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.

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.

Electrocardiography

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].

Other

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.

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.

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.

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.

Symptoms

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.

Diagnosis

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.

Treatment

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.

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