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2017 ; 2017
(ä): 7018393
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English Wikipedia
Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical
Issue for Clinicians and Forensic Pathologists
#MMPMID28286377
Neri M
; Riezzo I
; Pascale N
; Pomara C
; Turillazzi E
Mediators Inflamm
2017[]; 2017
(ä): 7018393
PMID28286377
show ga
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.