Ventricular hypertrophy (VH) is thickening of the walls of a ventricle (lower chamber) of the heart.

Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes.

[2] Overt signs of heart failure, such as edema, or shortness of breath without exertion are uncommon.

These adaptations are related to how the cardiomyocyte contractile units, called sarcomeres, respond to stressors such as exercise or pathology.

Eccentric hypertrophy is related to volume overload and leads to the addition of sarcomeres in series.

[4] Concentric hypertrophy is characterized by an addition of sarcomeres (the contractile units of cardiac cells) in parallel.

This is maladaptive largely because there is not a corresponding proliferation of the vasculature supplying the myocardium, resulting in ischemic areas of the heart.

Ultimately, this response can be compensatory for a duration, and allow for improved cardiac function in the face of stressors.

However, this type of hypertrophy can result in a dilated ventricle which is unable to effectively pump blood, leading to heart failure.

[5] When stressors that encourage this concentric hypertrophy are reduced or eliminated (either surgically corrected in the case of cardiac defects, or hypertension is reduced from diet and exercise) it is possible for the heart to undergo 'reverse remodeling', returning to a somewhat more 'normal' state instead of progressing to a dilated, pathologic phenotype.

It is the normal response to healthy exercise or pregnancy,[6] which results in an increase in the heart's muscle mass and pumping ability.

This increase in pumping ability is the result of the addition of sarcomeres in series, which enables the heart to contract with greater force.

[7] This is explained by the Frank Starling mechanism, which describes the sarcomere's ability to contract with greater force as more of the elements of its contractile units become engaged.

This response can be dramatic; in trained athletes have hearts that have left ventricular mass up to 60% greater than untrained subjects.

Though eccentric hypertrophy is termed 'athlete's heart' it is typically only found in individuals who are aerobically conditioned.

For example, weight lifters tend to undergo remodeling which more closely resembles concentric hypertrophy, as the heart does not experience a volume-overload, but instead responds to transient pressure overload as a consequence of increased vascular resistance from pressures exerted on arteries by sustained muscular contraction.

[citation needed] Though it is the case that eccentric hypertrophy is largely considered to be a healthy response to increased cardiac demand, it is also associated with risks.

Additionally, in pregnant individuals, a subpopulation progress to peripartum cardiomyopathy, characterized by a dilation of the left ventricle and a corresponding deficit in heart function.

There are suggestions that this progression is partially determined by underlying metabolic derangement (diabetes) and hypertension which may result in a more maladaptive cardiac response to pregnancy.

Electrical abnormalities are commonly found in individuals with LVH, both ventricular and super-ventricular tachycardia.

Additionally, cytoarchitecture and the extracellular environment of the myocardium are altered, specifically genes typically expressed in the fetal heart are induced, as are collagen and other fibrotic proteins.

Before progression to a dilated phenotype, mechanical obstruction of the outflow tract can occur, leading to reduced cardiac output.

[citation needed] Androgens, especially dihydrotestosterone (DHT), are active in the ventricle and promote hypertrophy.

[10][11] In the framework of continuum mechanics, the volumetric growth is often modeled using a multiplicative decomposition of the deformation gradient

In eccentric growth, cardiomyocyte lengthens in the direction of the cell's long axis,

The biomechanical model based on continuum theories of growth can be used to predict the progression of the disease, and therefore can potentially help developing treatments to pathological hypertrophy.

Electrocardiogram (EKG), a non-invasive assessment of the electrical system of the heart, can be useful in determining the degree of hypertrophy, as well as subsequent dysfunction it may precipitate.

[13] Specific changes in repolarization and depolarization events are indicative of different underlying causes of hypertrophy and can assist in the appropriate management of the condition.

[14] In either condition fewer than 10% of patients with significant hypertrophy display a normal EKG.

Important considerations in echocardiography of the hypertrophied heart include lateral and septal wall thickness, degree of outflow tract obstruction, and systolic anterior wall motion (SAM) of the mitral valve, which can exacerbate outflow obstruction.