Jugdutt B I
Department of Medicine, University of Alberta, Edmonton.
Can J Cardiol. 1993 Jan-Feb;9(1):103-14.
To review the evidence for the temporal pathophysiological evolution of structural, topographic and functional changes during remodelling post infarction, and how the timing and duration of therapeutic interventions for limiting remodelling might influence outcome.
Published English language literature.
The focus was on experimental and clinical studies relating to modification of post infarct remodelling as well as pertinent clinical trials with clinical outcome and mortality end-points.
An objective determination of the timing and duration of therapy from the indexed infarction, and the rationale for the approach and its possible relation to measured outcome parameters.
Several strategies targeted to salvage ischemic myocardium and unload the left ventricle have proven effective in limiting remodelling. Because remodelling begins very early and is a staged and progressive pathophysiological process, timing and duration of therapy are likely to have a profound effect on outcome. Different outcomes can be expected depending on whether therapy is begun very early (during the infarction process), early (after completion of the infarction process but before significant deposition of infarct collagen has occurred), late (after infarct collagen has peaked and infarct healing is completed) or very late (after healing is completed). Different outcomes can also be expected with therapy that spans one or more of these stages. Maximum benefit might be expected from therapy that is begun very early, spans the entire healing process and extends beyond. Two-dimensional echocardiograms can be used to assess the impact of therapies on remodelling and function. Very early thrombolysis and low dose intravenous nitroglycerin followed by prolonged angiotensin-converting enzyme inhibition and/or nitrate appear to be a very promising algorithm.
The optimal therapeutic strategy for limiting post infarct remodelling should recognize the pathophysiological staging of the process and be targeted at preventing infarction, early expansion and progressive dilation.
回顾心肌梗死后重构过程中结构、形态及功能改变的时间性病理生理演变证据，以及限制重构的治疗干预的时机和持续时间如何影响预后。
已发表的英文文献。
重点关注与心肌梗死后重构改变相关的实验和临床研究，以及具有临床结局和死亡率终点的相关临床试验。
根据索引梗死客观确定治疗的时机和持续时间，以及该方法的原理及其与测量的结局参数的可能关系。
几种旨在挽救缺血心肌和减轻左心室负荷的策略已被证明在限制重构方面有效。由于重构很早就开始，且是一个分阶段进行的渐进性病理生理过程，治疗的时机和持续时间可能对预后有深远影响。根据治疗是在极早期（梗死过程中）、早期（梗死过程完成后但梗死胶原显著沉积之前）、晚期（梗死胶原达到峰值且梗死愈合完成后）还是极晚期（愈合完成后）开始，可预期不同的结局。跨越这些阶段中的一个或多个阶段的治疗也可预期不同的结局。极早期开始、贯穿整个愈合过程并持续更长时间的治疗可能会带来最大益处。二维超声心动图可用于评估治疗对重构和功能的影响。极早期溶栓和低剂量静脉注射硝酸甘油，随后长期使用血管紧张素转换酶抑制剂和/或硝酸盐似乎是一种非常有前景的方案。
限制心肌梗死后重构的最佳治疗策略应认识到该过程的病理生理阶段，并旨在预防梗死、早期扩张和进行性扩张。
