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Right Ventricular Hypertrophy


Right ventricular hypertrophy (RVH) is the enlargement in the size of this chamber, which occurs as a result of underlying causes that increase the stress on its wall.


In cases with mild RVH, there may be no symptoms whereas the clinical picture in patients with severe hypertrophy is that of heart failure. For example, they experience dyspnea, chest pain, dizziness, peripheral edema, and possibly loss of consciousness. These individuals may also exhibit tachycardia and palpitations.

Physical exam
The clinician should perform a complete exam that consists of cardiac auscultation, palpation of the pulses, and other relevant aspects. Moreover, cardiac auscultation will reveal rate, rhythm, and any existing murmurs that can collectively provide details about the underlying etiology of the RVH.

Heart Disease
  • BACKGROUND: The outcome of the surgical repair in congenital heart disease correlates with the degree of myocardial damage.[ncbi.nlm.nih.gov]
  • This simple experimental model may have features similar to those of human congenital heart disease associated with pulmonary hypertension.[ncbi.nlm.nih.gov]
  • Three were reported from that hospital in 1942. 2 Ordinarily when a patient with heart disease of obscure origin is encountered an attempt is made to fit him into one of the well recognized etiologic categories of heart disease, but there is a large group[annals.org]
  • Abstract Cardiac MRI is a complementary and confirmatory modality to a clinical echocardiography in diagnosing patients with complex adult congenital heart disease, especially in presence of great vessel abnormalities.[ncbi.nlm.nih.gov]
  • METHODS: We identified children without congenital heart disease who underwent evaluation for suspected pulmonary hypertension that included both an electrocardiogram and echocardiography within a specified time frame.[ncbi.nlm.nih.gov]
Gallop Rhythm
  • rhythm, persistent jugular venous distention, systemic hypotension, peripheral vascular disease Laboratory findings Hyponatremia, persistently elevated B-type natriuretic peptide and A-type natriuretic peptide levels, elevated norepinephrine and renin[clevelandclinicmeded.com]
Vaginal Bleeding
  • A 33-year-old G4P1021 woman with uncontrolled Graves' disease presented at 29 weeks gestation with abdominal pain and vaginal bleeding. Fetal echocardiogram showed severe RV hypertrophy and a pericardial effusion.[ncbi.nlm.nih.gov]


All patients with any heart condition or presentation suggestive of cardiac disease should be evaluated thoroughly. The clinician should assess the clinical picture, personal and family history, and existing risk factors. Additionally, the workup includes a physical examination and laboratory tests.


The diagnosis of RVH requires an evaluation of the ECG, which provides key findings. The most common observation is a right axis deviation greater than 100 degrees. As with LVH, the deviation occurs because of the electrical activity that is produced by the depolarization of the myocardial cells. This axis shift should be present before considering RVH.

Further ECG evidence of this disease may include:

  • QRS abnormalities due to the increased voltage in leads V1, V5, and V6
  • P wave abnormalities (as reflected by P pulmonale and peaked T-waves inferiorly)
  • ST depression and T wave inversion in leads V2 through V6. These changes commonly occur in advanced RVH diseases such as pulmonary hypertension and pulmonary stenosis

Note the greater the number of features, the higher the sensitivity for RVH. Other specific findings include:

  • Right axis deviation >100 degrees
  • The R wave in V1 > 7mm
  • Presence of an rSR' pattern in V1; R' > 10mm
  • The sum of R in V1 and S in V5 or V6 > 10.5mm
  • Presence of qR complex in V1
  • ST- T wave abnormalities secondary to hypertrophy

Newer studies such as tissue Doppler imaging (TDI) and speckle tracking may be helpful. TDI can assess the peak systolic strain of the RV free wall, which is decreased in those with pulmonary hypertension [11].


More tests may be warranted during the evaluation of underlying causes or coexisting diseases. For example, chronic hypertension is often a component of the disease, which should be considered in these patients. Moreover, individuals with lung disease may require pulmonary function tests while those with congenital diseases will need a detailed assessment.

Right Axis Deviation
  • Example 4 Right ventricular hypertrophy in a patient with arrhythmogenic right ventricular cardiomyopathy (ARVC): Right axis deviation.[lifeinthefastlane.com]
  • The ECG shows right axis deviation and right ventricular hypertrophy. Pediatric cardiologist Dr. Mahmut Gokdemir has donated this ECG to our website. Click here for a more detailed ECG ECG 3.[metealpaslan.com]
  • The most common observation is a right axis deviation greater than 100 degrees. As with LVH, the deviation occurs because of the electrical activity that is produced by the depolarization of the myocardial cells.[symptoma.com]
Right Bundle Branch Block
  • In contrast, when an incomplete right bundle branch block exists, the rSR' pattern is a relatively sensitive but nonspecific predictor of RVH.[ncbi.nlm.nih.gov]
  • Abstract In pediatric electrocardiogram (ECG) analysis, mild right ventricular hypertrophy (RVH) and especially mild RVH with terminal right conduction delay (RVHtcd) are often confused with partial right bundle branch block (PRBBB).[ncbi.nlm.nih.gov]
  • Other causes of an R/S ratio of greater than 1 in lead V1: Posterior wall myocardial infarction (also causes ST segment depression in V1-V3, but T waves are symmetrically inverted, and the patient would be presenting with chest pains) Right bundle branch[healio.com]
  • This resembles, but is not, right bundle branch block (RBBB) . Secondary ST-T changes are common in V1–V3. The ST-T segment is usually discordant to the QRS complex. V5, V6, I and aVL displays smaller R-waves than normal.[ecgwaves.com]
Incomplete Right Bundle Branch Block
  • In contrast, when an incomplete right bundle branch block exists, the rSR' pattern is a relatively sensitive but nonspecific predictor of RVH.[ncbi.nlm.nih.gov]
  • right bundle branch block in the right precordial chest leads may signal the development of RVH In the limb leads right axis deviation develops and at times prominent Q waves simulating an IMI appear in leads 2,3, and aVF.[wikidoc.org]
  • right bundle branch block ST-T wave abnormalities ("strain") in inferior leads Right atrial hypertrophy/overload (“P pulmonale”) S greater than R in leads I, II, III, particularly in children (S1S2S3 pattern) Patients with VSD and EKG evidence of right[ncbi.nlm.nih.gov]
Biphasic T Wave
Right Ventricular Hypertrophy
  • Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy.[ncbi.nlm.nih.gov]
  • Although there was a significant relationship between electrocardiogram and echocardiography evidence of right ventricular hypertrophy, the sensitivity of an electrocardiogram in diagnosing echocardiography-documented right ventricular hypertrophy was[ncbi.nlm.nih.gov]
  • Your doctor might use a combination of these tests to confirm whether or not you have right ventricular hypertrophy. The treatment of right ventricular hypertrophy depends on the underlying cause.[healthline.com]
  • Coal workers' pneumoconiosis, emphysema, and right ventricular hypertrophy were assessed uniformly in all cases.[ncbi.nlm.nih.gov]
  • We examined the relationship between right ventricular hypertrophy in patients with TOF and the gene expression of factors in the mitogen-activated protein kinase (MAPK) signal pathway.[ncbi.nlm.nih.gov]
Electrocardiogram Change
  • There was no relationship between electrocardiogram changes and Doppler tricuspid regurgitation gradient.[ncbi.nlm.nih.gov]
  • There was no relationship between electrocardiogram changes and Doppler tricuspid regurgitation gradient. CONCLUSION.[pediatrics.aappublications.org]


The therapeutic approach targets the underlying diseases that are contributing to RVH. Patients with pulmonary hypertension may benefit from the use of vasodilators including epoprostenol. Furthermore, PDE5A inhibitors used for erectile dysfunction can be effective in dilating the pulmonary vasculature. Sildenafil and tadalafil are examples of this drug class.

In cases with systemic hypertension, the treatment regimen consists of antihypertensives such as ACE inhibitors, beta blockers, and others as well. Additionally, smoking cessation, lifestyle modifications, and weight loss are very advantageous in cardiac patients.

If the culprit of the hypertrophy is an underlying pulmonary valve abnormality or complex congenital anomalies, surgical intervention may be warranted.

Patients with obstructive sleep apnea (OSA) are encouraged to lose weight in addition to the standard treatment of this disorder.


The prognosis of RVH is dependent on its etiology and resultant pathology. As a predominant cause of RVH, pulmonary hypertension is linked to morbidity and mortality. Likewise, RVH sequela such as heart failure leads to poor outcomes.

Additionally, patients with biventricular hypertrophy are at high risk of developing serious events. Hence, cardiovascular diseases should be carefully managed and monitored as a means of improving the survival rates and quality of life in these patients.


RVH develops from numerous etiologies. This structural change may occur secondary to diseases such as pulmonary valve stenosis and pulmonic regurgitation. Additionally, lung pathologies including pulmonary hypertension and chronic obstructive pulmonary disease (COPD) and congenital diseases such as ventricular septal defect (VSD) and tetralogy of Fallot result in hypertrophy of the right ventricle. Further causes are obstructive sleep apnea (OSA), cardiac fibrosis, and exposure to high altitude.

Although systemic hypertension is a well-known cause of left ventricular hypertrophy (LVH), it may contribute to RVH as well. One study, in particular, examined the effects of systemic hypertension on the right ventricle. The findings demonstrated that this chamber undergoes similar changes as the left ventricle regarding wall dimensions and other measurements as well [1].


RVH, which frequently occurs in patients with systemic hypertension, is accompanied by LVH in almost 20% of patients observed in a specialist clinic. Furthermore, the presence of biventricular hypertrophy indicates an elevated cardiovascular risk.

Sex distribution
Age distribution


Chronic pressure overload

In patients with longstanding pressure overload, the response of the heart consists of gradual structural changes. As described by Laplace's Law, the elevated pressure results in increased stress in the walls. Consequently, the right ventricle undergoes hypertrophy as a compensatory mechanism. The pathological changes responsible for the enlargement are the proliferation of sarcomeres and the resultant growth of the myocytes [2]. Further alterations include the expansion of the extracellular matrix and fibrosis.

Eventually, the heart struggles to manage the pressure overload and undergoes dilation. The ensuing systolic and diastolic dysfunction result in RV failure.

Cellular changes in RVH

While the events leading to right ventricular failure are not clear, the cellular mechanisms have been elucidated. Specifically, there is enhanced myocyte apoptosis, which may account for the progressive decline in RV function [2]. Moreover, the α-subtype myosin heavy chain is observed to be reduced in comparison to the b-subtype myosin heavy chain in systolic dysfunction [3] [4].

Other cellular changes include certain modifications to the β-adrenoreceptor and the angiotensin type 1 receptor. The latter may be implicated in the overactivation of the renin-angiotensin system that occurs in right ventricular dysfunction.

Also, hypertrophy and dysfunction of the right ventricle may develop as a response to the ischemia observed in pulmonary artery hypertension (PAH) [5].

Further findings associated with RVH is the upregulation of mitochondrial nitric oxide synthase (mtNOS), which is reversed with the PDE5A inhibitor, sildenafil [6]. These observations have been previously reported in PAH studies that showed the hypertrophied tissue exhibited an increase in 1) PDE5 expression [7], 2) membrane potential in the mitochondria [8], and 3) glucose uptake [9].

All of these observations may provide insight regarding the treatment of these patients [10].


RVH is identified and diagnosed when patients develop symptoms of cardiac failure which include shortness of breath, chest pain, swelling of the lower extremities, and episodes of loss of consciousness. Once a patient experiences these, he or she should seek medical attention.

A healthy lifestyle can prevent or slow down the progression of systemic hypertension, which may contribute to the development of biventricular hypertrophy and cardiac failure. Cessation of smoking, modifying the diet, increasing physical activity, and weight control are beneficial strategies for the overall health of the patient, especially the cardiovascular aspect.

Also, good respiratory health is paramount in the protection of the right ventricular function. Smoking cessation and abstinence from alcohol should be a priority for all individuals.

OSA is likely a risk factor for RVH, especially in obese individuals. Patients that are snoring and experiencing nocturnal dyspnea should undergo evaluation for this condition.


Right ventricular hypertrophy (RVH) occurs as a response to the increased stress on the walls of the right ventricle. Among the numerous etiologies of RVH are pulmonary hypertension and diseases associated with right ventricular outflow obstruction. Furthermore, the enlargement of this ventricle is based on the hemodynamic and structural changes that occur as a consequence of the stressed right ventricle. Over time, the progression of the underlying diseases and the resultant weakened heart can lead to a decline in the cardiac function.

Mild RVH is usually asymptomatic, but severe cases will produce features of heart failure such as dyspnea, angina, and peripheral edema.

The diagnosis is achieved through a detailed personal and family history, a physical exam with a focus on the cardiovascular system, and tests such as the electrocardiogram (ECG). The latter study may reveal crucial findings such as right axis deviation and other abnormalities. Additionally, an echocardiogram will demonstrate the size of the chambers and overall performance of the heart.

The treatment is directed at the underlying conditions of hypertrophied ventricle. For example, pulmonary hypertension is managed with phosphodiesterase 5 (PDE5A) inhibitors to open the pulmonary arteries while essential hypertension is treated with standard antihypertensives. Furthermore, congenital heart anomalies may require surgical intervention.

Maintaining good general health and modification of lifestyle may prevent or slow the progression of diseases that cause RVH and heart failure.

Patient Information

What is right ventricular hypertrophy (RVH)?

The heart is comprised of 4 main chambers. The upper ones are called the atria, and the lower ones are referred to as the ventricles. When the wall of right sided ventricle increases in size, this is known as right ventricular hypertrophy.

A normal function of the right ventricle is necessary since it pumps blood to the lungs. Once oxygenated, the blood is then sent to the left side of the heart so that it can be pumped to the brain and the rest of the body.

Any condition that hinders or slows the pumping of the right ventricle will cause blood to back up in this chamber. Therefore, the right ventricle becomes stressed and has to grow in size to accommodate the accumulated blood.

These conditions include:

  • Pulmonary stenosis: The narrowing of the valve causes less blood flow from the right ventricle to the lungs
  • Ventral septal defect (VSD): This abnormality is present at birth. Depending on the severity, patients may not have symptoms until later.
  • Pulmonary hypertension
  • Tetralogy of Fallot: This is a complex heart abnormality that is present at birth. Infants can develop "blue baby syndrome" since there is less oxygen in the blood circulating throughout the body.


Patients with mild enlargement of the right ventricle may not produce symptoms. However, severe cases result in symptoms of heart failure such as shortness of breath, chest pain, dizziness, and fainting episodes. Also, they develop swelling in the legs, ankles, and feet. These patients may feel palpitations.


The clinician will evaluate the patient's symptoms, personal and medical history and perform a full physical exam. The clinician may identify abnormal heart sounds and rhythms through various tests.

The main tests are the ECG and the echocardiogram. The ECG will reveal characteristic findings that are associated with an enlarged heart. Also, the echocardiogram will determine the heart size and provide details about the function of the heart.


The doctor will determine the cause prior to treatment. Patients with high blood pressure will be treated with the standard antihypertensive therapies. Those with pulmonary hypertension can be treated with medications like sildenafil.

Also, all patients are urged to quit smoking, eat healthy, exercise regularly, maintain a healthy weight, and follow-up regularly with their doctor.



  1. Akintunde A, Akinwusi P, Opadijo O, Familoni O. Effect of systemic hypertension on right ventricular morphology and function: an echocardiographic study. Cardiovascular Journal of Africa. 2010;21(5):252-256.
  2. Bogaard HJ, Abe K, Vonk Noordegraaf A, Voelkel NF. The right ventricle under pressure: cellular and molecular mechanisms of right-heart failure in pulmonary hypertension. Chest. 2009; 135(3):794-804.
  3. Lowes BD, Minobe W, Abraham WT, et al. Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium. J Clin Invest. 1997;100(9):2315-24.
  4. Herron TJ, McDonald KS. Small amounts of alpha-myosin heavy chain isoform expression significantly increase power output of rat cardiac myocyte fragments. Circ Res. 2002; ;90(11):1150-2.
  5. Gómez A, Bialostozky D, Zajarias A, et al. Right ventricular ischemia in patients with primary pulmonary hypertension. Journal of the American College of Cardiology. 2001; 38(4):1137-42.
  6. Zaobornyj T, Valdez LB, Iglesias DE, Gasco M, Gonzales GF, Boveris A. Mitochondrial nitric oxide metabolism during rat heart adaptation to high altitude: effect of sildenafil, L-NAME, and L-arginine treatments.Am J Physiol Heart Circ Physiol. 2009; 296(6):H1741-7.
  7. Nagendran J, Archer SL, Soliman D. Phosphodiesterase type 5 is highly expressed in the hypertrophied human right ventricle, and acute inhibition of phosphodiesterase type 5 improves contractility. Circulation. 2007;116(3):238-48.
  8. Nagendran J, Gurtu V, Fu DZ, et al. A dynamic and chamber-specific mitochondrial remodeling in right ventricular hypertrophy can be therapeutically targeted. J Thorac Cardiovasc Surg. 2008;136(1):168-78, 178.e1-3.
  9. Oikawa M1, Kagaya Y, Otani H, et al. Increased [18F]fluorodeoxyglucose accumulation in right ventricular free wall in patients with pulmonary hypertension and the effect of epoprostenol. J Am Coll Cardiol. 2005; 45(11):1849-55.
  10. Nagendran J, Michelakis ED. Mitochondrial NOS is upregulated in the hypoxic heart: implications for the function of the hypertrophied right ventricle. Am J Physiol Heart Circ Physiol. 2009;296(6): H1723-6.
  11. Rajagopalan N1, Simon MA, Mathier MA, López-Candales A. Identifying right ventricular dysfunction with tissue Doppler imaging in pulmonary hypertension.Int J Cardiol. 2008;128(3):359-63.

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Last updated: 2018-06-21 19:20