In myocardial infarction (MI), a form of acute coronary syndrome, reduced blood flow through one or more coronary arteries initiates myocardial ischemia and necrosis. (See also“Coronary artery disease,” page 50.)
· Coronary artery stenosis or spasm
Predisposing risk factors
· Family history of heart disease
· Tobacco smoking
· Elevated serum triglyceride, total cholesterol, and low-density lipoprotein levels
· Diabetes mellitus, obesity
· Excessive intake of saturated fats, carbohydrates, or salt
· Sedentary lifestyle
· Stress or type A personality
· Drug use, especially cocaine and amphetamines
· Gender and age (most common in men and postmenopausal women)
If coronary artery occlusion causes prolonged ischemia, lasting longer than 30 to 45 minutes, irreversible myocardial cell damage and muscle death occur.
Occlusion of the circumflex branch of the left coronary artery causes a lateral wall infarction; occlusion of the anterior descending branch of the left coronary artery, an anterior wall infarction. True posterior or inferior wall infarctions generally result from occlusion of the right coronary artery or one of its branches.
Right ventricular infarctions can also result from right coronary artery occlusion, can accompany inferior infarctions, and may cause right-sided heart failure. In ST-elevation (transmural) MI, tissue damage extends through all myocardial layers; in non-ST-elevation (subendocardial) MI, damage occurs only in the innermost and, possibly, the middle layers.
All infarcts have a central area of necrosis surrounded by an area of potentially viable hypoxic injury, which may be salvaged if circulation is restored or may progress to necrosis. The zone of injury is surrounded by viable ischemic tissue.
The infarcted myocardial cells release cardiac enzymes and proteins. Within 24 hours, the infarcted muscle becomes edematous and cyanotic. During the next several days, leukocytes infiltrate the necrotic area and begin to remove necrotic cells, thinning the ventricular wall. Scar formation begins by the 3rd week after MI; by the 6th week, scar tissue is well established.
The scar tissue that forms on the necrotic area inhibits contractility. Compensatory mechanisms (vascular constriction, increased heart rate, and renal retention of sodium and water) try to maintain cardiac output. Ventricular dilation may also occur in a process called remodeling. MI may cause reduced contractility with abnormal wall motion, altered left ventricular compliance, reduced stroke volume, reduced ejection fraction, and elevated left ventricular end-diastolic pressure.
Signs and symptoms
· Persistent, crushing substernal chest pain that may radiate to the left arm, jaw, neck, or shoulder blades
· Cool extremities, perspiration, anxiety, restlessness
· Blood pressure and pulse initially elevated
· Shortness of breath and crackles
· Fatigue and weakness
· Nausea and vomiting
· Jugular vein distention
· S3 and S4 heart sounds, loud holosystolic murmur in apex
· Reduced urine output
Many older adults with MI may experience atypical symptoms (instead of chest pain), such as fatigue, dyspnea, falls, tingling of the extremities, nausea, vomiting, weakness, syncope, and confusion.
Diagnostic test results
· Serial 12-lead electrocardiography (ECG) reveals ST-segment depression or elevation. An ECG also identifies the location of MI, arrhythmias, hypertrophy, and pericarditis.
· Serial cardiac enzymes and proteins show a characteristic rise and fall—specifically, CK-MB, the proteins troponin T and I, and myoglobin.
· Complete blood count and other blood tests show elevated white blood cell count, C-reactive protein level, and erythrocyte sedimentation rate due to inflammation.
· Blood chemistry shows increased glucose levels following the release of catecholamines.
· Echocardiography shows ventricular wall motion abnormalities and detects septal or papillary muscle rupture.
· Chest X-rays show left-sided heart failure or cardiomegaly.
· Nuclear imaging scanning identifies areas of infarction and viable muscle cells.
· Cardiac catheterization identifies the involved coronary artery and provides information on ventricular function and volumes within the heart.
· Assessment of patients with chest pain in the emergency department within 10 minutes of symptom onset
· Morphine or meperidine (Demerol)
· Continuous cardiac monitoring
· I.V. fibrinolytic therapy
· Glycoprotein IIb/IIIa receptor blockers
· I.V. heparin
· Percutaneous transluminal coronary angioplasty with or without stent placement
· Atropine, lidocaine, transcutaneous pacing patches or a transvenous pacemaker, a defibrillator, and epinephrine
· Beta-adrenergic blockers, angiotensin-converting enzyme inhibitors, and magnesium sulfate
· Low-fat, low-cholesterol diet; smoking cessation; regular exercise
· Lifestye modifications
TISSUE DESTRUCTION IN MYOCARDIAL INFARCTION