Alteration of left ventricular performance by left bundle branch block simulated with atrioventricular sequential pacing

Abstract

The effects of atrioventricular (AV) sequential pacing-induced left bundle branch block (LBBB) on left ventricular (LV) performance were evaluated during cardiac catheterization in 9 randomly selected patients being investigated for chest pain. All patients were in normal sinus rhythm with a normal P-R interval and QRS duration. LV performance was assessed by both hemodynamic and angiographie measurements. The maximal rate of LV pressure increase (dP/dt), rate of maximal LV pressure decrease ( −dP dt ), LV end-diastolic pressure (LVEDP), end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume and percent ejection (EF) were measured during right atrial and AV sequential pacing at a constant pacing rate. The average pacing rate was 97 ± 3 beats/min (mean ± standard error of the mean). In each patient, both dP/dt and −dP dt decreased significantly (p < 0.001) during AV sequential pacing compared with atrial pacing at the same rate, from 1,541 ± 68 to 1,319 ± 56 mm Hg/s for dP/dt and from 1,506 ± 86 to 1,276 ± 92 for −dP dt . LVEDP did not change significantly when atrial (17 ± 3 mm Hg) and AV sequential pacing (16 ± 2 mm Hg) were compared. Mean LVEDV did not change during atrial (135 ± 13 ml) or AV sequential pacing (137 ± 14 ml). In contrast, the LVESV during AV sequential pacing was higher by 15 ml (23 % ) (from 48 ± 10 to 63 ± 12 ml) ( p < 0.001); as a result, the stroke volume was lower by 13 ml (15%) and the EF decreased by 10 %, from 66 to 56 % (−15 %). These changes in LV performance during acutely induced LBBB by AV sequential pacing as compared with atrial pacing at the same rate were independent of altered preload, because both LVEDP and LVEDV were similar during the 2 different pacing modes. Peak systolic pressure during AV sequential pacing was significantly lower than that during atrial pacing (161 ± 10 vs 145 ± 10 mm Hg, p < 0.01), and thus afterload was presumably altered during the different pacing modes. However, because the observed change in systolic pressure (afterload) was lower during AV sequential pacing, this change should improve rather than result in deterioration of ejection phase indexes. Because the opposite was observed, it is concluded the deterioration in LV function noted during AV sequential pacing must be due in part to the asynchronous pattern of ventricular activation induced by this intervention.