Histopathology of (a) normal myocardium and (b) myocardial<unk> . Scale bar indicates 50 μm. Rectangular "Boxcar" nuclei is a microscopic sign indicating myocardial<unk> . The ventricles are the chambers in the heart responsible for pumping blood either to the lungs (right ventricle) or to the rest of the body (left ventricle).<unk>  may be divided into two categories: concentric<unk>  and eccentric<unk> . These adaptations are related to how the cardiomyocyte contractile units, called sarcomeres, respond to stressors such as exercise or pathology. Concentric<unk>  is a result of pressure overload on the heart, resulting in parallel sarcomerogenesis (addition of sarcomere units). Eccentric<unk>  is related to volume overload and leads to the addition of sarcomeres in series. Concentric<unk>  results from various stressors to the heart including hypertension, congenital heart defects (such as Tetralogy of Fallot), valvular defects (aortic coarction or stenosis), and primary defects of the myocardium which directly cause<unk>  <unk> c cardiomyopathy). The underlying commonality in these disease states is an increase in pressures that the ventricles experience. For example, in tetralogy of Fallot, the right ventricle is exposed to the high pressures of the left heart due to a defect in the septum; as a result the right ventricle undergoes<unk>  to compensate for these increased pressures. Similarly, in systemic hypertension, the left ventricle must work harder to overcome the higher pressures of the vascular system and responds by thickening to deal with increased wall stress. Concentric<unk>  is characterized by an addition of sarcomeres (the contractile units of cardiac cells) in parallel. The result is an increase in thickness of the myocardium without a corresponding increase in ventricular size. 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<unk>  can result in a dilated ventricle which is unable to effectively pump blood, leading to heart failure. When stressors that encourage this concentric<unk>  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. Eccentric<unk>  is generally regarded as healthy, or physiologic<unk>  and is often termed "athlete's heart." It is the normal response to healthy exercise or pregnancy, which results in an increase in the heart's muscle mass and pumping ability. It is a response to 'volume-overload', either as a result of increased blood return to the heart during exercise, or a response to an actual increase in absolute blood volume as in pregnancy. This increase in pumping ability is the result of the addition of sarcomeres in series, which enables the heart to contract with greater force. 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. Rowers, cyclists, and cross-country skiers tend to have the largest hearts, with an average left ventricular wall thickness of 1.3 centimeters, compared to 1.1 centimeters in average adults. Though eccentric<unk>  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<unk> , 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. Though it is the case that eccentric<unk>  is largely considered to be a healthy response to increased cardiac demand, it is also associated with risks. For example, in athletes with significantly increased left ventricular weight there is also a corresponding increased risk for conduction abnormalities and sudden cardiac death. 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. As such, though it is convenient to consider clear cut distinctions between pathologic and physiologic cardiac<unk> , there may be a broader range of phenotypes than may be accounted for by gross cardiac phenotypes alone. The development of pathologic states in LVH is complex. 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. LVH may interfere with heart functionality in a number of ways. Before progression to a dilated phenotype, mechanical obstruction of the outflow tract can occur, leading to reduced cardiac output. Additionally, increased fibrosis of the ventricle can result in a failure to relax appropriately which impairs cardiac filling and may lead to diastolic dysfunction or heart failure with preserved ejection fraction.
Ventricular hypertrophy
Atrial enlargement
Myocardial disarray
Aortic unfolding
Cardiac fibrosis
Myocardial scarring
Ventricular remodeling
Hydrodilatation