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=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===
 
=== [[Cardiac Hypertrophy|Myocardial hypertrophy]]  ===
Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: '''concentric''' and '''eccentric''' hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.
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Chronic increase in cardiac work results in a geometric alteration of the chambers involved. Remodelling of the ventricular myocardium occurs in two forms: concentric and eccentric hypertrophy. Factors implicated in the development of hypertrophy include adrenergic stimulation, angiotensin II and increased intracellular calcium.
    
'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.
 
'''Concentric hypertrophy''' develops in response to pressure overload (increased afterload). Increased afterload causes replication of sarcomeres in parallel, resulting in an increase in wall thickness and a decrease in internal diameter with no overall change in the external diameter of the chamber. This is better understood by considering the '''Laplace''' law, which states that ventricular wall stress is elevated by increased pressure and increased chamber diameter; whereas wall stress decreases as the ventricular wall thickens. Therefore concentric hypertrophy occurs as a compensatory mechanism to normalise ventricular wall stress in the face of pressure overload.
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