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Research Article Free access | 10.1172/JCI106286

The role of inotropic variation in ventricular function during atrial fibrillation

Robert E. Edmands, Kalman Greenspan, and Charles Fisch

Department of Medicine, Indiana University School of Medicine and the Krannert Institute of Cardiology, Marion County General Hospital, Indianapolis, Indiana 46202

Find articles by Edmands, R. in: PubMed | Google Scholar

Department of Medicine, Indiana University School of Medicine and the Krannert Institute of Cardiology, Marion County General Hospital, Indianapolis, Indiana 46202

Find articles by Greenspan, K. in: PubMed | Google Scholar

Department of Medicine, Indiana University School of Medicine and the Krannert Institute of Cardiology, Marion County General Hospital, Indianapolis, Indiana 46202

Find articles by Fisch, C. in: PubMed | Google Scholar

Published April 1, 1970 - More info

Published in Volume 49, Issue 4 on April 1, 1970
J Clin Invest. 1970;49(4):738–746. https://doi.org/10.1172/JCI106286.
© 1970 The American Society for Clinical Investigation
Published April 1, 1970 - Version history
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Abstract

A series of experiments were performed upon intact anesthetized dogs to determine the relevance of a variety of hemodynamic variables to the irregular ventricular performance associated with atrial fibrillation. During experimentally induced atrial fibrillation central aortic pulse pressure was measured in relation to the duration of the preceding diastolic interval, the relative degree of cycle-length change, the magnitude of the preceding aortic end-diastolic pressure, the rate of ventricular tension development (at a fixed diastolic tension), and to ventricular end-diastolic pressure. While all of the latter variables bore a significant relation to the chosen parameters of ventricular function, the most linear correlation lay with the rate of ventricular tension development. It has been suggested, as a consequence, that the irregular ventricular performance observed during atrial fibrillation under these experimental conditions, may be more directly related to variation in the inotropic state of the ventricular myocardium than to an expression of the Frank-Starling concept, resulting from variable ventricular filling. The lability of the inotropic or contractile state has in turn been attributed to abrupt cycle-length change effecting inotropic alteration analogous to postextrasystolic potentiation of contractility and, at rapid rates, effecting an alternation of the contractile state.

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