Acute transient coronary sinus hypertension impairs left
ventricular function and induces myocardial edema.
Pratt, J. W., E. R. Schertel, S. L. Schaefer, K. E. Esham, D. E.
McClure, C. F. Heck, and P. D. Myerowitz.
Division of Thoracic and Cardiovascular Surgery, Department of
Surgery, The Ohio State University, Columbus, Ohio 43210, Department
of Surgery, Wilford Hall Medical Center, 59th Medical Wing/PSSG,
Lackland AFB, Texas 78236
APStracts 3:0059H, 1996.
This study was performed to evaluate the direct and indirect effects
of acute coronary sinus hypertension (CSH) on systolic and diastolic
left ventricular (LV) function. Coronary sinus pressure was elevated
to 25 mmHg for 3 hr in 8 pentobarbital anesthetized dogs and then
relieved. Left ventricular contractility was assessed by preload
recruitable stroke work (PRSW) and end-systolic elastance (Ees).
Diastolic function was assessed by the time constant of isovolumic
relaxation ([tau]) and the end-diastolic pressure volume relationship
(EDPVR). PRSW and Ees decreased progressively, and [tau] and the
slope of the EDPVR increased progressively with CSH. These changes
persisted after relief of CSH. [beta]-adrenergic and cholinergic
receptor blockade, performed in 6 dogs, did not alter the effects of
CSH on systolic or diastolic function. The LV wet-dry weight ratios
of the groups with CSH were significantly greater than that of a
control group without CSH. We conclude that CSH results in changes in
the left ventricle that depress contractility, prolong active
relaxation and increase diastolic stiffness. The dysfunction was not
the direct effect of CSH or autonomic reflex activation, but may have
been induced by fluid accumulation within the interstitium.
Received 24 July 1995; accepted in final form 24 January 1996.
APS Manuscript Number H695-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96