cardiovascular disorders
Acute Myocardial Infarction (MI)
Pathophysiology of Acute MI
Myocardial infarction is defined as myocardial necrosis in a clinical setting consistent with myocardial ischemia ( Pathophysiology references ). These conditions can be satisfied by a rise of Symptoms of ischemia ECG changes indicative of new ischemia (significant ST/T changes or left bundle branch block) Development of pathologic Q waves Imaging evidence of new loss of myocardium or new regional wall motion abnormality Angiography or autopsy evidence of intracoronary thrombus Slightly different criteria are used to diagnose MI during and after percutaneous coronary intervention or coronary artery bypass grafting, and as the cause of sudden death. MI can be classified into 5 types based on etiology and circumstances: Type 1: Spontaneous MI caused by ischemia due to a primary coronary event (eg, plaque rupture, erosion, or fissuring; coronary dissection) Type 2: Ischemia due to increased oxygen demand (eg, hypertension), or decreased supply (eg, coronary artery spasm or embolism, arrhythmia, hypotension) Type 3: Related to sudden unexpected cardiac death Type 4a: Associated with percutaneous coronary intervention (signs and symptoms of myocardial infarction with cTn values > 5 × 99th percentile URL) Type 4b: Associated with documented stent thrombosis Type 5: Associated with coronary artery bypass grafting (signs and symptoms of myocardial infarction with cTn values > 10 × 99th percentile URL) MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria. usually results from obstruction of the right coronary or a dominant left circumflex artery; it is characterized by high RV filling pressure, often with severe Tricuspid Regurgitation and reduced cardiac output. Aninferoposterior infarctioncauses some degree of RV dysfunction in about half of patients and causes hemodynamic abnormality in 10 to 15%. RV dysfunction should be considered in any patient who has inferoposterior infarction and elevated jugular venous pressure with hypotension or shock. RV infarction complicating LV infarction significantly increases mortality risk. Anterior infarctstend to be larger and result in a worse prognosis than inferoposterior infarcts. They are usually due to left coronary artery obstruction, especially in the anterior descending artery; inferoposterior infarcts reflect right coronary or dominant left circumflex artery obstruction. Infarction may be Transmural Nontransmural Transmural infarcts involve the whole thickness of myocardium from epicardium to endocardium and are usually characterized by abnormal Q waves on ECG. Nontransmural (including subendocardial) infarcts do not extend through the ventricular wall and cause only ST-segment and T-wave (ST-T) abnormalities. Subendocardial infarcts usually involve the inner one third of myocardium, where wall tension is highest and myocardial blood flow is most vulnerable to circulatory changes. These infarcts may follow prolonged hypotension. Because the transmural depth of necrosis cannot be precisely determined clinically, infarcts are usually classified as STEMI or NSTEMI by the presence or absence of ST-segment elevation or Q waves on the ECG. Volume of myocardium destroyed can be roughly estimated by the extent and duration of CK elevation or by peak levels of more commonly measured cardiac troponins. (NSTEMI, subendocardial MI) is myocardial necrosis (evidenced by Cardiac markers in blood; troponin I or troponin T and CK will be elevated) without acute ST-segment elevation. ECG changes such as ST-segment depression, T-wave inversion, or both may be present. ST-segment elevation myocardial infarction(STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed bynitroglycerin. Troponin I or troponin T and CK are elevated. Myocardial infarction in the absence of obstructive coronary artery disease (MINOCA) is found in about 5 to 6% of patients with acute MI who undergo coronary angiography ( Pathophysiology references ). Patients with MINOCA tend to be younger, women, and without dyslipidemia. They tend to have myocardial necrosis without significant coronary atherosclerosis. Plaque disruption and coronary vasospasm are common in MINOCA. Coronary thrombosis or embolism and spontaneous coronary artery dissection are causes of MINOCA. Medical management should be based on the underlying mechanism for MINOCA in each patient. 1.Thygesen K, Alpert JS, Jaffe AS, et al, the Writing Group on behalf of the Joint ESC/ACCF/AHA/WHF Task Force for the Universal Definition of Myocardial Infarction: ESC/ACCF/AHA/WHF Expert Consensus Document Third Universal Definition of Myocardial Infarction.Circulation126:2020–2035, 2012. doi: 10.1161/CIR.0b013e31826e1058 2.Tamis-Holland JE, Jneid H, Reynolds HR, et al: Contemporary diagnosis and management of patients with myocardial infarction in the absence of obstructive coronary artery disease: A scientific statement from the American Heart Association.Circulation139:e891–e908, 2019. doi.org/10.1161/CIR.0000000000000670 