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| Acute Myocardial Infarct |
| Etiology • Atherosclerotic coronary stenosis +/- thrombosis. • Less common causes: emboli from mural thrombi, paradoxical embolism, or endocarditis; coronary spasm; polyarteritis; Takayasu's disease; Kawasaki syndrome (infancy and childhood); extension of dissecting aortic aneurysm. • Anomalous origin of left coronary artery from pulmonary trunk. |
| Pathogenesis • Endothelium lining atheromatous plaque torn by ulceration, plaque hemorrhage, or fissuring. • Activated platelets adherent to exposed collagen and plaque contents yield ADP boosting massing of platelets, which produce coagulant factors thromboxane A2, serotonin, and platelet factors 3 &4 with expanding occlusive thrombosis, abetted by tissue thromboplastin release. , |
| Epidemiology • The same risk factors as for atherosclerosis, fatty diets, hypertension, diabetes, smoking, etc. • 1,500,000 cases yearly, with 30% mortality. • May occur at any age, but frequency rises with advancing age, 5% occurring under age 40, and only 45% under age 65. • Low incidence in women rises in postmenopausal years, when estrogen relacement is protective. |
| General Gross Description • Lesions not visible before 18-24 hours after onset. • Size variable up to entire transverse sectional area. • May involve partial (subendocardial) or full (transmural) thickness of left ventricular wall. • Earliest change is a poorly defined pale area, some with hemorrhagic changes. Area defined better with time, turning yellow with a pink margin of organizing tissue, and, finally, a discrete scar. |
| General Microscopic Description • Earliest changes, at 4-12 hrs., are nuclear necrosis, muscle coagulative necrosis, neutrophils, and non-contracting (dead) marginal wavy fibers, which may appear histologically viable. • Frank coagulative necrosis at 24-72 hours, loss of fiber nuclei, and heavy neutrophilic infiltrate. • Macrophagic phagocytic activity and early organization at 3-7 days; healed scar by 7 weeks. |
| Clinical Correlation Clinical Correlation: • Crushing chest pain and variants, including mimicry of acute abdomen, absent in 15% asymptomatic cases. • EKG's and serum creatine phosphokinase MB isoenzyme (CPK-MB) and lactic dehydrogenase (LDH) important. • Complications include arrhythmias, shock, heart failure, cardiac rupture, and pulmonary emboli. • 30% mortality with 20% dying before admission. • Late complications are mural thrombi and aneurysms. |
| References • Cotran RS etal. Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 495, 524-41 • Harrison's Principles of Internal Medicine, 13th Ed: Isselbach et. al. (eds). New York, McGraw-Hill, 1994, p.1066 |
| Acute Myocardial Infarct |
| Synopsis by: J. Hasson M.D. (T33010M54720)[136] |
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