This 81-year-old man received an Adapta dual chamber pacemaker for atrial disease, sinus node dysfunction and episodes of paroxysmal AF; he was seen on routine visit.
Tracing 3a: the first channel is lead I of the surface ECG with the markers superimposed, the second channel shows the ventricular EGM, and the third is the marker channel;
Tracing 3b: tracing recorded a few seconds later;
Tracing 3c: no optimization of atrial sensing possible despite programming to the best capabilities of the device; change in pacing mode and programming to DDI;
The proper function of mode switch requires accurate sensing of arrhythmic atrial signals, the amplitude of which is most often lower than the amplitude of signals of sinus origin. Therefore, the proper sensing of atrial arrhythmias cannot be inferred by a measurement of the signals during sinus rhythm. In this patient, this intermittent sensing was responsible for repetitive alternation between synchronous (DDD) and fallback (DDIR) mode, with unnecessary ventricular pacing and energy consumption. Inhibition by the QRS alternated with ventricular pacing synchronized to atrial sensing, which was programmed to the highest value allowed by the device, leaving no room for additional optimisation. Programming of the DDI mode seemed appropriate for this patient presenting with atrial disease, as it enabled atrial pacing when he was in sinus rhythm, and prevented the development of erratic ventricular pacing due to the absence of mode switch when he was in AF.
In contrast to the previous tracing, a rate slowing treatment was necessary for this patient whose AV conduction was preserved. A treatment with a beta-adrenergic blocker or a calcium antagonist was preferred as it was likely to be effective at rest as well as during exercise. These treatments are also likely to slow the sinus rate and promote atrial pacing and AV synchronization in DDI mode.
