Ultimately, this response can be compensatory for a duration, and allow for improved cardiac function in the face of stressors. This is maladaptive largely because there is not a corresponding proliferation of the vasculature supplying the myocardium, resulting in ischemic areas of the heart. The result is an increase in thickness of the myocardium without a corresponding increase in ventricular size. Ĭoncentric hypertrophy is characterized by an addition of sarcomeres (the contractile units of cardiac cells) in parallel. 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. 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 hypertrophy to compensate for these increased pressures. The underlying commonality in these disease states is an increase in pressures that the ventricles experience.
Ĭoncentric hypertrophy 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 hypertrophy ( hypertrophic cardiomyopathy). Eccentric hypertrophy is related to volume overload and leads to the addition of sarcomeres in series. Concentric hypertrophy is a result of pressure overload on the heart, resulting in parallel sarcomerogenesis (addition of sarcomere units parallel to existing units). These adaptations are related to how the cardiomyocyte contractile units, called sarcomeres, respond to stressors such as exercise or pathology. Ventricular hypertrophy may be divided into two categories: concentric hypertrophy and eccentric hypertrophy. 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). Rectangular "Boxcar" nuclei is a microscopic sign indicating myocardial hypertrophy. Physiology Histopathology of (a) normal myocardium and (b) myocardial hypertrophy. Overt signs of heart failure, such as edema, or shortness of breath without exertion are uncommon. Most commonly, chest pain, either with or without exertion is present, along with shortness of breath with exertion, general fatigue, syncope, and palpitations. Conversely, concentric hypertrophy can make itself known in a variety of ways. In individuals with eccentric hypertrophy there may be little or no indication that hypertrophy has occurred as it is generally a healthy response to increased demands on the heart. Importantly, pathologic and physiologic remodeling engage different cellular pathways in the heart and result in different gross cardiac phenotypes. For example, it occurs in what is regarded as a physiologic, adaptive process in pregnancy in response to increased blood volume but can also occur as a consequence of ventricular remodeling following a heart attack. Ventricular hypertrophy can result from a variety of conditions, both adaptive and maladaptive. Although left ventricular hypertrophy (LVH) is more common, right ventricular hypertrophy (RVH), as well as concurrent hypertrophy of both ventricles can also occur. Ventricular hypertrophy ( VH) is thickening of the walls of a ventricle (lower chamber) of the heart.
The diagram shows a typical heart (left) and one with ventricular hypertrophy (right). Medical condition Ventricular hypertrophy
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