Ertl G, Gaudron P, Hu K
Medizinische Klinik, Universität Würzburg.
Basic Res Cardiol. 1993;88 Suppl 1:125-37. doi: 10.1007/978-3-642-72497-8_9.
Changes of ischemic myocardium following coronary occlusion, including active and passive functions, and adaptive changes of non-ischemic surviving myocardium have been summarized under the term "left ventricular remodeling" post myocardial infarction. An increase in left ventricular volume may be a consequence, and associated with an adverse prognosis. Although left ventricular dilatation may increase stroke volume and, thus, be compensatory at first, in about one-fifth of patients it ultimately results in progressive dysfunction and heart failure. Major determinants of this process are time, infarct size, infarct location, global left ventricular function assessed 4 days after infarction by radionuclide ejection fraction and right heart catheter (stroke volume), and morphology of the infarct-associated coronary artery. The surviving myocardium hypertrophies and may also dilate structurally. Depression of left ventricular ejection fraction chronically after the infarct is due to deterioration of wall motion of chamber segments initially classified normal by radionuclide analysis. Biochemical changes may also occur, including reduction of phosphocreatine, prolongation of time to peak Cai2+, and changes in myosin isoforms. Systemic or local humoral factors may be involved in these changes, however, clear evidence is still lacking. Perfusion of surviving myocardium may be altered under various conditions due to morphologic and functional changes of coronary vasculature. Successful prevention of heart failure and death by angiotensin converting enzyme inhibitors in asymptomatic patients with left ventricular dysfunction post-myocardial infarction has supported the pathophysiologic concepts of remodeling.
冠状动脉闭塞后缺血心肌的变化，包括主动和被动功能，以及非缺血存活心肌的适应性变化，已被概括在心肌梗死后的“左心室重构”这一术语之下。左心室容积增加可能是其结果，并与不良预后相关。虽然左心室扩张可能会增加每搏输出量，因此起初具有代偿作用，但在约五分之一的患者中，它最终会导致进行性功能障碍和心力衰竭。这一过程的主要决定因素包括时间、梗死面积、梗死位置、心肌梗死后4天通过放射性核素射血分数和右心导管（每搏输出量）评估的整体左心室功能，以及梗死相关冠状动脉的形态。存活心肌会肥大，在结构上也可能会扩张。心肌梗死后长期左心室射血分数降低是由于最初经放射性核素分析归类为正常的心室节段壁运动恶化所致。还可能发生生化变化，包括磷酸肌酸减少、Ca2+峰值时间延长以及肌球蛋白同工型的变化。全身或局部体液因素可能参与这些变化，然而，仍缺乏明确证据。由于冠状动脉血管的形态和功能变化，在各种情况下存活心肌的灌注可能会改变。心肌梗死后左心室功能障碍的无症状患者使用血管紧张素转换酶抑制剂成功预防心力衰竭和死亡，支持了重构的病理生理概念。
