Pfeffer M A, Braunwald E
Department of Medicine, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.
Circulation. 1990 Apr;81(4):1161-72. doi: 10.1161/01.cir.81.4.1161.
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.
急性心肌梗死，尤其是大面积透壁性梗死，可导致梗死区和非梗死区心室形态发生改变。这种重塑可显著影响心室功能和生存预后。在早期，超声心动图已将梗死扩展识别为非收缩区的延长。非梗死区也会发生重要的延长，这与继发性容量负荷过重性肥厚一致，且可能呈进行性发展。梗死后心室扩大的程度与心肌初始损伤的程度有关，尽管腔径增大倾向于在射血分数持续降低的情况下恢复每搏输出量，但心室扩张与生存率降低相关。心室扩大的过程可受三个相互依存的因素影响，即梗死面积、梗死愈合和心室壁应力。预防或尽量减少梗死后心室大小增加及其对预后的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可导致心室容积减小。即使在心肌细胞挽救时间窗之后，恢复梗死区域的血流对减轻心室扩大也有有益作用。在急性梗死期，给予糖皮质激素和非甾体类抗炎药可干扰瘢痕形成过程，导致梗死变薄和更大程度的梗死扩展。改变扩张或变形力可显著影响心室扩大。即使是后负荷的短期增加对心室形态也有有害的长期影响。相反，合理使用硝酸甘油似乎与梗死扩展的减轻及临床结局的长期改善有关。实验和临床研究均表明，长期使用血管紧张素转换酶抑制剂治疗可有利地改变左心室的负荷条件，减少进行性心室扩大。采用前一种治疗方法时，心室扩大的减轻与生存期延长相关。目前正在评估心肌梗死后长期使用血管紧张素转换酶抑制剂治疗的长期临床后果。尽管针对减轻梗死后左心室重塑的研究尚处于早期阶段，但这似乎将是一个重要领域，未来的研究可能会改善梗死后的长期结局。
