This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Paulus, W. J. Articles by Andries, E. Search for Related Content PubMed PubMed Citation Articles by Paulus, W. J. Articles by Andries, E.

Circulation, Vol 81, 886-898, Copyright © 1990 by American Heart Association

ARTICLES

Wide-range load shift of combined aortic valvuloplasty-arterial vasodilation slows isovolumic relaxation of the hypertrophied left ventricle

WJ Paulus, GR Heyndrickx, P Buyl, MA Goethals and E Andries
Cardiovascular Center, Aalst, Belgium.

To assess the effects of left ventricular (LV) load on isovolumic relaxation rate of the hypertrophied LV, wide range LV load shifts were imposed by the sequential use of balloon aortic valvuloplasty (BAV) and arterial vasodilation in 14 patients with severe sclerocalcific aortic stenosis (aortic valve area, 0.45 +/- 0.16 cm2). Micromanometer tip- catheter LV pressure recordings (n = 14) and simultaneous LV angiograms (n = 9) were obtained before BAV, during nitroprusside infusion (NIT) before BAV, 48 hours after BAV, and 48 hours after BAV during NIT. LV peak systolic pressure (LVPSP) decreased from 237 +/- 33 mm Hg before BAV to 200 +/- 33 mm Hg (p less than 0.01) during NIT before BAV, to 201 +/- 27 mm Hg (p less than 0.01) after BAV and to 165 +/- 26 mm Hg (p less than 0.01) during NIT after BAV.LV end-systolic volume (LVESV) decreased from 55 +/- 34 ml before BAV to 25 +/- 23 ml (p less than 0.01) during NIT before BAV, to 30 +/- 32 ml (p less than 0.025) after BAV and to 15 +/- 12 ml (p less than 0.025) during NIT after BAV. LV end-systolic wall stress (LVESs) decreased from 90 +/- 30.10(3) dyne/cm2 before BAV to 41 +/- 13.10(3) dyne/cm2 (p less than 0.01) during NIT before BAV, to 55 +/- 16.10(3) dyne/cm2 (p less than 0.025) after BAV and to 26 +/- 6.10(3) dyne/cm2 (p less than 0.01) during NIT after BAV. Only after sequential BAV-NIT was the time of LV electromechanical systole (LVEST), which marked the onset of the LV isovolumic relaxation period, significantly reduced (from 419 +/- 26 msec before BAV to 363 +/- 28 msec after BAV-NIT [p less than 0.01]). The time constants of LV pressure decay with zero or nonzero asymptote pressure (TO and TPB) remained unchanged after BAV and during NIT before BAV. At the lowest LVPSP, LVESV, and LVESs after sequential BAV- NIT, both TO and TPB significantly prolonged from 35.7 +/- 6.3 to 46.7 +/- 12.6 msec (p less than 0.025) and from 46.6 +/- 12.5 to 73.2 +/- 23.3 msec (p less than 0.01). Phase-plane plots (LV dP/dt vs. LVP) of the LV pressure (P) signal during isovolumic relaxation were constructed for the four different loading states by matching corresponding LVP and LV dP/dt points. For a given LVP value, the corresponding LV dP/dt values on the phase plane plots were comparable before BAV, during NIT before BAV, and after BAV. The corresponding LV dP/dt value was higher during NIT after BAV, impling a slower relaxation rate at the same LVP after sequential BAV-NIT. A shift in the control of isovolumic LV relaxation kinetics from myofilamentary detachment to myoplasmic calcium removal, which proceeds slower in hypertrophied myocardium, could explain the observed slowing of LV isovolumic relaxation after drastic LV unloading of sequential BAV-NIT.

This article has been cited by other articles:

				L. van Heerebeek, N. Hamdani, M. L. Handoko, I. Falcao-Pires, R. J. Musters, K. Kupreishvili, A. J.J. Ijsselmuiden, C. G. Schalkwijk, J. G.F. Bronzwaer, M. Diamant, et al. Diastolic Stiffness of the Failing Diabetic Heart: Importance of Fibrosis, Advanced Glycation End Products, and Myocyte Resting Tension Circulation, January 1, 2008; 117(1): 43 - 51. [Abstract] [Full Text] [PDF]

				A. Borbely, J. van der Velden, Z. Papp, J. G.F. Bronzwaer, I. Edes, G. J.M. Stienen, and W. J. Paulus Cardiomyocyte Stiffness in Diastolic Heart Failure Circulation, February 15, 2005; 111(6): 774 - 781. [Abstract] [Full Text] [PDF]

				D. A. Kass, J. G.F. Bronzwaer, and W. J. Paulus What Mechanisms Underlie Diastolic Dysfunction in Heart Failure? Circ. Res., June 25, 2004; 94(12): 1533 - 1542. [Abstract] [Full Text] [PDF]

				J. G. F. Bronzwaer, C. Heymes, C. A. Visser, and W. J. Paulus Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy Am J Physiol Heart Circ Physiol, January 1, 2003; 284(1): H10 - H16. [Abstract] [Full Text] [PDF]

				W. Hayashida, J. Donckier, H. Van Mechelen, A. A. Charlier, and H. Pouleur Load-sensitive diastolic relaxation in hypertrophied left ventricles Am J Physiol Heart Circ Physiol, February 1, 1998; 274(2): H609 - H615. [Abstract] [Full Text] [PDF]

				T. Yamakado, E. Takagi, S. Okubo, K. Imanaka-Yoshida, T. Tarumi, M. Nakamura, and T. Nakano Effects of Aging on Left Ventricular Relaxation in Humans: Analysis of Left Ventricular Isovolumic Pressure Decay Circulation, February 18, 1997; 95(4): 917 - 923. [Abstract] [Full Text]

				S. Teramura, T. Yamakado, M. Maeda, and T. Nakano Effects of MCI-154, a Calcium Sensitizer, on Left Ventricular Systolic and Diastolic Function in Pacing-Induced Heart Failure in the Dog Circulation, February 4, 1997; 95(3): 732 - 739. [Abstract] [Full Text]

				W. J. Paulus, P. J. Vantrimpont, and A. M. Shah Paracrine Coronary Endothelial Control of Left Ventricular Function in Humans Circulation, October 15, 1995; 92(8): 2119 - 2126. [Abstract] [Full Text]