Increased dependence on slow filling for left ventricular diastolic filling in patients with coronary artery disease and a depressed systolic function--assessment with radionuclide ventriculography.

Contributions of rapid filling, slow filling and atrial systole to the left ventricular (LV) filling volume were analyzed with the use of radionuclide ventriculography at rest, both globally and regionally, in 34 patients with isolated disease of the left anterior descending coronary artery. The patients included 17 with a normal ejection fraction (EF greater than or equal to 50%; group 1) and 17 with a depressed EF (less than 50%; group 2), and the data were compared with those obtained from 13 normal subjects. A computer program subdivided the LV image into 4 regions, and time-activity curves were constructed globally and regionally by reverse-gating from the R wave. In both groups the contribution of rapid filling to the LV filling volume was decreased significantly in the affected septal and apical regions, and in the global left ventricle compared with that in normal subjects. In group 1, the contribution of atrial systole showed an increase in these affected regions and in the global left ventricle. In contrast, in group 2, the atrial contribution was not increased globally or regionally as much as was expected. However, the contribution of slow filling was either increased significantly or tended to increase in the affected regions and in the global left ventricle. There were negative correlations between the contribution of rapid filling and that of slow filling in the global left ventricle (r = -0.73, p less than 0.001) and in each of the septal, apical and lateral regions (r greater than or equal to -0.60, p less than 0.001), which suggested that the contribution of slow filling as well as of atrial systole undergoes an increase as rapid filling is impaired. Thus, in patients with coronary artery disease, the left ventricle relies on slow filling as well as atrial systole to affect diastolic LV filling in the affected regions and in the global left ventricle in the presence of LV systolic dysfunction.