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Pathological hypertrophy heart diagram
Pathological hypertrophy heart diagram







pathological hypertrophy heart diagram

Over time, this state can deteriorate into dilated and eccentric hypertrophy, in which individual cardiomyocytes reduce in width and lengthening becomes excessive, leading to extreme chamber enlargement with loss of wall and septal thickness, along with large increases in wall tension. Pathologic stress or hypertrophic cardiomyopathy activates neuroendocrine factors that stimulate cardiac hypertrophy, often resulting in concentric remodeling, in which cardiomyocytes mostly increase in width compared with length, resulting in wall and septal thickening and a loss of chamber area. Exercise and pregnancy result in physiologic hypertrophy, in which individual cardiomyocytes increase in length and width and the heart undergoes a balanced type of eccentric hypertrophy (chambers, walls, and septum enlarge in unison). The normal heart can develop different types of hypertrophic remodeling depending on the stress. Overview of different types of cardiac hypertrophy. Alternatively, select pathologic stimuli, or the transition to heart failure, can also elicit an eccentric or dilatory growth response in which the chamber effectively dilates with wall thinning, most likely through a predominate lengthening of individual myocytes (Figure 1). Pathologic growth of the myocardium can induce concentric remodeling of the ventricle that results in myocyte growth in a cross-sectional area, such as with hypertension or from hypertrophic cardiomyopathy due to mutations in sarcomeric genes (Figure 1). The hypertrophic growth of the myocardium is typically initiated by signal transduction pathways in response to either neuroendocrine factors or an ill-defined mechanical stretch– or wall tension–sensing apparatus ( 6– 10). Pathologic hypertrophy of the myocardium temporarily preserves pump function and reduces ventricular wall stress, but prolonged cardiac hypertrophy is a leading predictor for arrhythmias and sudden death as well as dilated cardiomyopathy and heart failure ( 2– 5). When contractile performance is perturbed or reduced in response to diverse (patho-)physiologic stimuli, the heart typically remodels and hypertrophies, in association with increases in myocyte cell volume ( 1). The primary function of the heart is to contract and pump blood. Cardiac hypertrophy and clinical considerations We focus our discussion on selected therapeutic targets that have more recently emerged and have a tangible translational potential given the available pharmacologic agents that could be readily evaluated in human clinical trials. The majority of these are based on intracellular signaling pathways considered central to pathologic cardiac remodeling and hypertrophy, which then leads to heart failure. Here we discuss therapeutic avenues emerging from molecular and genetic studies of cardiovascular disease in animal models. Cardiac hypertrophy is the strongest predictor for the development of heart failure, arrhythmia, and sudden death. Initially, such cardiac hypertrophic growth is often compensatory, but as time progresses these changes become maladaptive. The heart responds to many cardiopathological conditions with hypertrophic growth by enlarging individual myocytes to augment cardiac pump function and decrease ventricular wall tension. Cardiovascular disease is the number one cause of mortality in the Western world.









Pathological hypertrophy heart diagram