The remodeling of the left ventricle occurs as a response to a number of pathophysiologic events. It commonly occurs after a myocardial infarction as a response to loss of muscle mass, in the setting of myocarditis or idiopathic cardiomyopathy as a response to an intrinsic contractile dysfunction of cardiomyocytes or to acute loss of myocytes, or as a result of hypertension in a response to chronic pressure overload. All of these adverse events lead to a change in the size and shape of the left ventricle, and each alters the myocellular milieu and can provoke an adaptive response among constituent elements of the left ventricular wall.

Remodeling can also be expressed as a compensatory process, as a result of hypertrophy and dilation of nonischemic tissue after myocardial infarction or as a maladaptive response of hypertrophy secondary to long-standing systemic hypertension. The remodeling process itself can become autoinductive, leading to further progression of ventricular dysfunction<sup>54 Sabbah H.N., Stein P.D., Kono T. , et al. A canine model of chronic heart failure produced by multiple sequential coronary microembolizations Am J Physiol 1991 ;  260 : H1379-H1384

Cliquez ici pour aller à la section Références</sup> and the induction of apoptosis.<sup>58 Sharov V.G., Sabbah H.N., Shimoyama H. , et al. Evidence of cardiocyte apoptosis in myocardium of dogs with chronic heart failure Am J Pathol 1996 ;  148 : 141-149

Cliquez ici pour aller à la section Références</sup> At the same time, the inciting stimulus, such as ischemia or myocarditis, may continue to be active and lead to further tissue loss and progressive remodeling.

The change in shape and size of the left ventricle develops in response to focal loss of functional cardiac units, as in infarction, or in response to homogeneous degeneration of cardiomyocytes, as seen in various cardiomyopathies or in myocarditis. In the case of infarction, the unaffected myocardium hypertrophies, as evidenced by increases in both length and width of residual viable cardiocytes. Because myocytes lack the ability to replicate, global distortion ensues.

Progressive ventricular remodeling therefore occurs either as a result of a continuing pathologic process or as a result of compensatory mechanisms that occur in response to the initial insult. This progression can lead to a series of adverse neurohormonal and hemodynamic consequences manifested by ventricular enlargement, hypertrophy, and dilation. These features of ventricular remodeling ultimately result in the expression of clinical heart failure. In contrast, studies indicate that the modification of remodeling can limit the occurrence of heart failure in a number of disease states. The treatment of hypertension<sup>32 Kostis J.B., Davis B.R., Cutler J. , et al. for the SHEP Cooperative Research Group Prevention of heart failure by antihypertensive drug treatment in older persons with isolated systolic hypertension JAMA 1997 ;  278 : 212-216

Cliquez ici pour aller à la section Références</sup> and the prevention of the activation of the renin angiotensin system (RAS) after acute myocardial infarction<sup>47 Pfeffer M.A., Braunwald E., Moye L.A. , et al. on behalf of the SAVE Investigators Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction: Results of the Survival and Ventricular Enlargement Trial N Engl J Med 1992 ;  327 : 669-677  [cross-ref]

Cliquez ici pour aller à la section Références</sup> can limit the stimulus to ventricular remodeling and prevent the occurrence of heart failure. Infarct size is a major determinant of the remodeling process, just as continued arterial hypertension represents a continued stimulus to hypertrophic remodeling. The early administration of thrombolytic and β-adrenergic blocking agents has the potential to achieve limitation of ischemia and ischemic myocyte loss.