• Marli Smit, A R Coetzee, and A Lochner.
• Department of Anesthesiology and Critical Care, Stellenbosch University, Tygerberg Academic Hospital, Cape Town, South Africa. Electronic address: smitmarli@yahoo.com.
• J. Cardiothorac. Vasc. Anesth. 2020 Sep 1; 34 (9): 2501-2512.

AbstractIschemic heart disease, the leading cause of death worldwide, may result in devastating perioperative ischemia and infarction. The underlying pathophysiology, precipitating factors, and approach to prevention differ between patients presenting for noncardiac surgery, developing acute coronary syndrome versus stable angina. The first half of this article reviews the pathophysiology of acute coronary syndrome and stable angina. Acute coronary syndrome, otherwise known as Type 1 myocardial infarction, includes unstable angina, non-ST segment elevated myocardial infarction and ST segment elevated myocardial infarction. Acute coronary syndrome occurs as a result of vulnerable plaque rupture with subsequent varying degrees of thrombus formation, arterial spasm, and thus coronary occlusion. Stable angina, on the other hand, results from a myocardial oxygen delivery and demand mismatch in the setting of fixed coronary stenosis. After this discussion, the review article considers how both apply to perioperative myocardial infarctions and myocardial injury after noncardiac surgery. This article furthermore argues why myocardial oxygen delivery demand mismatch (Type 2) myocardial infarction is the most likely underlying pathophysiology responsible for perioperative myocardial infarctions. Being aware of this and knowledgeable about Type 2 infarctions may enable anesthetic providers to better predict the majority of triggers contributing to, and thus decreasing the incidence of, perioperative myocardial infarctions.Copyright © 2019 Elsevier Inc. All rights reserved.

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