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ISCHEMIC HEART DISEASE
Cardiac ischemia is usually secondary to coronary artery disease (CAD); it is themost common cause of death in the United States. It is most often seen in middle-age men and postmenopausal women.
Angina pectoris is due to transient cardiac ischemia without cell death resulting insubsternal chest pain.
· Stable angina (most common type) is caused by coronary artery atheroscle-rosis with luminal narrowing >75%. Chest pain is brought on by increased cardiac demand (exertional or emotional), and is relieved by rest or nitroglyc-erin (vasodilation). Electrocardiogram shows ST segment depression (suben-docardial ischemia).
· Prinzmetal variant angina is caused by coronary artery vasospasm and produces episodic chest pain often at rest; it is relieved by nitroglycerin (vasodilatation). Electrocardiogram shows transient ST segment elevation (transmural ischemia).
· Unstable or crescendo angina is caused by formation of a nonocclusive throm-bus in an area of coronary atherosclerosis, and is characterized by increasing frequency, intensity, and duration of episodes; episodes typically occur at rest. This form of angina has a high risk for myocardial infarction.
Myocardial infarction (MI) occurs when a localized area of cardiac muscle undergoescoagulative necrosis due to ischemia. It is the most common cause of death in the United States. The mechanism leading to infarction is coronary artery atheroscle-rosis (90% of cases). Other causes include decreased circulatory volume, decreased oxygenation, decreased oxygen-carrying capacity, or increased cardiac workload, due to systemic hypertension, for instance.
· Distribution of coronary artery thrombosis.The left anterior descendingartery (LAD) is involved in 45% of cases; the right coronary artery (RCA) is involved in 35% of cases; and the left circumflex coronary artery (LCA) is involved in 15% of cases.
Infarctions are classified as transmural, subendocardial, or microscopic.
· Transmural infarction (most common type) is considered to have occurredwhen ischemic necrosis involves >50% of myocardial wall. It is associated with regional vascular occlusion by thrombus. It causes ST elevated MIs (STEMIs) due to atherosclerosis and acute thromobosis.
· Subendocardial infarction is considered to have occurred when ischemicnecrosis involves <50% of myocardial wall. It is associated with hypoperfu-sion due to shock. ECG changes are not noted. This type of infarction occurs in a setting of coronary artery disease with a decrease in oxygen delivery or an increase in demand.
· Microscopic infarction is caused by small vessel occlusion due to vasculitis,emboli, or spasm. ECG changes are not noted.
The clinical presentation of MI is classically a sudden onset of severe “crushing” substernal chest pain that radiates to the left arm, jaw, and neck. The pain may be accompanied by chest heaviness, tightness, and shortness of breath; diaphoresis, nausea, and vomiting; jugular venous distension (JVD); anxiety and often “feeling of impending doom.” Electrocardiogram initially shows ST segment elevation. Q waves representing myocardial coagulative necrosis develop in 24–48 hours.
· Gross and microscopic sequence of changes.The microscopic and grosschanges represent a spectrum that is preceded by biochemical changes going from aerobic metabolism to anaerobic metabolism within minutes. The time intervals are variable and depend on the size of the infarct, as well as other factors.
Complications of MI include cardiac arrhythmias that may lead to sudden car-diac death; congestive heart failure; cardiogenic shock (>40–50% myocardium is necrotic); mural thrombus and thromboembolism; fibrinous pericarditis; ventricu-lar aneurysm; and cardiac rupture. Cardiac rupture most commonly occurs 3–7 days after MI, and has effects that vary with the site of rupture: ventricular free wall rupture causes cardiac tamponade; interventricular septum rupture causes left to right shunt; and papillary muscle rupture causes mitral insufficiency.
Sudden cardiac death is defined to be death within 1 hour of the onset of symp-toms. The mechanism is typically a fatal cardiac arrhythmia (usually ventricular fibrillation).
Coronary artery disease is the most common underlying cause (80%); other causes include hypertrophic cardiomyopathy, mitral valve prolapse, aortic valve stenosis, congenital heart abnormalities, and myocarditis.
Chronic ischemic heart disease is the insidious onset of progressive congestive heartfailure. It is characterized by left ventricular dilation due to accumulated ischemic myocardial damage (replacement fibrosis) and functional loss of hypertrophied non-infarcted cardiac myocytes.
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