This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

HARRY GROSS, M.D.; WILLIAM H. STERNBERG, M.D.

Arch Intern Med. 1939;64(2):249-267.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Since Heberden's¹ famous description of the clinical syndrome of angina pectoris and the subsequent finding of associated calcification of the coronary arteries by Jenner² and his pupil Parry,³ the controversy about the etiologic role of narrowing of the coronary arteries in Heberden's syndrome has never ceased to hold interest. Until recently all objections have been based on the frequent disparity between the anatomic and the clinical features. The difficulty in correlating morbid anatomy, on the one hand, with disturbed physiology, on the other, has been epitomized by Aschoff.⁴ Similar discrepancies between the location and size of the myocardial infarction and the corresponding vascular lesion have been indicated.

The occurrence of major myocardial damage with a minimum or even absence of coronary disease is not rare. S. A. Levine⁵ cited 11 of his own cases studied at autopsy in which major myocardial lesions were accompanied by corresponding disease of the coronary . . . [Full Text PDF of this Article]

Author Affiliations
NEW YORK

From the Medical Division and the Laboratory Division of Montefiore Hospital.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?