<B>Acute MI </B>

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Acute MI

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, abbetted 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, neutrophiles, 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 neutrophillic infiltrate.
• Macrophagic phagocytic activity and early organization at 3-7 days; healed scar by 7 weeks.

Clinical Correlations:
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:
•1. Robbins Pathological Basis of Disease, 5th Edition pp. 495, 524-541 •2. Harrison's Principles of Internal Medicine, 13th Edition, p. 1066 •3. Cardiovascular Pathology, edited by Malcolm D. Silver, 2nd Edition, pp. 674-676.