| • Outflow tract of left ventricle. Note: aortic valve;
endocardial surface of interventricular septum (aterisk);
posterior papillary muscle arising from posterior wall
(1 arrow); anterolateral wall of left ventricle (double asterisk).
• Subendocardial scarring, a healed infarct of posterior wall of left ventricle, and apical portions of anterior wall and interventricular septum (2 arrows). |
| Old 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. |
| Clinical |
• 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 troponin important. • Complications include arrhythmias, shock, heart
failure, and cardiac rupture. • Late complications are mural thrombi and aneurysms. |
| 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 Micro 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. |
| Reference |
• 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
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