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(Circulation. 1972;46:1048.)
© 1972 American Heart Association, Inc.

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Pathology of Angina Pectoris

ZEEV VLODAVER M.D.¹; HENRY N. NEUFELD M.D.¹; JESSE E. EDWARDS M.D.¹

¹ From the Departments of Pathology of the Charles T. Miller Hospital, St. Paul, Minnesota, and of the University of Minnesota, Minneapolis, Minnesota.

Among the wide variety of causes of angina pectoris, two major categories may be recognized: the anatomic, causing arterial obstruction, and the functional.

The anatomic causes may be divided according to anatomic sites as follows: (1) the major coronary arterial trunks and their epicardial branches, (2) the coronary ostia at the aorta, and (3) the intramyocardial "small" arteries. The major coronary arteries are by far the most common sites for anatomic lesions. Atherosclerosis in its various anatomic manifestations is responsible for about 90% of the cases of angina. Commonly, hypertension and, less commonly, valvular disease are associated. The balance of cases of angina result from various states given below. Nonatheromatous diseases of the major coronary arteries include embolism, primary dissecting aneurysm of a coronary artery, arteritis, and anomalous communication of a coronary artery. Coronary ostial narrowing results from various diseases of the aorta including atherosclerosis, saccular and dissecting aneurysm, inflammation, and calcification of the aorta in relation to origin of a coronary artery. Lesions causing obstruction of the intramyocardial arteries are commonly part of systemic diseases such as hematologic, embolic, metabolic, and degenerative.

Functional causes of angina pectoris include aortic valvular disease and functionally related conditions, thyroid disease, and pulmonary hypertension.

Key Words: Myocardial ischemia • Small coronary arteries • Myocardial infarction • Coronary ostial obstruction • Nonatheromatous coronary disease • Hypertension

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