心肌内出血与再灌注损伤的“波阵面”危及心肌挽救。

Intramyocardial Hemorrhage and the "Wave Front" of Reperfusion Injury Compromising Myocardial Salvage.

机构信息

Cedars-Sinai Medical Center, Los Angeles, California, USA; Department of Radiology, the First Affiliated Hospital of China Medical University, Shenyang, China.

Cedars-Sinai Medical Center, Los Angeles, California, USA; University of Calgary, Calgary, Alberta, Canada.

出版信息

J Am Coll Cardiol. 2022 Jan 4;79(1):35-48. doi: 10.1016/j.jacc.2021.10.034.

DOI:10.1016/j.jacc.2021.10.034

PMID:34991787

Abstract

BACKGROUND

Reperfusion therapy for acute myocardial infarction (MI) is lifesaving. However, the benefit of reperfusion therapy can be paradoxically diminished by reperfusion injury, which can increase MI size.

OBJECTIVES

Hemorrhage is known to occur in reperfused MIs, but whether hemorrhage plays a role in reperfusion-mediated MI expansion is not known.

METHODS

We studied cardiac troponin kinetics (cTn) of ST-segment elevation MI patients (n = 70) classified by cardiovascular magnetic resonance to be hemorrhagic (70%) or nonhemorrhagic following primary percutaneous coronary intervention. To isolate the effects of hemorrhage from ischemic burden, we performed controlled canine studies (n = 25), and serially followed both cTn and MI size with time-lapse imaging.

RESULTS

CTn was not different before reperfusion; however, an increase in cTn following primary percutaneous coronary intervention peaked earlier (12 hours vs 24 hours; P < 0.05) and was significantly higher in patients with hemorrhage (P < 0.01). In hemorrhagic animals, reperfusion led to rapid expansion of myocardial necrosis culminating in epicardial involvement, which was not present in nonhemorrhagic cases (P < 0.001). MI size and salvage were not different at 1 hour postreperfusion in animals with and without hemorrhage (P = 0.65). However, within 72 hours of reperfusion, a 4-fold greater loss in salvageable myocardium was evident in hemorrhagic MIs (P < 0.001). This paralleled observations in patients with larger MIs occurring in hemorrhagic cases (P < 0.01).

CONCLUSIONS

Myocardial hemorrhage is a determinant of MI size. It drives MI expansion after reperfusion and compromises myocardial salvage. This introduces a clinical role of hemorrhage in acute care management, risk assessment, and future therapeutics.

摘要

背景

急性心肌梗死（MI）的再灌注治疗是救命的。然而，再灌注损伤会使再灌注治疗的益处适得其反，从而增加 MI 面积。

目的

已知再灌注 MI 会发生出血，但出血是否在再灌注介导的 MI 扩大中起作用尚不清楚。

方法

我们研究了 ST 段抬高 MI 患者的心肌肌钙蛋白动力学（cTn）（n=70），这些患者通过心血管磁共振成像分类为出血性（70%）或原发性经皮冠状动脉介入治疗后非出血性。为了将出血的影响与缺血负担隔离开来，我们进行了控制性犬研究（n=25），并通过时相成像对 cTn 和 MI 大小随时间的变化进行了连续监测。

结果

再灌注前 cTn 没有差异；然而，在原发性经皮冠状动脉介入治疗后，cTn 的增加更早（12 小时与 24 小时；P<0.05），且在出血患者中显著更高（P<0.01）。在出血动物中，再灌注导致心肌坏死迅速扩大，最终导致心外膜受累，而在非出血病例中则没有（P<0.001）。在有或没有出血的动物中，再灌注后 1 小时 MI 大小和抢救无差异（P=0.65）。然而，在再灌注后 72 小时内，出血性 MI 中可抢救的心肌损失增加了 4 倍（P<0.001）。这与出血性病例中较大 MI 的观察结果一致（P<0.01）。