Key result
Longer paced QTc (505 vs 486 ms, P<=0.003) and QRS duration (182 vs 167 ms, P<=0.03) were associated with sustained ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy.
Why the study?
Do paced QTc and QRS duration predict the risk of sustained ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy?
Cohort (n=127)
Do paced QTc and QRS duration predict the risk of sustained ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy?
Pacing-induced increases in QTc and QRS duration are associated with an increased risk of sustained ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy.
Paced QTc and QRS may flag higher arrhythmia risk in CRT recipients; hypothesis-generating and should not yet change practice or device settings.
BACKGROUND AND OBJECTIVES: QRS duration (QRSd) and prolonged corrected QT interval (QTc) are associated with ventricular arrhythmic events. This study was designed to determine whether CRT by means of biventricular pacing alters the QTc and QRSd, and whether such changes are related to the risk of sustained ventricular tachyarrhythmias (sVTA). METHODS AND RESULTS: A total of 127 patients (102 men, mean age 63.9 +/- 8.9 years) with drug-resistant heart failure and QRS duration > or = 130 ms underwent CRT/CRT-ICD. The aetiology of the heart failure was ischaemic in 41 patients (32.3%). After a median follow-up of 24 months, 42 sVTA occurred in 35 patients (27.6%). Twenty-nine patients had a single sVTA, in five patients two sVTA and in one patient three sVTA occurred. The paced QTc was longer in sVTA patients (505 +/- 55 ms) compared with no sVTA patients (486 +/- 44 ms, P < or = 0.003). Similar responses for paced QRSd were observed (182 +/- 27 ms in sVTA patients vs 167 +/- 27 ms in no-sVTA patients, P < or = 0.03). This effect was independent from intrinsic QTc and QRSd and the aetiology of the heart failure. The mortality rate was significantly higher in patients with ventricular fibrillation and fast VT (P < or = 0.004) who experienced shock therapies. However, the sVTA were not the immediate cause of death. CONCLUSIONS: A pacing-induced increase in QTc and QRSd is related to sVTA in patients with CRT. Further studies are needed to determine whether optimization of CRT with the goal to achieve a narrow paced QRSd can reduce the occurrence of sVTA.
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Prochnau et al. (2011) conducted a cohort in drug-resistant heart failure (n=127). Paced QTc and QRS duration was evaluated on Sustained ventricular tachyarrhythmias (sVTA) (p=<= 0.003). Longer paced QTc (505 vs 486 ms, P<=0.003) and QRS duration (182 vs 167 ms, P<=0.03) were associated with sustained ventricular tachyarrhythmias in patients receiving cardiac resynchronization therapy.
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