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Myocardial Infarction and ThromboembolismA Comparative Study in Boston and in Kyushu, Japan
IRA GORE, MD;
ALBERT E. HIRST, MD;
KENZO TANAKA, MD
Arch Intern Med. 1964;113(3):323-330.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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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
. . . [Full Text PDF of this Article]
Author Affiliations
BOSTON; LOS ANGELES; FUKUOKA, JAPAN
Department of Pathology, Boston University Medical Center, Massachusetts Memorial Hospital; Veterans Administration Hospital, West Roxbury; and Department of Nutrition, Harvard School of Public Health, Boston (Dr. Gore); Department of Pathology, School of Medicine, Loma Linda University, Los Angeles (Dr. Hirst); Department of Pathology, Kyushu University Medical School, Fukuoka, Japan (Dr. Tanaka).
Professor of Pathology, Boston University School of Medicine; Chief of Pathology, Massachusetts Memorial Hospitals, Boston (Dr. Gore); Associate Professor of Pathology, School of Medicine, Loma Linda University, Los Angeles (Dr. Hirst); Professor of Pathology, Kyushu University, Kyushu, Japan (Dr. Tanaka).
From the Veterans Administration Hospital, West Roxbury, Mass, and the Department of Nutrition, Harvard School of Public Health, Boston.
Footnotes
Received for publication Oct 17, 1963; accepted Oct 24.
Supported in part by grants-in-aid from the National Heart Institute (H-7327, H-3726, HE-02048, and H-5610), the Nutrition Foundation and the Fund for Research and Teaching, Department of Nutrition, Harvard School of Public Health.
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