Essentials of Diagnosis
- Sudden but not instantaneous development of prolonged (> 30 minutes) anterior chest discomfort (sometimes felt as “gas” or pressure) that may produce arrhythmias, hypotension, shock, or cardiac failure.
- Rarely painless, masquerading as acute congestive heart failure, syncope, stroke, or shock.
- Electrocardiography: ST segment elevation or depression, evolving Q waves, symmetric inversion of T waves.
- Elevation of cardiac enzymes (CK-MB, troponin T, or troponin I).
- Appearance of segmental wall motion abnormality by imaging techniques.
Myocardial infarction results from prolonged myocardial ischemia, precipitated in most cases by an occlusive coronary thrombus at the site of a preexisting (though not necessarily severe) atherosclerotic plaque. More rarely, infarction may result from prolonged vasospasm, inadequate myocardial blood flow (eg, hypotension), or excessive metabolic demand. Very rarely, myocardial infarction may be caused by embolic occlusion, vasculitis, aortic root or coronary artery dissection, or aortitis. Cocaine is a cause of infarction, which should be considered in young individuals without risk factors.
The location and extent of infarction depend upon the anatomic distribution of the occluded vessel, the presence of additional stenotic lesions, and the adequacy of collateral circulation. Thrombosis in the anterior descending branch of the left coronary artery results in infarction of the anterior left ventricle and interventricular septum. Occlusion of the left circumflex artery produces anterolateral or posterolateral infarction. Right coronary thrombosis leads to infarction of the posteroinferior portion of the left ventricle and may involve the right ventricular myocardium and interventricular septum. The arteries supplying the atrioventricular node and the sinus node more commonly arise from the right coronary; thus, atrioventricular block at the nodal level and sinus node dysfunction occur more frequently during inferior or right-sided infarctions. Individual variation in coronary anatomy and the presence of collateral vessels can make the prediction of coronary anatomy from infarct location imperfect.
Infarctions are often classified as transmural if the classic electrocardiographic evolution of ST segment elevation to Q waves was observed or nontransmural or subendocardial if pain, enzyme elevations, and ST-T wave changes occurred in the absence of new Q waves. However, on pathologic examination, most infarctions involve the subendocardium predominantly, and some transmural extension is common even in the absence of Q waves. Thus, a better classification is Q wave versus non-Q wave infarction. The latter generally results from incomplete occlusion or spontaneous lysis of the thrombus and often signifies the presence of additional jeopardized myocardium; it is associated with a higher incidence of reinfarction and recurrent ischemia.
The size and anatomic location of an infarction determine the acute course, the early complications, and the long-term prognosis. Hemodynamic stability is related to extent of necrosis. In small infarctions, cardiac function is normal, whereas with more extensive damage, early heart failure and hypotension (cardiogenic shock) may appear. Preventing extension of an infarct and subsequent myocardial injury is a major goal of early management. The complications of acute infarction are discussed below.
Myocardial infarction redefined-a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol 2000;36:959.
Tavazzi L: Clinical epidemiology of acute myocardial infarction. Am Heart J 1999;138(2 Part 2):S48.
Essentials of Diagnosis
C. Laboratory Findings
E. Chest X-Ray
G. Scintigraphic Studies
H. Hemodynamic Measurements
B. Thrombolytic Therapy
C. Acute PTCA and Stenting for ST Segment Elevation Myocardial Infarction
D. Initial Management of Non-ST-Segment Elevation Myocardial Infarction
E. General Measures
G. Beta-Adrenergic Blocking Agents
I. Angiotensin-Converting Enzyme (ACE) Inhibitors
J. Antiarrhythmic Prophylaxis
K. Calcium Channel Blockers
A. Postinfarction Ischemia
C. Myocardial Dysfunction
D. Right Ventricular Infarction
E. Mechanical Defects
F. Myocardial Rupture
G. Left Ventricular Aneurysm
I. Mural Thrombus
A. Risk Stratification
B. Secondary Prevention
C. ACE Inhibitors in Patients With Left Ventricular Dysfunction
Revision date: June 20, 2011
Last revised: by Janet A. Staessen, MD, PhD