Elsevier

American Heart Journal

Volume 69, Issue 1, January 1965, Pages 22-30
American Heart Journal

Clinical communication
The masking of aortic stenosis by mitral stenosis

https://doi.org/10.1016/0002-8703(65)90212-7Get rights and content

Abstract

The clinical data (signs and symptoms, x-ray and electrocardiographic analysis) and hemodynamic findings in 10 patients with severe mitral and aortic stenosis have been presented.

All patients had signs, symptoms, and radiologic stigmata of mitral stenosis. Normal sinus rhythm was present in 7 of the 10 patients, and right ventricular hypertrophy in only 3. Many of the features usually considered to be a sine qua non of severe aortic stenosis were absent in these cases. However, all patients had at least one manifestation other than the typical murmur of aortic stenosis (e.g., angina, syncope, abnormal carotid pulse, left ventricular enlargement by x-ray or ECG examination, calcification of the aortic valve, or dilatation of the aortic root).

All patients with ECG evidence of left ventricular hypertrophy also had angina pectoris and significantly elevated timetension indices. This was due largely to a prolongation of the systolic ejection period. It is suggested that ECG evidence of left ventricular hypertrophy in this clinical setting, without significant mitral or aortic regurgitation, signifies severe left ventricular stress and severe aortic stenosis.

A decrease in cardiac output secondary to mitral stenosis reduces the differences in pressure across the aortic valve and, there-fore, reduces the total left ventricular stress, as reflected by the time-tension index. It is believed that this reduction in output is the basic cause of inconstancy of symptoms and signs of aortic stenosis in patients with tight mitral and aortic stenosis.

When aortic stenosis is suspected in patients with severe mitral stenosis, the only certain method of quantitative evaluation is catheterization of the left side of the heart, with simultaneous measurement of transvalvular pressure differences and blood flow.

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This work was supported in part by grants from the Life Insurance Medical Research Fund, The National Heart Institute, United States Public Health Service (Grants H-0450, HTS-5234, and HTS-5550), and the American Heart Association.

Postdoctoral Research Fellow, National Heart Institute, United States Public Health Service, Present address: Department of Medicine, Northwestern University Medical School, 303 East Chicago Ave., Chicago, Ill., 60611.

∗∗

Research Fellow, American Heart Association.

∗∗∗

Resident in Radiology, Peter Bebt Brigham Hospital

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