Donate Help Contact The AHA Sign In Home
American Heart Association
Circulation
Search: search_blue_button Advanced Search
Circulation. 1995;91:2423-2434

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Takano, H.
Right arrow Articles by Glantz, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Takano, H.
Right arrow Articles by Glantz, S. A.

(Circulation. 1995;91:2423-2434.)
© 1995 American Heart Association, Inc.


Articles

Left Ventricular Contractility Predicts How the End-Diastolic Pressure-Volume Relation Shifts During Pacing-Induced Ischemia in Dogs

Hiroshi Takano, MD; Stanton A. Glantz, PhD

From the Cardiovascular Research Institute, Department of Medicine, University of California, San Francisco.

Correspondence to Stanton A. Glantz, PhD, Professor of Medicine, Division of Cardiology, University of California at San Francisco, San Francisco, CA 94143-0124.

Background Two types of ischemia, pacing-induced and coronary occlusion–induced, have different effects on left ventricular diastolic properties. During pacing-induced ischemia, the diastolic pressure-volume relation is said to shift upward, whereas during coronary occlusion, it is said to shift rightward or downward. However, recent studies have shown that the relation can shift in any direction during both types of ischemia. The purpose of this study was to identify determinants of the shift of the end-diastolic pressure-volume relation (EDPVR) during pacing-induced ischemia.

Methods and Results We retrospectively analyzed 46 pacing-induced ischemia experiments performed in 15 open-pericardium anesthetized dogs. Pacing ischemia was induced by constricting left anterior descending and left circumflex coronary arteries and pacing the left atrium at 150 to 180 beats per minute for 3 minutes. Left ventricular volume was measured with a conductance catheter. Hemodynamics were recorded during baseline, coronary stenosis, rapid pacing, and pacing-induced ischemia (immediately after rapid pacing). For each condition, hemodynamics were recorded in steady state and then during a brief inferior vena caval occlusion (except for during rapid pacing) to obtain left ventricular end-diastolic and end-systolic pressure-volume relations. The shift of the EDPVR from coronary stenosis to pacing-induced ischemia was assessed by an upward shift index (end-diastolic pressure during pacing-induced ischemia minus the pressure during coronary stenosis at the largest end-diastolic volume common to both conditions, SI-S) and a rightward shift index (the largest end-diastolic volume during pacing-induced ischemia minus the largest volume during coronary stenosis, {Delta}EDVI-S). The index of left ventricular contractility, the end-systolic elastance (Ees), or the slope of the dP/dtmax–end-diastolic volume relation (dE/dtmax) during pacing-induced ischemia was the strongest determinant of the magnitude of SI-S and {Delta}EDVI-S and thus of the shift of the EDPVR. As Ees or dE/dtmax decreased, SI-S decreased and {Delta}EDVI-S increased.

Conclusions Our results suggest that left ventricular contractility is the best determinant of the shift of the EDPVR during pacing-induced ischemia. The more left ventricular contractility decreases, the more the EDPVR shifts downward and rightward.


Key Words: mechanics • ischemia • diastole • systole




This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
N. Varma, J. P. Morgan, and C. S. Apstein
Mechanisms underlying ischemic diastolic dysfunction: relation between rigor, calcium homeostasis, and relaxation rate
Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H758 - H771.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
S. B. Solomon and S. A. Glantz
Regional ischemia increases sensitivity of left ventricular relaxation to volume in pigs
Am J Physiol Heart Circ Physiol, June 1, 1999; 276(6): H1994 - H2005.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
M. Tayama, S. B. Solomon, and S. A. Glantz
Effect of lidocaine on left ventricular pressure-volume curves during demand ischemia in pigs
Am J Physiol Heart Circ Physiol, June 1, 1998; 274(6): H2100 - H2109.
[Abstract] [Full Text] [PDF]