TY - CHAP M1 - Book, Section TI - PATHOLOGY OF MYOCARDIAL INFARCTION AND SUDDEN DEATH A1 - Romero, Maria E. A1 - Fernandez-Jimenez, Rodrigo A1 - Ladich, Elena A1 - Fuster, Valentin A1 - Ibanez, Borja A1 - Virmani, Renu A2 - Fuster, Valentin A2 - Harrington, Robert A. A2 - Narula, Jagat A2 - Eapen, Zubin J. PY - 2017 T2 - Hurst's The Heart, 14e AB - SummaryThis chapter discusses the pathology of myocardial infarction (MI) and sudden death. Severe loss of myocardial contractility occurs within 60 seconds of the onset of ischemia; loss of viability (irreversible injury) takes at least 20-40 minutes after total occlusion of blood flow. MI has traditionally been viewed as a manifestation of necrotic cell death, but other forms of cardiomyocyte death have also been observed in reperfused MI; the extent to which the processes considered to comprise the spectrum of cell death—necrosis, apoptosis, autophagy, and necroptosis—each contribute to infarct size is currently unclear. Collateral circulation, preconditioning, and reperfusion can influence infarct size. If ischemic myocardium is reperfused early, the degree of myocardial salvage greatly exceeds the damage associated with reperfusion injury. Myocardium may adapt to chronic ischemia by decreasing its contractility but preserving viability; this reversibly, dysfunctional tissue is commonly referred to as hibernating myocardium. Left ventricular remodeling begins within the first few hours after an MI and continues to progress, and the infarcted myocardium undergoes rapid turnover during the first 1-2 weeks after MI. MI also generates a systemic inflammatory response. Histologic evaluation (see accompanying Hurst’s Central Illustration) has been classically considered the gold standard for the evaluation of myocardial tissue, but cardiac magnetic resonance has become the in vivo gold standard for quantifying myocardial salvage. SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/04/19 UR - accesscardiology.mhmedical.com/content.aspx?aid=1191187922 ER -