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冠心病中的可逆性左心室功能障碍(第一部分):心肌顿抑

[Reversible left ventricular dysfunction in coronary disease (part one): myocardial stunning].

作者信息

Vlahović A, Popović A

机构信息

Centar za kardiovaskularna istrazivanja Dr Aleksandar D. Popović, Institut za kardiovaskularne bolesti Dedinje, Beograd.

出版信息

Med Pregl. 2000 Jan-Feb;53(1-2):39-44.

Abstract

INTRODUCTION

The concept of myocardial stunning has been proposed by Braunwald and Kloner in early 1980's and is defined as transient postischemic myocardial dysfunction that persists after reperfusion, despite the absence of irreversible damage and restoration of normal or near normal coronary flow. Thus, the hallmark of stunned myocardium is the mismatch between coronary flow and myocardial function.

MYOCARDIAL STUNNING

The two most plausible hypotheses used to explain the pathogenetic mechanisms of myocardial stunning are calcium and oxyradical hypotheses. According to the first one, myocardial stunning is the result of impaired calcium homeostasis caused either by calcium overload or decreased responsiveness of myofilaments to calcium. The oxyradical hypothesis postulates that generation of free oxygen radicals depresses myocardial function after the ischemic episode. The exact mechanism is unknown, but it is probably due to extreme reactivity of oxyradicals that bind to some cellular components, impairing membrane permeability and function of various cell organelle. Stunned myocardium can be seen in numerous clinical situations in which myocardial ischemia has been followed by reperfusion. These include: coronary artery bypass surgery, acute myocardial infarction, stable, unstable and variant angina, percutaneous transluminal coronary angioplasty and cardiac transplantation.

DISCUSSION AND CONCLUSION

In majority of these situations, stunned myocardium is usually well tolerated. However, there is a group of high-risk patients in whom prolonged myocardial dysfunction due to stunning can cause serious hemodynamic instability, which requires pharmacological and/or mechanical support. Therefore, in order to avoid these situations, some authors have suggested that stunned myocardium should be prevented, rather than treated. Since stunned myocardium is by definition reperfused, with normal or near normal coronary flow, treatment is reserved only for those patients in whom stunned region is large enough to cause low cardiac output and hypotension. Revascularisation is usually unnecessary; however, there are situations in which episodes of repetitive stunning cause chronic myocardial dysfunction along with hibernated myocardium, when myocardial revascularization would be beneficial.

摘要

引言

心肌顿抑的概念由布劳恩瓦尔德和克洛纳于20世纪80年代初提出,定义为再灌注后持续存在的短暂性缺血后心肌功能障碍,尽管不存在不可逆损伤且冠状动脉血流已恢复正常或接近正常。因此,顿抑心肌的标志是冠状动脉血流与心肌功能不匹配。

心肌顿抑

用于解释心肌顿抑发病机制的两个最合理假说是钙假说和氧自由基假说。根据第一个假说,心肌顿抑是钙稳态受损的结果,钙稳态受损是由钙超载或肌丝对钙的反应性降低引起的。氧自由基假说假定,缺血发作后游离氧自由基的产生会抑制心肌功能。确切机制尚不清楚,但可能是由于氧自由基与某些细胞成分结合的极端反应性,损害了膜通透性和各种细胞器的功能。在许多心肌缺血后再灌注的临床情况中都可见到顿抑心肌。这些情况包括:冠状动脉搭桥手术、急性心肌梗死、稳定型、不稳定型和变异型心绞痛、经皮腔内冠状动脉成形术和心脏移植。

讨论与结论

在大多数这些情况下,顿抑心肌通常耐受性良好。然而,有一组高危患者,由于顿抑导致的长期心肌功能障碍可引起严重的血流动力学不稳定,这需要药物和/或机械支持。因此,为了避免这些情况,一些作者建议应预防顿抑心肌,而不是治疗。由于根据定义,顿抑心肌是再灌注的,冠状动脉血流正常或接近正常,仅对那些顿抑区域大到足以导致低心输出量和低血压的患者进行治疗。通常不需要血管重建;然而,在某些情况下,反复顿抑发作会导致慢性心肌功能障碍以及心肌冬眠,此时心肌血管重建可能有益。

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