Coronary occlusion is generally the result of two distinct but often coincident processes: One, atherosclerosis, progresses slowly to produce narrowing; the other, thrombosis, often apparently sudden, completes the obstruction of the lumen. While atherosclerosis-thrombosis is the usual sequence in the pathogenesis of coronary occlusion, occasionally atheroma alone is the cause and, exceptionally, thrombosis complicates relatively minor intimal disease. This description of two separate factors producing coronary obstruction does not exclude the probability that certain phases of blood coagulation, ie, deposition of fibrin, platelets, or both, may contribute to the development of atherosclerosis, a thesis originally proposed by Rokitansky 1 and revived and documented by Duguid and others2-4 who have found histologic evidence of incorporation of fibrin into atheromatous lesions.
The part played by increased thrombogenic activity in the blood of patients with ischemic heart disease is disputed. While some authors5-7 have reported increased coagulability based upon one or
GORE I, HIRST AE, TANAKA K. Myocardial Infarction and Thromboembolism: A Comparative Study in Boston and in Kyushu, Japan. Arch Intern Med. 1964;113(3):323–330. doi:10.1001/archinte.1964.00280090009003
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