Left ventricular filling dynamics: influence of left ventricular relaxation and left atrial pressure.
TL;DR: PRFR is determined by both the left atrial pressure and the left ventricular relaxation rate and should be used with caution as an index ofleft ventricular diastolic function.
Abstract: 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.
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TL;DR: Mitral E velocity, corrected for the influence of relaxation (i.e., the E/Ea ratio), relates well to mean PCWP and may be used to estimate LV filling pressures.
2,911 citations
Cites background from "Left ventricular filling dynamics: ..."
...The mitral E wave velocity is directly influenced by left atrial pressure and inversely altered by changes in the time constant of relaxation (7,8)....
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TL;DR: Mitral flow velocity recordings have clinical potential in assessing left ventricular diastolic function that merits further investigation, despite the indirect method of estimation and certain limitations.
1,549 citations
TL;DR: These new Doppler applications have been shown to provide an accurate estimate of LV relaxation and appear to be relatively insensitive to the effects of preload compensation.
1,024 citations
Cites background from "Left ventricular filling dynamics: ..."
...However, other factors such as atrial and ventricular compliance, mitral valve inertance and left atrial (LA) pressure are also determinants of transmitral Doppler flow (11,13,15)....
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01 Feb 1989
TL;DR: An interpretation of the mitral valve, tricuspid valve, and systemic and pulmonary venous inflow velocities in the normal patient and in various disease states is provided.
Abstract: Evaluation of diastolic filling of the heart has been difficult because of its complexity and the numerous interrelated contributing factors. Previous determinations have depended on high-fidelity, invasive measurements of instantaneous pressure, volume, mass, and wall stress, which could not be done on a routine clinical basis. With the advent of Doppler echocardiography, intracardiac blood flow velocities can now be noninvasively assessed. For application of this technique to evaluation of diastolic function in patients with heart disease, it is necessary to understand what the Doppler-derived variables represent. It is also necessary to know how they are affected by changes in loading conditions and changes in myocardial relaxation. In this review, we provide an interpretation of the mitral valve, tricuspid valve, and systemic and pulmonary venous inflow velocities in the normal patient and in various disease states.
770 citations
TL;DR: To determine the effect of filling pressure on the pattern of left ventricular filling in humans, the mitral flow velocity profile was measured by pulsed wave Doppler echocardiography during right and left heart catheterization in 11 patients before and during nitroglycerin infusion.
641 citations
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TL;DR: The present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate.
Abstract: The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall was studied in isovolumic relaxation for isovolumic and ejecting beats (r less than or equal to 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 +/- 4.5 ms at 110/min to 48.2 +/- 6.0 ms at 160/min (P less than 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 +/- 5.0 ms in isovolumic beats to 45.8 +/- 2.9 ms in the ejecting beats (P less than 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. Calcium chloride and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 +/- 13.4 vs. 46.3 +/- 7.0 ms, P less than 0.02). During recovery from ischemia, T increased significantly from 59.3 +/- 9.6 to 76.8 +/- 13.1 ms when compared with the preischemic control beat (P less than 0.05). Thus, the present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.
1,078 citations
TL;DR: LV diastolic filling, evaluated noninvasively by radionuclide angiography, is abnormal in a high percentage of patients with CAD at rest independent of LV systolic function or previous myocardial infarction.
Abstract: To assess left ventricular (LV) diastolic filling at rest in patients with coronary artery disease (CAD), we analyzed high-resolution time-activity curves (10-20 msec/frame) obtained from gated radionuclide angiograms in 231 patients. Peak LV filling rate (PFR), expressed in end-diastolic volumes per second (EDV/sec), was subnormal in CAD patients (1.8 +/- 0.6 [+/- SD] vs normal mean of 3.3 +/- 0.6, p les than 0.001) and time to PFR (TPFR), measured from end-systole to PFR, was prolonged (171 +/- 41 msec vs normal mean of 136 +/- 23 msec, p less than 0.001). These indexes were also abnormal in the 141 patients with normal resting LV ejection fraction (PFR = 2.1 +/- 0.5 EDV/sec; TPFR = 175 +/- 36 msec) and in 123 patients without Q waves on the ECG (PFR = 2.1 +/- 0.5 EDV/sec; TPFR = 168 +/- 38 msec). Abnormal LV filling at rest (PFR less than 2.5 EDV/sec or TPFR greater than 180 msec) was found in 91% of all patients with CAD, 86% of patients with normal resting LV ejection fractions, 85% of patients without Q waves, and 82% of patients with normal resting LV ejection fraction, no resting regional wall motion abnormalities and no Q waves. Thus, LV diastolic filling, evaluated noninvasively by radionuclide angiography, is abnormal in a high percentage of patients with CAD at rest independent of LV systolic function or previous myocardial infarction.
596 citations
TL;DR: This work has shown that despite the recent progress in understanding of relaxation of the heart, the underlying mechanisms are still not fully understood and these mechanisms can now be discerned.
Abstract: EARLY DETECTION of impaired relaxation has been emphasized recently for the evaluation of global and regional ventricular function in patients with heart disease. Although early relaxation abnormalities have been found in various cardiac diseases, the underlying mechanisms are not as yet fully understood. Given the recent progress in our understanding of relaxation of the heart,' these mechanisms can now be discerned
465 citations
TL;DR: Volume loading slows isovolumic relaxation rate in the intact canine heart and appears to be a reflection of the dependence of relaxation on both end-diastolic and mean aortic systolic pressures.
Abstract: We studied the effects of volume loading on left ventricular isovolumic relaxation rate in 16 intact anesthetized dogs. End-diastolic pressure, mean aortic systolic pressure, dp/dtmnx, and heart rate were measured at end expiration and end inspiration. Volume loading to approximately 5, 10, 15, and 20 mm Hg above initial end-diastolic pressure was performed. In nine dogs, simultaneous ventricular dimensions were measured with previously implanted tantalum screws using biplane cineangiography. Similar volume loading was done in open-chest and open-pericardium states. Relaxation rate was measured in 3413 beats using T, the time constant of exponential isovolumic pressure fall. T was calculated as reported previously by others and also from a linear regression of dp/dt against p, to eliminate the effects of extracavity pressure changes. T always increased significantly with volume loading, indicating slower relaxation. (For example, with the chest intact, mean T increased from 26 ± 2 (SEM) msec before volume loading to 41.5 ± 4 msec after volume loading.) Using multiple linear regression analysis, we found, in agreement with previous reports, that T decreased significantly as dp/dtMAX, and heart rate increased. In contrast to previous reports, we also found that T increased significantly as end-diastolic and mean aortic systolic pressure increased. These four variables taken together accurately predicted T [SEE (standard error of estimate) = 3.2 msec, R = 0.94, P < 0.001]. Geometric variables, including ventricular dimensions and ejection fraction, did not have a statistically significant effect on T independent of the hemodynamic variables. Opening the chest or pericardium did not have a consistent effect on T. Volume loading slows isovolumic relaxation rate in the intact canine heart. This effect appears to be a reflection of the dependence of relaxation on both end-diastolic and mean aortic systolic pressures.
449 citations
TL;DR: It is indicated that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.
Abstract: To study left ventricular relaxation and filling in different forms of left ventricular hypertrophy, echocardiograms of the left ventricle in 24 patients with hypertrophic obstructive cardiomyopathy and in 24 patients with chronic left ventricular pressure overload (due to aortic stenosis in 6 and to severe arterial hypertension in 18) were analyzed by computer and compared with those of 28 normal subjects. The relaxation time index (minimal left ventricular dimension to mitral valve opening) was 13 ± 15 ms in normal subjects. This index was prolonged in patients with cardiomyopathy (93 ± 37 ms) and overload (66 ± 31 ms). During the interval from minimal left ventricular dimension to mitral valve opening both groups with left ventricular hypertrophy showed a marked increase in left ventricular dimension of 4.0 ± 2.2 mm and 3.0 ±1.8 mm, respectively, which was significantly greater (p The rapid filling phase and the increase in dimension during this period were significantly reduced in hypertrophic obstructive cardiomyopathy and chronic pressure overload. In contrast to findings in the patients with cardiomyopathy, in those with pressure overload the reduced increase in left ventricular dimension during the rapid diastolic filling period was compensated for by a greater dimensional increase due to atrial contraction, resulting in a normal end-diastolic dimension. These data indicate that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.
405 citations