Jackson Benjamin M, Gorman Joseph H, Moainie Sina L, Guy T Sloane, Narula Navneet, Narula Jagat, John-Sutton Martin G, Edmunds L Henry, Gorman Robert C
Harrison Department of Surgical Research, Philadelphia, Pennsylvania 19104, USA.
J Am Coll Cardiol. 2002 Sep 18;40(6):1160-7; discussion 1168-71. doi: 10.1016/s0735-1097(02)02121-6.
This study tests the hypothesis that hypocontractile, borderzone myocardium adjacent to an expanding infarct becomes progressively larger and more hypocontractile as remodeling continues. Early infarct expansion following anteroapical myocardial infarction (MI) is associated with progressive ventricular dilation and heart failure. The contribution of perfused, hypocontractile, borderzone myocardium to this process is unknown. Using a sheep model of anteroapical infarction, sonomicrometry array localization and serial microsphere injections were used to track changes in regional myocardial contractility, geometry, and perfusion. Eight sheep were studied before and after infarction and two, five, and eight weeks later. Thirty intertransducer chord lengths were analyzed to measure regional contractility and serial changes in regional geometry at end systole. Beginning as a narrow band of fully perfused hypocontractile myocardium adjacent to the infarction, borderzone myocardium extends to involve additional contiguous myocardium that progressively loses contractile function as the heart remodels. Three distinct myocardial zones develop as a result of transmural MI: infarct, borderzone (perfused but hypocontractile), and remote (perfused and normally functioning).This study demonstrates that hypocontractile, fully perfused borderzone myocardium extends to involve contiguous normal myocardium during postinfarction remodeling. This borderzone myocardium is a unique type of perfused, hypocontractile myocardium, which is distinct from hibernating or stunned myocardium. Preventing extension of borderzone myocardium by medical or surgical means offers the prospect of preventing late-onset heart failure following transmural expanding MIs.
随着重塑的持续，与不断扩大的梗死灶相邻的收缩功能减退的边缘区心肌会逐渐增大且收缩功能进一步减退。前壁心尖部心肌梗死（MI）后的早期梗死灶扩展与进行性心室扩张和心力衰竭相关。灌注良好但收缩功能减退的边缘区心肌在这一过程中的作用尚不清楚。利用前壁心尖部梗死的绵羊模型，采用超声心动图阵列定位和连续微球注射来追踪局部心肌收缩性、几何形态和灌注的变化。对8只绵羊在梗死前后以及梗死2周、5周和8周后进行研究。分析30条换能器间弦长以测量收缩末期的局部收缩性和局部几何形态的连续变化。边缘区心肌起初是梗死灶旁一条狭窄的灌注良好但收缩功能减退的心肌带，随着心脏重塑，其范围扩展至相邻的心肌，这些心肌逐渐丧失收缩功能。透壁性心肌梗死导致形成三个不同的心肌区域：梗死区、边缘区（灌注良好但收缩功能减退）和远隔区（灌注良好且功能正常）。本研究表明，在梗死后重塑过程中，收缩功能减退但灌注良好的边缘区心肌会扩展至相邻的正常心肌。这种边缘区心肌是一种独特类型的灌注良好但收缩功能减退的心肌，有别于冬眠心肌或顿抑心肌。通过药物或手术手段阻止边缘区心肌扩展，有望预防透壁扩展性心肌梗死后的迟发性心力衰竭。
