Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and/or diaphoresis. Diagnosis is by electrocardiography (ECG) and the presence or absence of serologic markers. Treatment is antiplatelet drugs, anticoagulants, nitrates, beta-blockers, statins, and reperfusion therapy. For ST-segment-elevation myocardial infarction, emergency reperfusion is via fibrinolytic drugs, percutaneous intervention, or, occasionally, coronary artery bypass graft surgery. For non-ST-segment-elevation myocardial infarction, reperfusion is via percutaneous intervention or coronary artery bypass graft surgery. Show
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:
MI affects predominantly the left ventricle (LV), but damage may extend into the right ventricle (RV) or the atria. An inferoposterior infarction causes 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 infarcts tend 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 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. ST-segment elevation myocardial infarction (STEMI, transmural MI) is myocardial necrosis with ECG changes showing ST-segment elevation that is not quickly reversed by nitroglycerin. Troponin I or troponin T and CK are elevated.
Usually, the first symptom of infarction is deep, substernal, visceral pain, described as aching or pressure, often radiating to the back, jaw, left arm, right arm, shoulders, or all of these areas. The pain is similar to angina pectoris Symptoms and Signs Angina pectoris is a clinical syndrome of precordial discomfort or pressure due to transient myocardial ischemia without infarction. It is typically precipitated by exertion or psychologic stress... read more but is usually more severe and long-lasting; more often accompanied by dyspnea, diaphoresis, nausea, and/or vomiting; and relieved little or only temporarily by rest or nitroglycerin. However, discomfort may be mild; about 20% of acute MIs are silent (ie, asymptomatic or causing vague symptoms not recognized as illness by the patient), more commonly in patients with diabetes. Patients often interpret their discomfort as indigestion, particularly because spontaneous relief may be falsely attributed to belching or antacid consumption. Some patients present with syncope. Women are more likely to present with atypical chest discomfort. Older patients may report dyspnea more than ischemic-type chest pain. In severe ischemic episodes, the patient often has significant pain and feels restless and apprehensive. Nausea and vomiting may occur, especially with inferior MI. Dyspnea and weakness due to LV failure, pulmonary edema, shock, or significant arrhythmia may dominate. Skin may be pale, cool, and diaphoretic. Peripheral or central cyanosis may be present. Pulse may be thready, and blood pressure is variable, although many patients initially have some degree of hypertension during pain. In right ventricular (RV) infarction, signs include elevated RV filling pressure, distended jugular veins (often with Kussmaul
sign Neck veins
(See also algorithm .) Evaluation begins with initial and serial ECG and serial measurements of cardiac markers Cardiac markers Acute coronary syndromes result from acute obstruction of a coronary artery. Consequences depend on degree and location of obstruction and range from unstable angina to non–ST-segment elevation... read more to help distinguish between unstable angina Unstable Angina Unstable angina results from acute obstruction of a coronary artery without myocardial infarction. Symptoms include chest discomfort with or without dyspnea, nausea, and diaphoresis. Diagnosis... read more , ST segment elevation myocardial infarction (STEMI), and non ST segment elevation myocardial infarction (NSTEMI). This distinction is the center of the decision pathway because fibrinolytics Fibrinolytics Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more benefit patients with STEMI but may increase risk for those with NSTEMI. Also, urgent cardiac catheterization is indicated for patients with acute STEMI but not generally for those with NSTEMI. Acute lateral left ventricular infarction (tracing obtained within a few hours of onset of illness)There is striking hyperacute ST-segment elevation in leads I, aVL, V4, and V6 and reciprocal depression in other leads. Lateral left ventricular infarction (after the first 24 hours)ST segments are less elevated; significant Q waves develop and R waves are lost in leads I, aVL, V4, and V6. Lateral left ventricular infarction (several days later)Significant Q waves and loss of R-wave voltage persist. ST segments are now essentially isoelectric. The ECG will probably change only slowly over the next several months. Acute inferior (diaphragmatic) left ventricular infarction (tracing obtained within a few hours of onset of illness)There is hyperacute ST-segment elevation in leads II, III, and aVF and reciprocal depression in other leads. Inferior (diaphragmatic) left ventricular infarction (after the first 24 hours)Significant Q waves develop with decreasing ST-segment elevation in leads II, III, and aVF. Inferior (diaphragmatic) left ventricular infarction (several days later)ST segments are now isoelectric. Abnormal Q waves in leads II, III, and aVF indicate that myocardial scars persist. Pathologic Q waves are not necessary for the diagnosis. The ECG must be read carefully because ST-segment elevation may be subtle, particularly in the inferior leads (II, III, aVF); sometimes the reader’s attention is mistakenly focused on leads with ST-segment depression. If symptoms are characteristic, ST-segment elevation on ECG has a specificity of 90% and a sensitivity of 45% for diagnosing myocardial infarction. Serial tracings (obtained every 8 hours for 1 day, then daily) showing a gradual evolution toward a stable, more normal pattern or development of abnormal Q waves over a few days tends to confirm the diagnosis. If right ventricular (RV) infarction is suspected, a 15-lead ECG is usually recorded; additional leads are placed at V4-6R, and, to detect posterior infarction, V8 and V9. Right ventricular (VR) leads VR1 through VR6ECG diagnosis of MI is more difficult when a left bundle branch block configuration is present because it resembles STEMI changes. ST-segment elevation concordant with the QRS complex strongly suggests MI as does > 5-mm ST-segment elevation in at least 2 precordial leads. But generally, any patient with suggestive symptoms and new-onset (or not known to be old) left bundle branch block is treated as for STEMI. Cardiac markers (serum markers of myocardial cell injury) are cardiac enzymes (eg, creatine kinase-MB isoenzyme [CK-MB]) and cell contents (eg, troponin I, troponin T, myoglobin) that are released into the bloodstream after myocardial cell necrosis. The markers appear at different times after injury, and levels decrease at different rates. Sensitivity and specificity for myocardial cell injury vary significantly among these markers, but the troponins (cTn) are the most sensitive and specific and are the markers of choice. Several highly sensitive assays of cardiac troponin (hs-cTn) that are also very precise are available. These assays can reliably measure cTn levels (T or I) as low as 0.003 to 0.006 ng/mL (3 to 6 pg/mL); some research assays go as low as 0.001 ng/mL (1 pg/mL). Previous, less sensitive methods of measuring cTn were unlikely to detect cTn except in patients who had an acute cardiac disorder. Thus a "positive" cTn result (ie, above the limit of detection) was very specific. However, the hs-cTn tests can detect small amounts of cTn in many healthy people. Thus, hs-cTn levels need to be referenced to the normal range and are defined as "elevated" only when higher than 99% of the reference population. Furthermore, although an elevated cTn level indicates myocardial cell injury, it does not indicate the cause of the damage (although any cTn elevation increases the risk of adverse outcomes in many disorders). In addition to acute coronary syndrome (ACS), many other cardiac and non-cardiac disorders can cause the hs-cTn measurement to be elevated (see table ); not all elevated hs-cTn measurements represent myocardial infarction, and not all myocardial necrosis results from an acute coronary syndrome event even when the etiology is ischemic. However, by detecting lower levels of cTn, hs-cTn assays enable earlier identification of MI than other assays and have replaced other cardiac marker tests in many centers. Patients suspected of having a myocardial infarction should have a hs-cTn level measured on presentation and 2 to 3 hours later (at 0 and 6 hours if using a standard cTn assay). The patient's pre-test probability of disease is estimated clinically based on:
A high pre-test probability plus an elevated cTn level is highly suggestive of myocardial infarction, whereas a low pre-test probability plus a normal cTn is unlikely to represent myocardial infarction. Diagnosis is more challenging when test results are discordant with pre-test probability, in which case serial cTn levels often help. A patient with low pre-test probability and an initially slightly elevated cTn that remains stable on repeat testing probably has non-ACS cardiac disease (eg, heart failure, stable coronary artery disease). However, if the repeat level rises significantly (ie, > 20 to 50%) the likelihood of myocardial infarction becomes much higher. If a patient with high pre-test probability has a normal cTn level that rises > 50% when the cTc is re-measured, myocardial infarction is likely; continued normal levels (often including at 6 hours and beyond when suspicion is high) suggest the need to pursue an alternate diagnosis. Angiography is obtained urgently for patients with STEMI, patients with persistent chest pain despite maximal medical therapy, and patients with complications (eg, markedly elevated cardiac markers, presence of cardiogenic shock, acute mitral regurgitation, ventricular septal defect, unstable arrhythmias). Patients with uncomplicated NSTEMI whose symptoms have resolved typically undergo angiography within the first 24 to 48 hours of hospitalization to detect lesions that may require treatment. After initial evaluation and therapy, coronary angiography may be used in patients with evidence of ongoing ischemia (ECG findings or symptoms), hemodynamic instability, recurrent ventricular tachyarrhythmias, and other abnormalities that suggest recurrence of ischemic events. Some experts also recommend that angiography be done before hospital discharge in patients with STEMI who have inducible ischemia on stress imaging or an ejection fraction < 40%. Risk should be estimated via formal clinical risk scores (eg, Thrombosis in Myocardial Infarction [TIMI]) or a combination of the following high-risk features:
For patients receiving reperfusion (fibrinolysis or PCI), in-hospital mortality is 5 to 6%, versus 15% for patients eligible for reperfusion who do not receive reperfusion therapy. In centers with established primary PCI programs, in-hospital mortality is reported to be < 5%.
Mortality rates tend to be higher in women and in patients with diabetes. Mortality rate of patients who survive initial hospitalization is 8 to 10% in the year after acute myocardial infarction. Most fatalities occur in the first 3 to 4 months. Persistent ventricular arrhythmia, heart failure, poor ventricular function, and recurrent ischemia indicate high risk. Many authorities recommend stress ECG before hospital discharge or within 6 weeks. Good exercise performance without ECG abnormalities is associated with a favorable prognosis; further evaluation is usually not required. Poor exercise performance is associated with a poor prognosis. Cardiac performance after recovery depends largely on how much functioning myocardium survives the acute attack. Acute damage adds to scars from previous infarcts. When > 50% of left ventricular mass is damaged, prolonged survival is unusual. 
On arrival to the emergency department, the patient's diagnosis is confirmed. Drug therapy and timing of revascularization depend on the clinical picture and diagnosis. For STEMI, reperfusion strategy can
include fibrinolytic therapy or immediate PCI. For patients with NSTEMI, angiography may be done within 24 to 48 hours of admission if the patient is clinically stable. If the patient is unstable (eg, ongoing symptoms, hypotension or sustained arrhythmias), then angiography must be done immediately (see figure
Approach to myocardial infarction
Approach to myocardial infarction Approach to myocardial infarction
All patients should be given antiplatelet
drugs Antiplatelet Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more
, anticoagulants
Anticoagulant Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more , and if chest pain is present, antianginal
drugs. The specific drugs used depend on the reperfusion strategy and other factors; their selection and use is discussed in Drugs for Acute Coronary
Syndrome Drugs for Acute Coronary Syndromes Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more
. Other drugs, such as beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins, should also be given (see table Drugs for
Coronary Artery Disease Drugs for Coronary Artery Disease* Patients with acute myocardial infarction should be given the following (unless contraindicated):
All patients are given aspirin 160 to 325 mg (not enteric-coated), if not contraindicated, at presentation and 81 mg once a day indefinitely thereafter. Chewing the first dose before swallowing quickens absorption. Aspirin reduces short-term and long-term mortality risk. In patients undergoing PCI, a loading dose of clopidogrel (300 to 600 mg orally once), prasugrel (60 mg orally once), or ticagrelor (180 mg orally once) improves outcomes, particularly when administered 24 hours in advance. For urgent PCI, prasugrel and ticagrelor are more rapid in onset and may be preferred.
Consider a glycoprotein IIb/IIIa inhibitor during PCI for high-risk lesions (high thrombus burden, no reflow). Abciximab, tirofiban, and eptifibatide appear to have equivalent efficacy, and the choice of drug should depend on other factors (eg, cost, availability, familiarity). This agent is continued for 6 to 24 hours. Chest pain can be treated with nitroglycerin or sometimes morphine. Nitroglycerin is preferable to morphine, which should be used judiciously (eg, if a patient has a contraindication to nitroglycerin or is in pain despite nitroglycerin therapy).
Nitroglycerin
Nitrates Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more is initially given sublingually, followed by continuous
IV drip if needed. Morphine 2 to 4 mg IV, repeated every 15 minutes as needed, is highly effective but can depress respiration, can reduce myocardial contractility, and is a potent venous vasodilator. Evidence also suggests that morphine use interferes with some P2Y12 receptor inhibitors. A large retrospective trial showed that morphine may increase mortality in patients with acute myocardial infarction
(1, 2
Treatment references Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and/or diaphoresis... read more
Standard therapy for all patients with unstable angina includes beta-blockers, ACE inhibitors, and statins. Beta-blockers Beta-Blockers Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more are recommended unless contraindicated (eg, by bradycardia, heart block, hypotension, or asthma), especially for high-risk patients. Beta-blockers reduce heart rate, arterial pressure, and contractility, thereby reducing cardiac workload and oxygen demand. ACE inhibitors Other Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more may provide long-term cardioprotection by improving endothelial function. If an ACE inhibitor is not tolerated because of cough or rash (but not angioedema or renal dysfunction), an angiotensin II receptor blocker Other Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more may be substituted. Statins Other Drugs Treatment of acute coronary syndromes (ACS) is designed to relieve distress, interrupt thrombosis, reverse ischemia, limit infarct size, reduce cardiac workload, and prevent and treat complications... read more are also standard therapy regardless of lipid levels and should be continued indefinitely.
For STEMI
patients, emergency PCI is the preferred treatment of ST-segment elevation myocardial infarction when available in a timely fashion (door to balloon-inflation time < 90 minutes) by an experienced operator
(3
Treatment references Acute myocardial infarction is myocardial necrosis resulting from acute obstruction of a coronary artery. Symptoms include chest discomfort with or without dyspnea, nausea, and/or diaphoresis... read more
Unstable NSTEMI patients (ie, those with ongoing symptoms, hypotension, or sustained arrhythmias) should proceed directly to the cardiac catheterization laboratory to identify coronary lesions requiring PCI or coronary artery bypass grafting (CABG). For uncomplicated NSTEMI patients, immediate reperfusion is not as urgent because a completely occluded infarct-related artery at presentation is uncommon. Such patients typically undergo angiography within the first 24 to 48 hours of hospitalization to identify coronary lesions requiring PCI or CABG. Fibrinolytics are not indicated for any NSTEMI patients. Risk outweighs potential benefit.
Patients who did not have coronary angiography during admission, have no high-risk features (eg, heart failure, recurrent angina, ventricular tachycardia or ventricular fibrillation after 24 hours, mechanical complications such as new murmurs, shock), and have an ejection fraction > 40% whether or not they received fibrinolytics usually should have stress testing of some
sort before or shortly after discharge (see table Functional Evaluation After Myocardial Infarction
Functional Evaluation After Myocardial Infarction Functional Evaluation After Myocardial Infarction
The acute illness and treatment of myocardial infarction should be used to strongly motivate the patient to modify risk factors. Evaluating the patient’s physical and emotional status and discussing them with the patient, advising about lifestyle (eg, smoking, diet, work and play habits, exercise), and aggressively managing risk factors may improve prognosis. On discharge, all patients should be on appropriate antiplatelet drugs, statins, antianginals, and other drugs based on comorbidities.
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