Sharpe Norman
Department of Medicine, University of Auckland, Auckland, New Zealand.
Heart Fail Monit. 2003;4(2):55-61.
Left ventricular (LV) remodeling, which can result from myocardial damage or ventricular pressure or volume overload, has genomic, cellular, and interstitial components with associated changes in ventricular size, shape, wall thickness, and function. It is a process that is detectable and measurable clinically, generally progressive, and associated with adverse outcomes. However, it is amenable to intervention, prevention, or reversal. Following myocardial infarction (MI), LV remodeling is particularly likely in patients with transmural or anterior infarction and in those with failed reperfusion or LV failure. Infarct artery patency and neurohormonal blockade are key management considerations for prevention or reversal of LV remodeling. Combination treatment with angiotensin-converting enzyme inhibition and beta-blockade is of proven benefit following MI, improving LV remodeling and long-term outcomes.
左心室（LV）重构可由心肌损伤、心室压力或容量超负荷引起，具有基因组、细胞和间质成分，并伴有心室大小、形状、壁厚和功能的相关变化。它是一个临床上可检测和测量的过程，通常呈进行性发展，并与不良后果相关。然而，它适合进行干预、预防或逆转。心肌梗死（MI）后，透壁性或前壁梗死患者以及再灌注失败或左心室衰竭患者尤其容易发生左心室重构。梗死动脉通畅和神经激素阻断是预防或逆转左心室重构的关键管理考虑因素。心肌梗死后，血管紧张素转换酶抑制和β受体阻滞剂联合治疗已被证明有益，可改善左心室重构和长期预后。
