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

Circulation, Vol 83, 674-680, Copyright © 1991 by American Heart Association

ARTICLES

Left ventricular diastolic dysfunction limits use of maximum systolic elastance as an index of contractile function

MR Zile, G Izzi and WH Gaasch
Department of Medicine (Cardiology), Medical University of South Carolina, Charleston 29425.

We tested the hypothesis that maximum systolic elastance (Emax) fails to detect a decline in left ventricular (LV) contractile function when diastolic dysfunction is present. Canine hearts were studied in an isolated blood-perfused heart apparatus (isovolumic LV); contractile dysfunction was produced by 60 or 90 minutes of global ischemia, followed by 90 minutes of reperfusion. Nine normal hearts underwent 60 minutes of ischemia, and five underwent 90 minutes of ischemia. After the ischemia-reperfusion sequence, developed pressure, pressure-volume area, and myocardial ATP level were significantly less than those at baseline in all 14 hearts. In the group undergoing 60 minutes of ischemia, LV diastolic pressure did not increase, whereas Emax decreased from 5.2 +/- 2.5 to 2.9 +/- 1.4 mm Hg/ml (p less than 0.05). In the group undergoing 90 minutes of ischemia, diastolic pressure increased (from 10 +/- 2 to 37 +/- 20 mm Hg, p less than 0.05), and Emax did not change significantly (from 5.1 +/- 4.3 to 4.3 +/- 2.5 mm Hg/ml). A second series of experiments was performed in 13 hearts with pressure-overload hypertrophy (aortic-band model with echocardiography and catheterization studies before the ischemia-reperfusion protocol). Five had evidence for pump failure, whereas eight remained compensated. After 60 minutes of ischemia and 90 minutes of reperfusion, developed pressure, pressure-volume area, and myocardial ATP level were significantly less than those at baseline in all 13 hearts. In the group with compensated LV hypertrophy, LV diastolic pressure did not change, whereas Emax decreased from 6.9 +/- 3.0 to 3.1 +/- 2.3 mm Hg/ml (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				S. Klotz, I. Hay, G. Zhang, M. Maurer, J. Wang, and D. Burkhoff Development of Heart Failure in Chronic Hypertensive Dahl Rats: Focus on Heart Failure With Preserved Ejection Fraction Hypertension, May 1, 2006; 47(5): 901 - 911. [Abstract] [Full Text] [PDF]

				R. W. Landymore, A. J. Bayes, J. T. Murphy, and J. H. Fris Preconditioning prevents myocardial stunning after cardiac transplantation Ann. Thorac. Surg., December 1, 1998; 66(6): 1953 - 1957. [Abstract] [Full Text] [PDF]

				G. Li, J. A. Sullivan, J. M. You, and R. I. Hall Effect of Pressure on Myocardial Function After 6-Hour Preservation With Blood Cardioplegia Ann. Thorac. Surg., January 1, 1998; 65(1): 115 - 124. [Abstract] [Full Text] [PDF]

				B. D. Hoit, Y. Shao, M. Gabel, and R. A. Walsh Disparate Effects of Early Pressure Overload Hypertrophy on Velocity-Dependent and Force-Dependent Indices of Ventricular Performance in the Conscious Baboon Circulation, February 15, 1995; 91(4): 1213 - 1220. [Abstract] [Full Text]