Rumberger J A
Division of Cardiovascular Diseases and Internal Medicine, Mayo Clinic Rochester, Minnesota 55905.
Mayo Clin Proc. 1994 Jul;69(7):664-74. doi: 10.1016/s0025-6196(12)61345-7.
To discuss the important predictors of ventricular enlargement after myocardial infarction and the appropriate time frame for the initiation of medical and pharmacologic therapy.
A review of the important contributions relative to the process known as "postinfarction ventricular remodeling" is provided; current clinical implications and areas for future investigation are discussed.
Ventricular dilatation is an important factor in the prognosis after infarction. Stretching and thinning of the myocardium within the infarct region can be seen within hours after the acute event and may be accompanied by delayed but potentially progressive stretching and thinning in the noninfarct regions. Development of left ventricular hypertrophy in the nonischemic myocardium, in response to increased wall stress, can be observed but may be insufficient for proper compensation. This process is referred to as postinfarction remodeling and can result in progressive and long-term changes in ventricular architecture and function in the absence of additional ischemic injury.
The most effective way to limit the extent of postinfarction ventricular remodeling is to limit infarct size by prompt medical intervention within the first few hours. In addition to traditional post-infarction medications such as beta-blockers, nitrates, and aspirin, long-term benefit may be derived by use of adjunctive pharmacologic therapy such as angiotensin converting enzyme inhibitors, which have been shown to be valuable in limiting the extent of ventricular chamber dilatation after infarction. Studies in animal models and conclusions from clinical trials have shown that angiotensin converting enzyme inhibitors also decrease late mortality and cardiac morbidity after infarction, likely through favorable effects on both hemodynamic and neurohumoral factors specific to this class of medication.
These investigations notwithstanding, further studies are necessary for a complete understanding of the pathogenesis of postinfarction ventricular remodeling and the appropriate timing of specific pharmacologic therapy intended to limit ventricular dilatation. The hemodynamic and neurohumoral interactions on and within the heart must be thoroughly understood relative to microscopic and macroscopic changes in cardiac size, shape, and function after myocardial infarction.
探讨心肌梗死后心室扩大的重要预测因素以及启动药物和药理治疗的合适时间范围。
对与“梗死后心室重构”这一过程相关的重要贡献进行综述；讨论当前的临床意义和未来研究领域。
心室扩张是梗死后预后的一个重要因素。在急性事件发生后的数小时内，梗死区域内的心肌会出现拉伸和变薄，并且在非梗死区域可能会伴有延迟但可能逐渐进展的拉伸和变薄。可以观察到非缺血心肌因壁应力增加而发生左心室肥厚，但可能不足以进行适当的代偿。这个过程被称为梗死后重构，并且在没有额外缺血损伤的情况下，可导致心室结构和功能的渐进性和长期变化。
限制梗死后心室重构程度的最有效方法是在最初几小时内通过及时的药物干预来限制梗死面积。除了传统的梗死后药物如β受体阻滞剂、硝酸盐和阿司匹林外，使用辅助药理治疗如血管紧张素转换酶抑制剂可能会带来长期益处，已证明这些药物在限制梗死后心室腔扩张程度方面具有重要价值。动物模型研究和临床试验结论表明，血管紧张素转换酶抑制剂还可降低梗死后的晚期死亡率和心脏发病率，这可能是通过对这类药物特有的血流动力学和神经体液因素产生有利影响实现的。
尽管进行了这些研究，但仍需要进一步研究以全面了解梗死后心室重构的发病机制以及旨在限制心室扩张的特定药理治疗的合适时机。相对于心肌梗死后心脏大小、形状和功能的微观和宏观变化，必须深入了解心脏上和心脏内的血流动力学和神经体液相互作用。
