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Pacemaker can be life-saving in high grade atrioventricular (AV) blocks. But this reality is occasionally challenged by arrhythmias induced by ventricular pacing. Some of the events are related to automated pacemaker algorithms. Managed ventricular pacing (MVP) is one such example which has delivered benefits but has also been associated with ventricular tachyarrhythmias (VT). Our case is possibly the first report of hysteresis induced symptomatic VT.

A 68-yr-old lady underwent a VVI pacemaker implantation 10 years back for infra-hisian complete heart block. Now she presents with 3 episodes of syncope within the last 2 months. Detailed neurological evaluation and pacemaker checkup was initially unremarkable. Real time electrograms during device interrogation were suspicious of lead noise resulting in oversensing. She became alright when the pacing mode was made VOO immediately. After discussion with patient relatives she underwent ventricular lead replacement and upgradation to a dual chamber pacemaker. However, in the immediate post-operative period she became unresponsive requiring immediate resuscitation. Monitor suggested short runs of polymorphic VT which was reproducibly suppressed with higher rate obligatory pacing @ 110 bpm. The runs of VT resurfaced immediately as the rate was lower than 90. She was managed by overdrive pacing at a lower rate of 110 bpm. Over the next 2 months the lower rate was brought down to 70 bpm in a stepwise manner. A retrospective analysis of her initial stored device electrogram suggested that it was all PMVT and no noise at all. The cause of her polymorphic VT is not clear. Relative hypomagnesemia, late presenting long QT syndrome and long term VVI pacing in isolation or combination remain the probable offender. She is presently doing well on oral propranolol.

Typical atrio-ventricular nodal re-entrant tachycardia (AVNRT) can occasionally remain easily inducible after slow pathway (SP) modification in lower Triangle of Koch (TOK). Analysis of resetting response by delivering atrial premature depolarizations (APD) from various sites (TOK, right atrium, coronary sinus and left atrium) can pin-point the culprit SP serving as the antegrade limb of the tachycardia circuit. However, the maneuver is under-utilized by most centers. We describe a case where anatomical SP modification in TOK failed to cure the arrhythmia. The resetting maneuver performed subsequently, helped us to rule out leftward inferior extension of SP and suggested right inferior SP as essential part of AVNRT circuit. Further ablation was performed at M1-M2 region (on the right side) to achieve success.

A 65-year-old gentleman with dual chamber pacemaker presented with presyncope. The ECG raised concerns of oversensing which was confirmed by magnet response. The device interrogation revealed noise in ventricular channel temporally associated with P wave. The pacing thresholds were normal. Although the ventricular lead impedance was within normal limit the impedance trend suggested 100 Ω decline over last 1 year. RV lead insulation failure was speculated and supported by the bipolar and unipolar intracardiac electrogram. Device was programmed to DOO temporarily. He underwent RV lead replacement uneventfully.