the right atrium via the tricuspid valve and propel it to the lungs through the pulmonary artery, forming a low-resistance pulmonary circulation.[14] In terms of physiology, the RV operates within a low-pressure system, generating systolic pressures of 15 to 30 mmHg and diastolic pressures of 1 to 7 mmHg, which contrasts with the higher pressures in the systemic left ventricle.[15] It pumps the same stroke volume as the left ventricle—approximately 70 mL in a resting adult—to maintain balanced cardiac output, achieving this with about 25% of the workload due to the lower pulmonary vascular resistance.[14] Key structural components support this function, including the tricuspid valve for inflow regulation, three papillary muscles (anterior, posterior, and septal) that anchor the valve leaflets to prevent regurgitation, and the moderator band, a muscular extension from the septum to the anterior wall that conducts the right bundle branch of the cardiac conduction system.[13] Embryologically, the RV arises primarily from the primitive ventricle and proximal bulbus cordis during the fourth week of development, with the inlet region incorporating contributions from the sinus venosus to form the smooth-walled venous pole.[16] Under normal conditions, slight physiological adaptations occur, such as mild increases in RV wall thickness and cavity dimensions in endurance athletes due to chronic volume loading from elevated cardiac output; however, wall thickness remains below 5 mm and is distinguished from pathological changes by its reversibility upon detraining.[17]Physiological vs pathological hypertrophy
Right ventricular hypertrophy can manifest as either a physiological adaptation or a pathological remodeling process, distinguished primarily by their underlying stimuli, structural patterns, and functional outcomes. Physiological hypertrophy represents an adaptive response to increased physiological demands, such as those encountered during intense endurance exercise or pregnancy, resulting in a reversible increase in right ventricular wall thickness without compromising cardiac function.[1] In athletes, this often takes the form of eccentric hypertrophy, characterized by chamber dilation and proportional wall thickening to accommodate higher stroke volumes, while maintaining normal or enhanced contractility.[18] Similarly, during pregnancy, volume overload from expanded plasma volume induces mild right ventricular hypertrophy, which is eccentric in nature and fully reverses postpartum without evidence of fibrosis or long-term dysfunction.[19] These adaptations preserve right ventricular ejection fraction (typically >50%) and overall compliance, ensuring efficient hemodynamic performance under stress.[20] In contrast, pathological right ventricular hypertrophy arises from sustained pressure overload, such as in pulmonary hypertension or congenital heart defects, leading to concentric remodeling with disproportionate wall thickening relative to chamber size.[1] This maladaptive process involves myocyte hypertrophy initially as a compensatory mechanism to normalize wall stress, but it progresses to fibrosis, impaired diastolic relaxation, and eventual systolic dysfunction.[21] Unlike physiological forms, pathological hypertrophy is often irreversible, even after relief of the overload, and is associated with reduced right ventricular compliance, increased arrhythmogenic risk, and a decline in ejection fraction below 45%.[22] Key histological differences include the absence of interstitial fibrosis and apoptosis in physiological hypertrophy, whereas pathological states exhibit these features, contributing to progressive remodeling and heart failure.[23] The transition from compensated to decompensated pathological hypertrophy is marked by a shift from adaptive myocyte hypertrophy to maladaptive cellular loss, particularly through apoptosis, which exacerbates fibrosis and impairs contractility.[24] In early stages, pressure overload triggers hypertrophic signaling to maintain output, but prolonged stress leads to myocyte dropout and ventricular dilation, distinguishing it sharply from the benign, non-fibrotic profile of physiological hypertrophy.[25] This progression underscores the importance of early intervention in pressure-overload conditions to prevent irreversible decompensation.| Aspect | Physiological Hypertrophy | Pathological Hypertrophy |
|---|---|---|
| Stimulus | Volume overload (e.g., exercise, pregnancy) | Pressure overload (e.g., pulmonary hypertension) |
| Pattern | Eccentric (dilation with proportional thickening) | Concentric (wall thickening without dilation) |
| Reversibility | Fully reversible with detraining or postpartum | Often irreversible, even after load relief |
| Function | Preserved ejection fraction (>50%), no arrhythmias | Reduced ejection fraction (<45%), arrhythmias |
| Histology | No fibrosis or apoptosis | Fibrosis and apoptosis prevalent |