Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure

• Published in: Circulation (New York, N.Y.) N.Y.), 1986-07, Vol.74 (1), p.187-196
• Main Authors: ISHIDA, Y, MEISNER, J. S, TSUJIOKA, K, GALLO, J. I, YORAN, C, FRATER, R. W. M, YELLIN, E. L
• Format: Article
• Language: English
• Subjects: Angiotensin II - pharmacology; Animals; Atrial Function; Biological and medical sciences; Blood Flow Velocity; Blood Pressure - drug effects; Cardiac Volume - drug effects; Dogs; Electrocardiography; Electromagnetic Phenomena; Fundamental and applied biological sciences. Psychology; Heart; Heart - physiology; Hemodynamics - drug effects; Manometry; Models, Cardiovascular; Myocardial Contraction - drug effects; Oscillometry; Phonocardiography; Time Factors; Ventricular Function; Vertebrates: cardiovascular system
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.cir.74.1.187

Peak rapid filling rate (PRFR) is often used clinically as an index of left ventricular relaxation, i.e., of early diastolic function. This study tests the hypothesis that early filling rate is a function of the atrioventricular pressure difference and hence is influenced by the left atrial pressure as well as by the rate of left ventricular relaxation. As indexes, we chose the left atrial pressure at the atrioventricular pressure crossover (PCO), and the time constant (T) of an assumed exponential decline in left ventricular pressure. We accurately determined the magnitude and timing of filling parameters in conscious dogs by direct measurement of phasic mitral flow (electromagnetically) and high-fidelity chamber pressures. To obtain a diverse hemodynamic data base, loading conditions were changed by infusions of volume and angiotensin II. The latter was administered to produce a change in left ventricular pressure of less than 35% (A-1) or a change in peak left ventricular pressure of greater than 35% (A-2). PRFR increased with volume loading, was unchanged with A-1, and was decreased with A-2; T and PCO increased in all three groups (p less than .005 for all changes). PRFR correlated strongly with the diastolic atrioventricular pressure difference at the time of PRFR (r = .899, p less than .001) and weakly with both T (r = .369, p less than .01) and PCO (r = .601, p less than .001). The correlation improved significantly when T and PCO were both included in the multivariate regression (r = .797, p less than .0001). PRFR is thus determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index of left ventricular diastolic function.