Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1983;67:399-404

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ozawa, Y.
Right arrow Articles by Craige, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ozawa, Y.
Right arrow Articles by Craige, E.

Circulation, Vol 67, 399-404, Copyright © 1983 by American Heart Association


ARTICLES

Origin of the third heart sound. II. Studies in human subjects

Y Ozawa, D Smith and E Craige

We report noninvasive and invasive studies designed to clarify the mechanism of the third heart sound (S3) in humans. The noninvasive observations were made using a miniature accelerometer attached to the skin surface at the cardiac apex. In subjects with no S3, the tracings were either flat or showed very low undulations throughout diastole. Those with an S3, however, demonstrated a distinct reduction of acceleration, or negative jerk, of the rapid filling movement at the apex at the time of the sound. The invasive studies in the cardiac catheterization laboratory consisted of frame-by-frame measurements of left ventricular dimensions in the transverse and long axes during early diastole in patients with diastolic overload abnormalities to investigate the temporal sequence of filling in these two principal axes. The maximal long-axis filling rate occurred after the short axis, a finding that helps to resolve a discrepancy noted in the time of maximal short-axis filling and S3 production. These studies support the concept that the S3 is due to a sudden intrinsic limitation of longitudinal expansion of the left ventricular wall during early diastolic filling, resulting in a negative jerk that is transmitted to the skin surface.


This article has been cited by other articles:


Home page
Arch Intern MedHome page
G. Marcus, J. Vessey, M. V. Jordan, M. Huddleston, B. McKeown, I. L. Gerber, E. Foster, K. Chatterjee, C. E. McCulloch, and A. D. Michaels
Relationship between accurate auscultation of a clinically useful third heart sound and level of experience.
Arch Intern Med, March 27, 2006; 166(6): 617 - 622.
[Abstract] [Full Text] [PDF]


Home page
JAMAHome page
G. M. Marcus, I. L. Gerber, B. H. McKeown, J. C. Vessey, M. V. Jordan, M. Huddleston, C. E. McCulloch, E. Foster, K. Chatterjee, and A. D. Michaels
Association Between Phonocardiographic Third and Fourth Heart Sounds and Objective Measures of Left Ventricular Function
JAMA, May 11, 2005; 293(18): 2238 - 2244.
[Abstract] [Full Text] [PDF]