| • View of the superior surface of a transverse section of
the heart, with the anterior surface facing upwards.
• Note the acute infarct involving the anterior wall of
left ventricle and the adjoining anterior aspect of the
IV septum (2 white arrows). The lesion has vague
margins and colored shades of tan and pink.
• Note contrasting old scars in the posterior wall, septum, and adjoining right ventricle (2 black arrows) |
| 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. |
| Clinical |
| Clinical Correlation:
• Crushing chest pain and variants, including mimicry
of acute abdomen, absent in 15% asymptomatic cases. • EKG^s and troponin, serum creatine phosphokinase MB isoenzyme
(CPK-MB) and lactic dehydrogenase (LDH) important. • Complications include arrhythmias, shock, heart
failure, cardiac rupture, and pulmonary emboli. • 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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