Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

作者：Bodh I. Jugdutt · 发表于：Circulation · 年份：2003 · DOI：10.1161/01.cir.0000085658.98621.49 · 被引用次数：629 · 研究领域：Cardiac Structural Anomalies and Repair、Cardiac Fibrosis and Remodeling、Cardiovascular Function and Risk Factors

Ventricular Remodeling After Infarction and the Extracellular Collagen MatrixWhen Is Enough Enough?Bodh I. Jugdutt, MD L eft ventricular (LV) remodeling after myocardial in- farction (MI) contributes significantly to LV dilation and dysfunction, and disability and death.Two paradigms, pertinent to antiremodeling therapy after MI (Figure 1), have evolved over the last 3 decades.Paradigm 1, LV remodeling is a major mechanism for disability and death, 1,2 has received a great deal of attention.In contrast, paradigm 2, remodeling of the extracellular collagen matrix (ECCM) plays a major role in LV remodeling, [3][4][5][6][7] whereby decrease, disruption, and/or defective composition of the ECCM promote LV dilation and rupture, 4 -7 has received little attention.A host of clinical trials showed that angiotensin-converting enzyme (ACE) inhibitors (ACE-Is) with or without aldosterone antagonists, angiotensin II (AngII) type 1 (AT 1 ) receptor blockers (ARBs), ␤-adrenergic blockers or reperfusion improve outcome in survivors of MI. 8 -10 Concurrent evidence has underscored the importance of preserving the ECCM during healing after MI. [2][3][4][5][6][7] However, the antifibrotic action of ACE-Is, aldosterone antagonists and ARBs on ECCM in the infarct zone (IZ) and noninfarct zone (NIZ), 6,7,9,11 and the reperfusion-induced damage to the ECCM in the IZ, 5,7,12 remain unreconciled with the benefits.8 -10,13 Nevertheless, excessive ECCM, as in dilated ischemic cardiomyopathy after remo...