Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.
Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.
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DOI：
10.1155/2017/7018393
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发表时间：
2017
影响因子：
4.6
通讯作者：
Turillazzi E
中科院分区：
文献类型：
--
作者：
Neri M;Riezzo I;Pascale N;Pomara C;Turillazzi E
急性心肌梗死（AMI）是导致发病率和死亡率的主要原因。再灌注策略是当前AMI的标准治疗。然而，它们可能导致反常的心肌细胞功能障碍，称为缺血再灌注损伤（IRI）。不同形式的IRI是公认的，其中只有前两种是可逆的：再灌注诱导的心律失常，心肌顿抑，微血管阻塞，和致命的心肌再灌注损伤。猝死是急性心肌梗死（AMI）中缺血诱发致死性室性心律失常最常见的模式。IRI的确切机制尚不完全清楚。分子、细胞和组织的改变，如细胞死亡、炎症、神经体液激活和氧化应激被认为是IRI中最重要的。然而，确切的病理生理机制的理解仍然是一个挑战，临床医生。此外，心肌IRI对于法医病理学家也是一个关键问题，因为尽管AMI后及时再灌注仍可能发生猝死，这是心脏病学实践中最常见的诉讼领域之一。在本文中，我们探讨了有关心肌IRI的病理生理学的文献，侧重于钙蛋白酶系统，氧化-亚硝化应激和基质金属蛋白酶的可能作用，旨在培养IRI的病理生理学知识，也在法医学方面的理解AMI后猝死。
Acute myocardial infarction (AMI) is a leading cause of morbidity and mortality. Reperfusion strategies are the current standard therapy for AMI. However, they may result in paradoxical cardiomyocyte dysfunction, known as ischemic reperfusion injury (IRI). Different forms of IRI are recognized, of which only the first two are reversible: reperfusion-induced arrhythmias, myocardial stunning, microvascular obstruction, and lethal myocardial reperfusion injury. Sudden death is the most common pattern for ischemia-induced lethal ventricular arrhythmias during AMI. The exact mechanisms of IRI are not fully known. Molecular, cellular, and tissue alterations such as cell death, inflammation, neurohumoral activation, and oxidative stress are considered to be of paramount importance in IRI. However, comprehension of the exact pathophysiological mechanisms remains a challenge for clinicians. Furthermore, myocardial IRI is a critical issue also for forensic pathologists since sudden death may occur despite timely reperfusion following AMI, that is one of the most frequently litigated areas of cardiology practice. In this paper we explore the literature regarding the pathophysiology of myocardial IRI, focusing on the possible role of the calpain system, oxidative-nitrosative stress, and matrix metalloproteinases and aiming to foster knowledge of IRI pathophysiology also in terms of medicolegal understanding of sudden deaths following AMI.