[The analysis of left ventricular filling dynamics by radionuclide ventriculography using ECG's R wave and the second heart sound gating techniques].

To assess the impairment of early diastolic left ventricular (LV) filling and the effect of atrial contraction on total LV filling in patients (pts) with coronary artery disease (CAD), LV volume (LVV) changes during rapid filling (RF) and atrial contraction (AC) phases were studied by equilibrium radionuclide ventriculography in 10 normals (N) and 17 pts with CAD including eight without (CAD-1) and nine with (CAD-2) previous myocardial infarction (MI). The data were acquired in a list-mode fashion as a series of X, Y coordinates, time markers and an ECG's R wave (R) plus the second heart sound (S2) markers. LVV curves were obtained from three types of multi-gated images by (1) R-synchronized forward reformatting for the analysis of systolic phase (ejection fraction; EF and peak ejection rate; PER), (2) S2-synchronized forward reformatting for the analysis of RF phase (peak filling rate; PFR-RF and filling fraction; FF) and (3) R-synchronized backward reformatting for the analysis of AC phase (peak filling rate; PFR-AC and LVV increment with atrial contraction/stroke volume; AC/SV). EF and PER were significantly lower (p less than 0.001) in CAD-2 (36.0 +/- 8.1% and -1.5 +/- 0.4 EDV/sec) than in N (58.2 +/- 5.8% and -2.4 +/- 0.4 EDV/sec), but those in CAD-1 (52.7 +/- 6.4% and -2.2 +/- 0.3 EDV/sec) were almost the same as N. However PFR-RF and FF were reduced both in CAD-1 (1.5 +/- 0.4 EDV/sec and 23.0 +/- 7.0%) and CAD-2 (1.3 +/- 0.4 EDV/sec and 19.0 +/- 8.0%) compared with N (2.3 +/- 0.4 EDV/sec and 37.0 +/- 8.3%). PFR-AC and AC/SV were significantly greater (p less than 0.01) in CAD-1 (1.3 +/- 0.3 EDV/sec and 0.30 +/- 0.06) than N (0.8 +/- 0.3 EDV/sec and 0.13 +/- 0.07), but those in CAD-2 (0.6 +/- 0.4 EDV/sec and 0.18 +/- 0.09) showed no increase like in CAD-1. These results indicate that 1) the impairment of early diastolic filling precedes the evidence of systolic dysfunction in pts with CAD and 2) AC could compensate the impaired early filling in pts without prior MI, whereas in pts with prior MI this compensatory mechanism is absent presumably because of elevated LV filling pressure.