• 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|
• 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
• 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.
• The same risk factors as for
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.
• 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
• 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.
• 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