{"id":"1979","type":{"id":"30","name":"Pathophysiologic Disorders","urlId":"pathophysiologic-disorder","subtypes":[],"schema":"http:\/\/schema.org\/Article","numTerms":0},"subtype":{"id":"22","name":"Cardiovascular Disorders","urlId":"cardiovascular-disorder"},"urlId":"myocardial-infarctions-types-definitions","role":"term","course":{"id":"38","urlId":"pathology","name":"Clinical Pathology"},"children":[],"name":"Myocardial Infarctions: Types \u0026 Definitions","demo":0,"description":"\u003E ### **Myocardial Infarction: Definitions \u0026 Types**\t\n\n**Injury vs. Infarction**\nMyocardial injury: Cardiac troponin values are elevated above the 99th percentile upper reference limit. \nMyocardial infarction: Myocardial injury (that is, elevated troponin levels) coupled with ischemia.\n\nReview [ischemic heart disease](\/term\/pathology\/ischemic-heart-disease).\n\n**Timing**\nIncident infarction is the patient\u0027s first myocardial infarction.\nRecurrent infarctions occur more than 28 days after the incident infarction.\nReinfarctions occur within 28 days of an incident or recurrent infarction.\n\n**Silent Infarctions**\nMost myocardial infarctions present with symptoms such as chest pain, dyspnea, and weakness; however, silent myocardial infarctions, which are asymptomatic, account for approximately 1 in 5 cases.\n\t\n**MINOCA**\nAlthough many myocardial infarctions occur in the presence of obstructive coronary artery disease, a significant number of heart attacks are classified as MINOCA: myocardial infarction with [non-obstructive coronary artery disease](\/term\/pathology\/ischemic-heart-disease). \n\n**Takotsubo cardiomyopathy**\nSimilar symptoms as heart attack: Takotsubo cardiomyopathy (sometimes called \u0022broken heart syndrome\u0022).\n\n\u0022Takotsubu\u0022 refers to the Japanese octopus trap, which resembles the extended shape of the left ventricle in patients with this condition. \n\nPatients have left ventricular dysfunction and damage due to increased catecholamines, which can be induced by physical or emotional triggers.\n\n[ECG](\/term\/physiology\/electrocardiogram-ecg) often shows ST-segment elevation, mild to severe biomarker elevation, and normal or non-obstructive coronary arteries.\n\nFormerly believed to be benign, we now know that this condition is associated with increased mortality. \n\t \n\u003E ### **Myocardial Infarction Types**\t\n\n**Based on ECG changes**\n* **ST-elevation myocardial infarction (STEMI)**: ECG shows ST-segment Elevation. \n\u2014 Often associated with totally occluded coronary arteries.\n* **Non-ST-Elevated Myocardial Infarctions (NSTEMI)**: No ST-segment Elevation, but can have ST-depression or inverted T-waves.\n\u2014 Often, though not always, associated with partial occlusions.\n* Some patients also develop pathological Q waves.\n\n**Mural Thickness**\n* **Transmural**: the ischemia traverses the width of the myocardial tissue.\n* **Subendocardial**: only the inner one-third of the myocardium. \n# Be aware that earlier publications often equated transmural MI with Q-wave MIs; however, autopsy reports failed to confirm this association, and these classification schemes have largely been replaced by the labels STEMI and NSTEMI.  \n\n**Etiology**\n# Based on 2018 publication by the Joint European Society of Cardiology\/American Heart Association\/World Heart Federation Task Force for the Universal Definition of Myocardial Infarction.  \n\t\n**MI Type 1**: \n\u2014 Spontaneous myocardial infarctions caused by **thrombi**, and are usually the result of plaque rupture or erosion. \n\u2014 Remind ourselves that plaque rupture occurs when thin-capped plaques with lipid cores produce red thrombi, and, that erosion occurs when thick-capped plaques produce white thrombi.\n\u2014 MI Type 1 is often, though not always, associated with obstructive coronary artery disease.\n\n**MI Type 2**:\n\u2014 Occur secondary to other conditions; they are the result of conditions that produce non-thrombotic mismatches between oxygen supply and demand, including microvascular dysfunction, hypertension, atherosclerosis, and vasospasm.\n\u2014 Thus, treatment for and prevention of MI Type 2 involves discovery of the underlying causes. \n\t\n**MI Type 3**:\n\u2014 There is evidence of ischemia, but biomarkers are unobtainable due to death or other events that preclude collection. \n\n**MI Types 4 and 5** are associated with revascularization procedures:\n\u2014 Type 4a is associated with Percutaneous Coronary Intervention (PCIs).\n\u2014 Type 4b is specifically associated with stent and scaffold PCIs.\n\u2014 Type 4c is characterized by restenosis associated with PCI.\n\u2014 Type 5 is associated with coronary artery bypass grafting. \n\n\u003E ### **Myocardial Infarction vs Injury**\t\n\nWe start this investigation when a patient has elevated cardiac troponin values.\n\nIf elevated levels are stable, the patient likely has chronic myocardial injury (which could be caused by structural heart disease, for example).\n\nHowever, if the troponin levels rise and fall, we\u0027ll need to determine whether ischemia is present.\n\nIf no ischemia is present, then the patient has myocardial injury, which could be caused by [myocarditis](\/term\/pathology\/myocarditis) or other conditions.\n\nIf ischemia is present, then the patient has an acute myocardial infarction, and we need to establish the presence or absence of thrombus.\n\nIf thrombus is present, it\u0027s a myocardial infarction Type 1.\n\nIf there is no thrombus, then we conclude that an underlying condition has produced a mismatch between oxygen supply and demand, and we classify the event as Type II MI. 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