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This 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.

eFig 37-01

Hurst's Central Illustration: Histologic Findings After Myocardial Infarction.

Timelines of histologic findings after myocardial infarction in nonreperfused and reperfused* infarctions. Myocardial salvage occurs if reperfusion takes place within 4-6 hours after onset of chest pain or electrocardiographic changes, and the infarct is likely to be subendocardial without transmural extension. *Reperfused within 4-6 hours after onset of chest pain or electrocardiographic changes.

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The major cause of acute myocardial infarction (MI) is coronary atherosclerosis with superimposed luminal thrombus, which accounts for more than 80% of all infarcts. MIs resulting from nonatherosclerotic diseases of the coronary arteries are rare. In past decades, there have been several trends regarding the epidemiology and outcome of patients hospitalized with acute MI. Over the time span from 1975 to 2009, patients became significantly older, were more likely to be women, and were more likely to receive effective cardiac medications. Despite a greater prevalence of comorbidities, hospital survival rates have globally improved over time.1 However, mortality has remained unchanged for patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation MI,2 mostly because of secular trends as a result of changing population.3 Reperfusion (blood flow restoration into the ischemic territory) is the only available treatment to stop the progression of ischemic damage during an MI, but comes at a price, inducing additional harm to the myocardium.4 Reperfusion injury, which accounts for up to 40% of total infarct size, is thus considered “a necessary evil.”5


Mechanisms of Myocardial Injury


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