Asynchronous left ventricular diastolic filling in patients with isolated disease of the left anterior descending coronary artery: assessment with radionuclide ventriculography.

Abstract

To study the relationship between global and regional filling of the left ventricle, we conducted resting gated radionuclide ventriculographic studies in 15 control subjects (group 1) and 22 patients with isolated disease of the left anterior descending coronary artery (group 2). None had had a previous myocardial infarction. A computer program subdivided the image of the left ventricle into four regions. The time-activity and first-derivative curves of the global and regional left ventricles were computed. In the global left ventricle, the normalized peak filling rate (PFR) was decreased (p < .01) and the ratio of the time to PFR (time interval from global end-systole to PFR) to the diastolic time, TPFR/DT, was greater (p < .02) in group 2 than in group 1. In the regional left ventricle, in the side perfused by the stenosed vessel (septal and apical), PFR was slightly decreased in the apical (p < .05), but not the septal region (p = NS); TPFR/DT was greater in the apical (p < .02) and in the septal region (p < .01) in group 2. In the normally perfused lateral side, there were no significant differences in PFR or in TPFR/DT between group 1 and group 2. Total At/DT, which was defined as the ratio of the sum of the absolute values of the time differences from global PFR to regional PFR (septal, apical, and lateral) to the diastolic time, was significantly greater in group 2 (0.09 0.05 vs 0. 16 + 0.05; p < .001). This indicates the existence of asynchronous diastolic filling in the different regions of the left ventricle in group 2. A negative correlation existed between total At/DT and global PFR (r -.64, p < .001). Thus, in patients with one-vessel disease, asynchronous diastolic filling occurs due to the filling disturbance in the affected regions, which may cause impairment of the filling of the global left ventricle. Circulation 69, No. 5, 933-942, 1984. LEFT VENTRICULAR diastolic filling has been reported to be impaired in many patients with coronary artery disease in whom there is no evidence of previous myocardial infarction. 8

Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine.

“…The ischemic process impairs myocardial relaxation6' 7,[22][23][24][25][26] and results in asynchrony of left ventricular filling.7 27 When a filling pressure or a driving pressure increases, as indicated by an elevation in left ventricular end-diastolic pressure in our study, the peak rate of left ventricular filling should increase substantially. One of the factors that contributes to a blunting of the effect of an increase in a driving pressure on the left ventricular filling rate is impairment of myocardial distensibility with ischemia, which we have discussed above.…”

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.…”

Effect of Dobutamine on Regional Diastolic Left Ventricular Asynchrony in Patients With Left Ventricular Hypertrophy. On-Line Quantification Using Automated Segmental Motion Analysis System.

“…11 LV nonuniformity is an important determinant of LV diastolic dysfunction because it delays LV relaxation and thus impairs diastolic filling. 4,6,7 LV asynchronies have been evaluated by left ventriculography, 7 radionuclide angiography 12,13 and echocardiography, 14 but none of these methodologies provides real-time evaluation. In this study, we have shown the diastolic asynchrony in patients with LVH using our newly developed A-SMA system, which uses an on-line system for analyzing color kinesis images, thus enabling us to quantify regional wall motion in real time.…”