Introduction: Permanent pacemaker (PPM) implanta-tion is regarded as curative in the prevention and treat-ment of bradycardia-induced ventricular arrhythmias. We present a case that raises the question whether a common pacemaker programming may cause synco-pal ventricular tachycardia.

Methods: A 65-year old man presented to our emer-gency department with recurrent syncope preceded by palpitations. Six months prior, the patient had a PPM implanted in another clinic for paroxysmal high-grade atrio-ventricular (AV) block, symptomatic by syncope and documented on 24-hour ECG monitoring. Baseli-ne ECG showed sinus rhythm, normal PR interval and complete left bundle branch. The operator opted for a single-chamber pacemaker, programmed VVI 60/min, hysteresis at 50/min. At the current presentation, ECG showed complete AV block, idioventricular rhythm at 55/min with long QTc interval (663 ms), intermittent paced QRS complexes and short runs of torsades de pointes (TdP).The patient required electrical cardio-version for a prolonged TdP episode. He was not taking any medication and had no significant family history. Clinical examination was unremarkable after stabili-zation. Serum electrolyte levels were also normal. In-terrogation of the PPM showed normal function and it was reprogrammed VVI 75/min. The following ho-urs, he remained in paced rhythm, with progressive shortening of the QT and disappearance of ventricu-lar arrhythmia. Echocardiogram during paced rhythm showed mild intraventricular dyssynchrony, left ventri-cular ejection fraction of 48% and no other significant abnormalities. Myocardial ischemia was excluded by normal coronary angiogram.

Results: T he case had two particularities: unusually fast idioventricular rhythm during AV block and long QT during this rhythm, without common causes for QT prolongation. The QT prolongation was proba-bly linked to electrical remodeling due to alternation between spontaneous (or eventually paced) ventricu-lar rhythm and idioventricular rhythm. The QRS vec-tors were markedly different between the two rhythms, which has been previously suggested as a cause for QT prolongation. Hysteresis allowed for long periods of the ventricular rhythm, which was the sole cause of TdP we identified. Management by upgrading to dual-chamber pacing or faster VVI pacing rate could have sufficed. However, since we could not completely ex-clude another (unrecognized) substrate for ventricu-lar arrhythmia, we chose to upgrade to dual-chamber implantable cardioverter-defibrillator, according to current guidelines. The procedure was performed une-ventfully, and the device was programmed DDD 60/ min with long AV interval and a ventricular fibrillati-on zone at >200/min. The patient was asymptomatic at one month.

Conclusions: Programming is of key importance even for simple devices. In rare cases, single-chamber hyste-resis can favor slow ectopic rhythms, which can be de-leterious.