C Definition ardiac remodeling may be defined as expression of the genome in molecular, cellular, and interstitial changes that are manifested clinically as changes in the size, shape, and function of the heart after cardiac injury. The process is influenced by hemodynamic load, neurohumoral activation, and other factors still under investigation. The myocyte is the major cardiac cell involved. Other participants include the intersti-tium, fibroblasts, collagen, and the coronary vasculature. Relevant processes include ischemia, cell necrosis, and apoptosis.
Cardiac remodeling may occur after myocardial infarction, pressure overload (aortic stenosis, hypertension), inflammatory heart muscle disease (myocarditis), idiopathic dilated cardiomyopathy, and volume overload (valvular regurgitation). It has been described as both an adaptive and maladaptive process: the adaptive component enables the heart to maintain function in response to pressure or volume overload in the acute phase of cardiac injury. Increments in load, such as in mitral insufficiency, modulate ventricular remodeling to maintain forward flow. However, after cardiac injury (eg, myocardial infarction), continued remodeling often leads to progressive decompensation.
The time course of remodeling is influenced by the severity of the initial insult, secondary events, associated disorders (eg, diabetes and hypertension), and treatment. Its magnitude carries prognostic significance: the greater the remodeling, the poorer the prognosis.
Although an exact picture of all the pathways and cells involved in left ventricular remodeling is still unclear, the following scenario has been proposed. Myocyte stretching triggers an increase in local norepinephrine activity and the release of angiotensin and endothelin.
These changes stimulate expression of altered proteins and myocyte hypertrophy. The end result is further deterioration in cardiac performance and increased neurohumoral activation. In addition, increased aldosterone and cytokine activation may also stimulate collagen synthesis, leading to fibrosis and remodeling of the extracellular matrix.
Progressive left ventricular dysfunction occurs in part as a result of ongoing myocyte death. Apoptosis increases after ischemia, reperfusion, and myocardial infarction, perhaps as an important regulatory mechanism in the adaptive response to pressure overload, to offset cardiac hypertrophy. Triggers of apoptosis include cytokines, oxidative stress, and mitochondrial damage.
Collagenase activation and increasing distension pressure, combined with unusual wall stress due to myocyte loss, are believed to cause the myocyte slippage that contributes to chamber remodeling. As the heart remodels, its geometry changes; it becomes less elliptical and more spherical.
What is myocardial remodeling, and what is its importance in heart failure? Photo Gallery
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