[The effect of changes in stroke volume on QT dispersion during long-term DDD and VVI pacing].

UNLABELLED: The aim of this study was to evaluate the alterations of stroke volume (SV) on the QT dispersion (QTD) as a result of different pacing modes (DDD, VVI) and programmed AV delays (AVD).

MATERIAL AND METHODS: We studied 60 patients (pts) (22 F, 38 M) in mean age 67.5 +/- 7.5 yrs in whom DDD pacemakers were implanted due to complete atrioventricular block (AVB III degree). 10 pts had coronary artery disease (CAD)--"CAD" subgroup, 14 pts arterial hypertension (AH)--"AH" subgroup, 27 pts CAD and AH--"AH + CAD" subgroup. The control group consisted of 9 pts without structural heart disease, but with AVB III degree, paced in DDD mode. Previous myocardial infarction was recognised in 7 patients in "CAD" subgroup and in 7 patients in "AH + CAD" subgroup. Left ventricular hypertrophy was detected in 4 men in "AH" subgroup and in 8 patients in "AH + CAD" subgroup. In all cases basic rate of the pacemaker was programmed at 70/min. Resting ECG showed all atrial and ventricular complexes captured. AVD optimization was based on the measurements of SV by Doppler echocardiography. QT intervals (QT) were measured from 12-lead ECG at 50 mm/sec. speed. QTD was calculated as the difference between maximal and minimal QT. It was measured at optimal AVD (with highest SV--opt. DDD) and "unoptimal" AVD (unopt. DDD) programmed AV intervals and then in VVI mode (with lowest SV) after 24 hrs following reprogramming of the pacemaker.

RESULTS: In the whole population, in DDD mode, we found a strong correlation between SV and QTD (r = -0.655; p < 0.01). In VVI mode SV was significantly lower than in unopt. DDD (78.7 ml vs 90.0 ml, p < 0.001) and QTD was significantly greater (74.3 ms vs 69.2 ms, p < 0.05). The modifications in AVD and conversion of pacing mode (VVI to DDD) leading to maximal SV resulted in decreased QT dispersion. The highest SV (128.9 ml at opt. DDD) and the lowest QTD (48.3 ms at opt. DDD) were seen in the controls, but changes in dispersion were the least and insignificant during different pacing modes. In CAD; AH + CAD pts, we observed the lowest SV (61.7 ml; 74.9 ml at VVI respectively) and the highest QTD (77.8 ms; 80.9 ms at VVI respectively). In these pts, the modifications of AVD and conversion of pacing mode (VVI to opt. DDD) leading to maximal SV (106.8 ml; 115.9 ml in CAD and AH + CAD pts, respectively) resulted in decreased QTD (53.9 ms; 56.6 ms, respectively). During DDD pacing there was significant correlation of QTD to SV (r = -0.680; r = -0.656, respectively). In CAD pts with myocardial infarction or in AH pts with LV hypertrophy the correlation of SV to QTD was stronger (r = -0.937, r = -0.886, p < 0.025, respectively). We didn't find the correlation in the control group (r = -0.318).

CONCLUSIONS: Programming of different AVD and pacing modes significantly influences QTD in CAD and/or AH pts. QTD reflects hemodynamic status of these paced pts.