VENTRICULAR REMODELING AFTER MYOCARDIAL-INFARCTION - EXPERIMENTAL-OBSERVATIONS AND CLINICAL IMPLICATIONS
VENTRICULAR REMODELING AFTER MYOCARDIAL-INFARCTION - EXPERIMENTAL-OBSERVATIONS AND CLINICAL IMPLICATIONS
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DOI：
10.1161/01.cir.81.4.1161
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发表时间：
1990-04-01
期刊：
影响因子：
37.8
通讯作者：
BRAUNWALD, E
中科院分区：
文献类型：
--
作者：
PFEFFER, MA;BRAUNWALD, E
急性心肌梗死，特别是大面积和跨壁的心肌梗死，可引起心室梗死区和非梗死区地形的改变。这种重构对脑室功能和生存预后有重要影响。在早期，超声心动图已确认梗死扩张为非收缩区域的延长。非梗死区也经历了重要的延长，这与继发性容量过载肥厚一致，并且可以是进行性的。梗死后心室扩大的程度与心肌初始损伤的程度有关，尽管在射血分数持续降低的情况下，腔体大小的增加倾向于恢复卒中容量，但心室扩张与生存率降低有关。心室扩大的过程可受三个相互依赖的因素影响，即梗死面积、梗死愈合和心室壁应力。预防或减少梗死后心室大小增加及其对预后不良影响的最有效方法是限制初始损伤。急性再灌注治疗一直显示导致心室容积减少。即使超过了挽救心肌细胞的时间框架，重新建立梗死区域的血流对减轻心室增大也有有益的作用。急性梗死期间，糖皮质激素和非甾体类抗炎药可干扰割伤过程，使梗死灶变薄，梗死灶扩大程度增大。扩张或变形力的改变对心室增大有重要影响。即使短期后负荷的增加也会对心室地形产生有害的长期影响。相反，明智地使用硝酸甘油似乎与梗死扩展的衰减和临床结果的长期改善有关。实验和临床研究均表明，血管紧张素转换酶抑制剂的长期治疗有利于改变左心室的负荷条件，减少进行性心室增大。在前一种治疗中，这种心室增大的衰减与生存期的延长有关。目前正在评估心肌梗死后长期血管紧张素转换酶抑制剂治疗的长期临床后果。尽管针对梗死后左心室重构的研究尚处于早期阶段，但这似乎将是未来研究可能改善梗死后长期预后的重要领域。
An acute myocardial infarction, particularly one that is large and transmural, can produce alterations in the topography of both the infarcted and noninfarcted regions of the ventricle. This remodeling can importantly affect the function of the ventricle and the prognosis for survival. In the early period, infarct expansion has been recognized by echocardiography as a lengthening of the noncontractile region. The noninfarcted region also undergoes an important lengthening that is consistent with a secondary volume-overload hypertrophy and that can be progressive. The extent of ventricular enlargement after infarction is related to the magnitude of the initial damage to the myocardium and, although an increase in cavity size tends to restore stroke volume despite a persistently depressed ejection fraction, ventricular dilation has been associated with a reduction in survival. The process of ventricular enlargement can be influenced by three interdependent factors, that is, infarct size, infarct healing, and ventricular wall stresses. A most effective way to prevent or minimize the increase in ventricular size after infarction and the consequent adverse effect on prognosis is to limit the initial insult. Acute reperfusion therapy has been consistently shown to result in a reduction in ventricular volume. The reestablishment of blood flow to the infarcted region, even beyond the time frame for myocyte salvage, has beneficial effects in attenuating ventricular enlargement. The process of scarification can be interfered with during the acute infarct period by the administration of glucocorticosteroids and nonsteroidal antiinflammatory agents, which result in thinner infarcts and greater degrees of infarct expansion. Modification of distending or deforming forces can importantly influence ventricular enlargement. Even short-term augmentations in afterload have deleterious long-term effects on ventricular topography. Conversely, judicious use of nitroglycerin seems to be associated with an attenuation of infarct expansion and long-term improvement in clinical outcome. Long-term therapy with an angiotensin converting enzyme inhibitor can favorably alter the loading conditions on the left ventricle and reduce progressive ventricular enlargement as demonstrated in both experimental and clinical studies. With the former therapy, this attenuation of ventricular enlargement was associated with a prolongation in survival. The long-term clinical consequences of long-term angiotensin converting enzyme inhibitor therapy after myocardial infarction is currently being evaluated. Although studies directed at attenuating left ventricular remodeling after infarction are in the early stages, it does seem that this will be an important area in which future research might improve long-term outcome after infarction.