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Circulation. 2000;102:IV-24-IV-33

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(Circulation. 2000;102:IV-24.)
© 2000 American Heart Association, Inc.


Special Anniversary Issue

Valvular Heart Disease

Shahbudin H. Rahimtoola, MB, FRCP; Robert L. Frye, MD

From the Griffith Center, Division of Cardiology, Department of Medicine, Los Angeles County and University of Southern California Medical Center, Keck School of Medicine of the University of Southern California; and the Division of Cardiology, Department of Internal Medicine, Mayo Clinic and Foundation, Mayo Medical School, Rochester, Minn.

Science is about the systematic collection of data and the interpretation of that data. Dr Stanley B. Prusiner 1997 Nobel Laureate in Physiology/Medicine

Era Before 1950

In 1950, rheumatic valvular heart disease (VHD) was the most common cause of VHD. The link between streptococcal infection and rheumatic fever was established, and a successful trial of penicillin prophylaxis against rheumatic fever was reported.1 In 1944, Jones published a seminal article on diagnosis of rheumatic fever.2 The American Heart Association (AHA) and Circulation played an important role in communicating the importance of (1) penicillin prophylaxis, which resulted in a dramatic reduction of rheumatic fever and rheumatic VHD, and (2) diagnosis of rheumatic fever, by revising the Jones criteria in 1956, 1965, 1984, and most recently in 1992.3

It was well recognized that the mitral valve was the valve most commonly affected in rheumatic heart disease. As a consequence, closed-chest mitral commissurotomy for mitral stenosis (MS) was the most common early and successful cardiac surgical intervention. 1950 was the first year of Circulation, and one of the articles published that year described the surgical experience in 8 patients.4

The etiology of mitral regurgitation (MR) in 1950 was rheumatic carditis; mitral valve prolapse (MVP) was not even recognized. As late as 1958, the following quote reflects the lack of recognition of MVP: "mid- and late systolic clicks are commonly produced by the tensing of pleuropericardial adhesions"; thus, MVP was considered to be of extracardiac origin.5

Circulation in 1950 had a smaller number of articles regarding VHD . . . [Full Text of this Article]




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