Impaired left ventricular diastolic filling in patients with coronary artery disease: assessment with radionuclide angiography.

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.

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

“…',',"' Based on experimental and clinical evidence that the impairment of left ventricular relaxation may occur before systolic dysfunction in many disease states,1'5 and based on the assumption that the rate of ventricular relaxation is an important determinant of early diastolic filling, many clinicians have attempted to determine early abnormalities in left ventricular relaxation by estimating early filling function, and in particular, by using the PRFR as an index.7', 10,11,13,14,16 The loading interventions used in this study, increased preload and afterload, are known to change the rate of left ventricular relaxation in ways that are consistent with the results of this study (see Brutsaert et al',2 for reviews). However, we do not know what these interventions would do to diastolic function in the diseased heart, nor do we know how changes in the rate of isovolumetric relaxation will affect diastolic events after the onset of filling.…”

“…3' 4, 7, 12, 14 Because this direct index of isovolumetric relaxation requires an invasive measurement of left ventricular pressure, many investigators assume that left ventricular relaxation can be assessed indirectly by estimating early diastolic filling. For example, peak rapid filling rate (PRFR) has been derived from radionuclide angiography, 10 11, 16 peak rates of chamber or wall dimension change have been measured from M mode echocardiograms,6, 9 15 and peak rapid filling velocity has been determined with Doppler ultrasound. '3 These approaches are based on the principle that the falling ventricular pressure contributes to the generation of the atrioventricular pressure difference that accelerates the blood across the mitral valve.…”

Acute and chronic effects of nicardipine on systolic and diastolic left ventricular performance in patients with heart failure: A pilot study

“…The peak filling rate was normalized to end-diastolic volume and was calculated as the slope of the filling curve between two "cursors" placed 80 ms apart to give the greatest rate of filling. The time to peak filling rate was the distance from end-systole to the midpoint of the segment of curve used for measurement of peak filling rate (Bonow et al, 1981a;Mancini et al, 1983). Blood pressure was measured with a calibrated mercury sphygmomanometer using standard techniques.…”

Detection of Diastolic Abnormality by Dyssynchrony Imaging Correlation With Coronary Artery Disease in Patients Presenting With Visibly Normal Wall Motion

“…[23][24][25] Earlier studies have demonstrated the presence of abnormal diastolic function in patients with CAD without evidence of systolic wall motion abnormalities by radionuclide angiography or digitized cineangiography. [26][27][28] Kondo et al have also demonstrated that delayed outward LV wall motion in the isovolumic relaxation phase by digital subtraction high-frame-rate echocardiography was indicative of CAD. 29 In our experience, a positive myocardial velocity occurring during the isovolumic relaxation phase as detected by the spectral tissue Doppler mapping technique (MOMI) was indicative of critical coronary artery stenosis in patients complaining of chest pain with visibly normal LV contraction.…”