Evaluation of Time Course of Left Ventricular Isovolumic Relaxation in Humans
Weiss and coworkers  first determined, in an open-chest, right-heart-bypass animal model, that left-ventricular-pressure decay during isovolumic relaxation can be approximated by a monoexponential function. Their technique required that the derived or best-fit monoexponential curve for the pressure data decay asymptotically toward zero pressure. [1, 2]. Subsequent evaluation of the time course of pressure fall during isovolumic relaxation has questioned whether the monoexponential decay of isovolumic pressure decline should proceed to a zero or nonzero asymptote [3–5]. Inherent in this calculation is the assumption that pressure decline during isovolumic relaxation is mono-exponential. This postulate is empiric and is not necessarily predicated by any physiologic mechanism . However, in those cases where a monoexponential model applies, calculation of the time constant provides a single index which characterizes the shape of the pressure curve during isovolumic relaxation. Such an index is important if the effects of relaxation on diastolic performance and overall cardiac function are to be evaluated in diseases such as hypertrophic cardiomyopathy and exercise-induced myocardial ischemia.
KeywordsAsymptote Model Coronary Artery Disease Group Semilog Plot Pressure Decline Monoexponential Decay
Unable to display preview. Download preview PDF.
- 3.Craig WE, Murgo JP (1980). Evaluation of isovolumic relaxation in normal man during rest, exercise, and isoproterenol infusion. Circulation 62 (suppl II): II - 92 (abstract).Google Scholar
- 6.Pasipoularides A, Palacios I, Frist W, et al (1985). Contribution of activation-inactivation dynamics to the impairment of relaxation in hypoxic cat papillary muscle. Am J Physiol: Regulatory Integrative Comp Physiol 248: R54 - R62.Google Scholar
- 7.Pasipoularides A, Murgo JP, Miller JW, Craig WE. Nonobstructive left ventricular ejection pressure gradients in man. (Submitted for publication)Google Scholar
- 8.Sabbah HN, Stein PD (1986). Investigation of the theory and mechanism of the origin of the second heart sound. Circ Res 39: 874–882.Google Scholar
- 9.Brown DL, Craig WE, Layton SA, et al (1981). Exercise induced abnormalities of left ventricular relaxation in coronary artery disease. Circulation 64 (suppl IV): 28 (abstract).Google Scholar
- 10.Murgo JP, Craig WE (1980). Relaxation abnormalities in hypertrophic cardiomyopathies. Circulation 62 (suppl II): 206 (abstract).Google Scholar
- 11.Craig WE, Pasipoularides A (1986). Ventricular diastolic dynamics: Effects of wall asynchrony on global relaxation indices. In Proceedings of the 21st Annual Meeting of the Association for the Advancement of Medical Instrumentation,Chicago, IL.Google Scholar
- 12.Murgo JP, Craig WE, Pasipoularides A (1982). The relationship between diastolic function and ejection in hypertrophic cardiomyopathy. In Proceedings of Symposium on Diastolic Function of the Heart,Hamburg, Germany.Google Scholar
- 13.Pagani M, Pizzinelli P, Gussoni M, et al (1983). Diastolic abnormalities of hypertrophic cardiomyopathy reproduced by asynchrony of the left ventricle in conscious dogs. J Am Coll Cardiol 1: 641 (abstract).Google Scholar
- 15.Brutsaert DL, Housmans PR, Goethals MA (1980). Dual control of relaxation: Its role in the ventricular function in the mammalian heart. Circ Res 47: 637–652.Google Scholar