Optimization of the AV delay in a non-dependent patient

Tracing
N° 9
Manufacturer Medtronic Device CRT Field AV & VV delays optimization
Patient

66-year-old man implanted with a triple-chamber defibrillator Viva XT CRT-D for idiopathic dilated cardiomyopathy with complete AV block; pacemaker interrogation 3 days post implant.

Graph and trace

The first line corresponds to an electrocardiographic lead with superimposed markers (MA), the second line to the bipolar right ventricular EGM (EGM3) and the third line to the bipolar atrial recording (EGM1);

  1. the programmed paced AV delay is short (100ms); atrial paced rhythm and biventricular pacing (AP-BV cycles); on the atrial EGM, we can see that ventricular depolarization occurs just in the middle of the atrial depolarization; probable complete biventricular capture;
  2. the paced AV delay is extended to 130 ms; the ventricular stimulus is less premature compared to the previous atrial EGM; modified pattern of the ventricular EGM corresponding to a fusion (pattern close to that of complete biventricular capture);
  3. the paced AV delay is extended to 160 ms; the ventricular stimulus now occurs at the end of the atrial depolarization; modified pattern of the ventricular EGM which is completely different from the pattern during the complete biventricular capture;
  4. the QRS pattern is variable depending on the degree of fusion which varies from cycle to cycle according to the degree of spontaneous atrioventricular conduction;
  5. the paced AV delay is extended to 200 ms; the device senses a spontaneous ventricular event and paces accordingly (VVT mode corresponding to the programmed response to a sensed ventricular event); markers indicating a fusion between the VS and BV;
  6. programming in AAI mode;
  7. spontaneous QRS pattern very close to that obtained in VVT mode; this demonstrates that despite this algorithm (response to a sensed ventricular event), the degree of biventricular capture often remains modest.
Comments

In patients with preserved atrioventricular conduction, which represents the majority of CRT patients, the prolongation of the AV delay leads to a progressive fusion with spontaneous activation. The AV delay setting changes the delay interval between atrial systole and ventricular systole, interferes with the quality of filling but also with the degree of capture and fusion with intrinsic activation; this setting must therefore be performed under electrocardiographic control.

As with the previous patient, the shortest AV delay was associated with an amputated A wave but was also with the longest AV delay enabling complete biventricular capture. While prolonging the AV delay improved the quality of filling, it was also associated with a fused pattern gradually approaching the spontaneous pattern. The overall difficulty in setting the AV delay is to determine the optimum degree of fusion for the patient. One of the few elements of certainty is that the CRT device was implanted to modify the patient's activation sequence deemed to be deleterious to his cardiac function. While it is difficult to determine which is the optimal activation sequence, it appears essential that it be completely different from that observed before implantation. A too high degree of fusion does not seem to be desirable. A setting of the AV delay paced at 130 ms was selected in this patient without the certainty that this programming truly corresponds to the optimal AV delay.