Faculty of Forensic Medicine, Guangdong Province Translational Forensic Medicine Engineering Technology Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, 510080, China.
Department of Clinical Medicine, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, 510080, China.
Sci Rep. 2024 Apr 26;14(1):9589. doi: 10.1038/s41598-024-57047-5.
Lysophosphoglycerides (LPLs) have been reported to accumulate in myocardium and serve as a cause of arrhythmias in acute myocardial ischemia. However, in this study we found that LPLs level in the ventricular myocardium was decreased by the onset of acute myocardial ischemia in vivo in rats. Decreasing of LPLs level in left ventricular myocardium, but not right, was observed within 26 min of left myocardial ischemia, regardless of whether arrhythmias were triggered. Lower LPLs level in the ventricular myocardium was also observed in aconitine-simulated ventricular fibrillation (P < 0.0001) and ouabain-simulated III atrioventricular block (P < 0.0001). Shot-lasting electric shock, e.g., ≤ 40 s, decreased LPLs level, while long-lasting, e.g., 5 min, increased it (fold change = 2.27, P = 0.0008). LPLs accumulation was observed in long-lasting myocardial ischemia, e.g., 4 h (fold change = 1.20, P = 0.0012), when caspase3 activity was elevated (P = 0.0012), indicating increased cell death, but not coincided with higher frequent arrhythmias. In postmortem human ventricular myocardium, differences of LPLs level in left ventricular myocardium was not observed among coronary artery disease- and other heart diseases-caused sudden death and non-heart disease caused death. LPLs level manifested a remarkable increasing from postmortem 12 h on in rats, thus abolishing the potential for serving as biomarkers of sudden cardiac death. Token together, in this study we found that LPLs in ventricular myocardium were initially decreased by the onset of ischemia, LPLs accumulation do not confer arrhythmogenesis during acute myocardial ischemia. It is necessary to reassess the roles of LPLs in myocardial infarction.
溶血磷脂酸 (LPLs) 已被报道在心肌中积累，并作为急性心肌缺血时心律失常的原因。然而，在这项研究中，我们发现，在体内大鼠急性心肌缺血发作时，心室肌中的 LPLs 水平降低。在左心肌缺血后 26 分钟内，无论是否引发心律失常，左心室心肌中 LPLs 水平的降低是观察到的，而右心室心肌中 LPLs 水平的降低则未观察到。在乌头碱模拟的心室颤动（P < 0.0001）和哇巴因模拟的 III 度房室传导阻滞（P < 0.0001）中，心室肌中的 LPLs 水平也较低。短暂的电休克，如 ≤ 40 秒，会降低 LPLs 水平，而长时间的电休克，如 5 分钟，则会增加其水平（倍数变化 = 2.27，P = 0.0008）。在长时间的心肌缺血，如 4 小时（倍数变化 = 1.20，P = 0.0012）中，LPLs 积累被观察到，此时 caspase3 活性升高（P = 0.0012），表明细胞死亡增加，但与更高频的心律失常不一致。在人体心室肌的死后样本中，在冠状动脉疾病和其他心脏病引起的猝死与非心脏病引起的死亡之间，左心室心肌中的 LPLs 水平没有差异。在大鼠死后 12 小时后，LPLs 水平表现出显著增加，因此消除了作为心脏性猝死生物标志物的潜力。综上所述，在这项研究中，我们发现心室肌中的 LPLs 最初是由缺血发作引起的，LPLs 的积累不会在急性心肌缺血期间引起心律失常发生。有必要重新评估 LPLs 在心肌梗死中的作用。
