ETIOPATHOGENESIS OF MYOCARDIAL INFARCTION

ETIOPATHOGENESIS OF MYOCARDIAL INFARCTION

• Etiology of IHD has been categorized into

  • Coronary atherosclerosis

  • Superadded changes in coronary atherosclerosis

  • Non-atherosclerotic causes

• Coronary atherosclerosis

  • 90% cases of IHD

  • Risk factors of atherosclerosis

  • Pathogenesis of atherosclerosis

  • Distribution

    • Can occur in one or more of the three major coronary arteries

    • Highest incidence is in anterior descending branches of left coronary

    • Next in decreasing frequency is right coronary artery and circumflex branches of left coronary artery

  • Location – area of severest involvement is about 3 to 4 cm from the coronary ostia and at or near the bifurcation of arteries

  • Morphology of atherosclerotic plaque

  • Atherosclerotic plaque may bulge into lumen causing obstruction of lumen

  • Further complications calcification, thrombosis, ulceration, hemorrhage, rupture and aneurysm formation can occur

• Superadded changes in atherosclerosis

  • Acute coronary syndromes including acute MI, unstable angina and sudden ischemic death are due to superadded changes in pre existing atherosclerotic plaque

  • These changes are

    • Acute changes in ahtheromatous plaque

    • Coronary artery thrombosis

    • Local platelet aggregation and coronary spasm

• Acute changes in atheromatous plaque –

  • hemorrhage, fissuring or ulceration resulting in thrombosis and embolization of atheromatous debris

  • These changes occur due to coronary artery spasm, tachycardia, intraplaque hemorrhage and hypercholerolemia

• Coronary artery thrombosis

  • Ulceration of fixed chronic atheromatous plaque leads to initiation of thrombosis as the lipid core of the plaque is highly thrombogenic

  •  small fragments of thrombotic material embolizes to terminal branches causing microinfarcts of myocardium

• Local platelet aggregation and coronary spasm

  • Platelet aggregates on atheromatous plaque short of forming thrombus

  • These platelet aggregates release vasospasmic mediators such as thromboxane A2 causing vasospasm of already existing atherosclerotic plaque

• Non-atherosclerotic causes

  • Vasospasm – in association with platelet aggregation and as in cocaine abuse

  • Stenosis of coronary ostia- in conditions like aortic atherosclerotic plaque encroaching on opening of coronary ostia or extension of syphilitic aortitis

  • Arteritis – as in rheumatic arteritis, poly arteritis nodosa, thromboangitis obliterans, or other bacterial infection

  • Embolism – emboli from else where in the body may occlude coronary arteries and their branches

  • Thrombotic diseases – conditions with hypercoagulability of blood such as in shock, polycythemia vera, sickle cell anemia and thrombotic thrombocytopenic purpura

  • Trauma – penetrating or blunt  injury

  • Aneurysm –

    • dissecting aneurysm of the aorta into the coronary artery may produce thrombotic coronary occlusion

    • Rarely congenital, mycotic and syphilitic aneurysms may occur in coronary arteries

  • Compression – from outside by primary or secondary tumors of the heart may result in occlusion

References

1. Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition.

2. Harsh mohan. Text book of Pathology.8th edition.2019