Early predictors of left ventricular remodeling after acute myocardial infarction.
Ventricular remodeling after acute myocardial infarction is characterized by alteration in left ventricular (LV) size, shape, and wall thickness and involves both the infarcted and the noninfarcted regions of the ventricle. These structural changes are the result of several distinct pathologic processes that contribute to progressive LV dilation: rearrangement of wall structure, myocyte hypertrophy, and increasing muscle mass without an increase in wall thickness (eccentric hypertrophy). The pathogenesis of LV remodeling is multifactorial. Multiple factors may in fact contribute at different stages from the time of coronary occlusion until the development of ventricular dilation: These include the magnitude of the loss of contractile elements, the abrupt alteration in systolic and diastolic loading conditions, the activation of circulating neurohormones and local autocrine trophic factors, and the patency of the infarct-related artery. Although remodeling occurring early after infarction may be an appropriate compensatory response to preserve ventricular function, recent observations have suggested that this long process has a deleterious effect on LV function and prognosis. Thus attempts to inhibit these structural changes have been the focus of recent experimental and clinical studies. This review focuses on interactive factors that influence postinfarction LV remodeling, emphasizing the role of some new emerging determinants such as the extent of surviving myocardium within the infarcted and noninfarcted zones.
Bolognese
L
L
Division of Cardiology, Careggi Hospital, Viale Morgagni, Florence, Italy.
Cerisano
G
G
D019898:Autocrine Communication / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D003331:Coronary Vessels / Q000473:pathology; D005544:Forecasting; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000473:pathology; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D018377:Neurotransmitter Agents / Q000502:physiology; D011379:Prognosis; D014654:Vascular Patency; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
D018377:Neurotransmitter Agents