LETTER TO THE EDITOR
Pressure relaxation of the left ventricle and filling pressures
Adelino F. Leite-Moreiraa,
Jorge Correia-Pinto,
Stefan G. De Hert and
Thierry C. Gillebert
a Department of Physiology, Faculty of Medicine, Al. Prof. Hernâni Monteiro, 4200-319 Porto, Portugal
amoreira{at}med.up.pt
We read with great interest the article by Senzaki et al. (1). In a careful study, the authors contrasted various methods for assessing the time constant tau of left ventricular (LV) pressure decay. They observed that pressure relaxation consistently deviated from a monoexponential (ME) decay in dilated cardiomyopathy and concluded that this deviation induced inaccuracies in the interpretation of the time constant tau. They proposed that the use of the hybrid-logistic (HL) method (2) resulted in more consistent data fits in various heart diseases.
The manuscript by Senzaki et al. yields important novel information on the analysis of LV pressure decay by focusing on the goodness of fit. Pressure decay is the best reflection of myocardial relaxation so far (3). Impaired myocardial relaxation will interfere with LV filling and result in elevated end-diastolic pressure (4). Senzaki et al. did not discuss the information that LV pressure decay might provide on incomplete myocardial relaxation and, as a consequence, on increased end-diastolic pressure. From a clinical and physiological point of view, it appears to us that this issue is at least as important as the goodness of fit.
We compared the ME method with the HL method. Single beat aortic clamping was performed in healthy hearts from dogs and rabbits (4). Leg elevation and phenylephrine administration were performed in coronary surgery patients (5). The goodness of fit was improved by the use of the HL-method in accordance to the paper under scrutiny. In these experimental and clinical studies, load dependence of LV pressure decay was less pronounced with the HL-method, but still was present and even highly significant. Changes in end-diastolic LV pressure induced by increasing cardiac load were closely correlated with relaxation rate, assessed both by the ME and HL methods (4,5). Of note, the ME method provided a better prediction of changes in end-diastolic pressure than did the HL method. The predictive value of the ME method was confirmed in more than 120 coronary surgery patients subjected to leg elevation (6).
Senzaki et al. suggested that increased load dependence of pressure decay in congestive heart failure, as was observed in dogs by Ishizaka (7) and in patients by Eichhorn (8), would not have been observed if these authors would have used the HL method. However, it should be noted that Ishizaka (7) not only reported increased load dependency of pressure decay (ME method) in cardiomyopathic hearts but also an upward shift of the diastolic pressure-volume loops. Eichhorn showed in a subsequent study (9) that load dependency of relaxation could predict the chronic response to a beta-adrenergic blocking agent and decreased in parallel with decreases in LV filling pressures.
Independently from its mathematical limitations and drawbacks, the ME time constant of LV pressure decay remains a good predictor of load-dependent changes of diastolic LV pressures. For this reason the previous reports on increased load dependence of pressure decay in cardiac overload and in diseased hearts keep for us their scientific and clinical value.
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References
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1. Senzaki H, Fetics B, Chen CH, Kass DA. Comparison of ventricular pressure relaxation assessments in human heart failure. Quantitative influence on load and drug sensitivity analysis. J Am Coll Cardiol. 1999;34:1529–1536[Abstract/Free Full Text]
2. Matsubara H, Takaki M, Yasuhara S, Araki J, Suga H. Logistic time constant of isovolumic relaxation pressure-time curve in the canine left ventricle. Better alternative to exponential time constant. Circulation. 1995;92:2318–2326[Abstract/Free Full Text]
3. Gillebert TC, Leite-Moreira AF, De Hert SG. The hemodynamic manifestation of normal myocardial relaxation. A framework for experimental and clinical evaluation. Acta Cardiologica. 1997;52:223–246[Medline]
4. Leite-Moreira AF, Correia-Pinto J, Gillebert TC. Afterload-induced changes in myocardial relaxation. A mechanism for diastolic dysfunction. Cardiovasc Res. 1999;43:344–353[Abstract/Free Full Text]
5. De Hert SG, Gillebert TC, Ten Broecke PW, Moulijn AJ. Length-dependent regulation of left ventricular function in coronary surgery patients. Anesthesiology. 1999;91:379–387[CrossRef][Medline]
6. De Hert SG, Gillebert TC, Ten Broecke PW, Mertens E, Rodrigus IE, Moulijn AJ. Contraction-relaxation coupling and impaired left ventricular performance in coronary surgery patients. Anesthesiology. 1999;90:748–757[CrossRef][Medline]
7. Ishizaka S, Asanoi H, Wada O, Kameyama T, Inoue H. Loading sequence plays an important role in enhanced load sensitivity of LV relaxation in conscious dogs with tachycardia-induced cardiomyopathy. Circulation. 1995;92:3560–3567[Abstract/Free Full Text]
8. Eichhorn EJ, Willard JE, Alvarez L, et al. Are contraction and relaxation coupled in patients with and without heart failure? Circulation. 1992;85:2132–2139[Abstract/Free Full Text]
9. Eichhorn EJ, Heesch CM, Risser RC, Marcoux L, Hatfield B. Predictors of systolic and diastolic improvement in patients with dilated cardiomyopathy treated with metoprolol. J Am Coll Cardiol. 1995;25:154–162[Abstract]
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