Why ICD still send out atrial pacing pulse after ventricular
extrasystole occurrence in a patient with old myocardial infarction
Kang Li,MD,Yansheng Ding,MD ,Jing Zhou*,MD
Department of Cardiology, Peking University First Hospital, Beijing,
China
*Corresponding author: Jing Zhou
zhoujing123@gmail.com
Postal address:
Xishiku Str.8,Xicheng District,Beijing,China,100034
Conflict of interest:None
A 78-year-old male with ischemic cardiomyopathy and old myocardial
infarction (the posterior inferior left ventricle and interventricular
septum), left ventricular ejection fraction 30%,initially had a
dual-chamber implantable cardioverter-defibrillator (ICD) placed 6 years
ago. After that, AAI pacing was dominant in managed ventricular pacing
mode (MVP mode :AAIR<=>DDDR and
AAI<=>DDD,Medtronic), the pacing rate was
previously set to 55 times / min),with paroxysmal atrial fibrillation
and frequent premature ventricular contraction (PVC), without sustained
ventricular tachycardia recording or discharge events. And judging from
QRS morphology of the PVC: it maybe originated from the scar zone of old
myocardial infarction in the
posterior inferior left
ventricle.(Figure-1:①)
He underwent a routine ICD (Medtronic Evera S DR DDBC3D4) replacement
when the existing device reached the recommended replacement time. Both
leads were tested at that time and found to be fine,located in the right
auricle and the right ventricular apex. Just after the replacement
procedure,we found something like
troubleshooting(Figure-1: ②).
Why did ICD still send out atrial pacing(AP) pulse and follow-up
ventricular safety pacing (VSP) after the occurrence of PVC?
Obviously,there was a significant delay from the onset of PVC to the
sense of PVC by the ventricular electrode(VS). The interval between PVC
and previous AP was 920ms, and the right ventricular electrode was
delayed for 90ms to detect PVC(Figure-1: ②). Because of the default
pacing rate of 60 times / min, ICD sended out AP pulse according to the
pacing interval of 1000ms, which was 10 ms earlier than the delayed
perception of PVC. Then the ventricular electrode sensed the ventricular
activation of PVC,and sended out the VSP after the AP
pulse(Figure-1:②). When VSP
function was turned off, ICD still sended out AP pulse after PVC as a
result of the conduction delay of 90ms, but no VSP was released again.
AP produced atrial activation and failed to transmit down due to falling
into ventricular refractory period(Figure-1:③).
We adjusted the pacing rate of ICD from 60 to 55 times / min, then the
pacing interval was 1090ms. The ventricular electrode could sense the
PVC(920ms + 90ms = 1010ms) from the delayed conduction to the left
ventricular posterior inferior origin without overlapping the AP pulse.
After MVP turned on, it took 40 ms for AP+VS to transmit the ventricular
activity from the atrioventricular node to the right ventricular
electrode, and 90 ms for AP+PVC to transmit the scar zone of ventricular
myocardium due to old myocardial infarction to the right ventricular
electrode(Figure-2:①). We modified the sense polarity of the right
ventricular electrode from “tip to ring” to “tip to coil”, but there
seemed to be no significant difference in the delay of ventricular
perception.
Later, when the patient’s oral dosage of beta blocker was increased, the
AV delay was prolonged and the conduction block was more severe than
before. Because of MVP function, inhibiting ventricular pace(VP),thus
AP+VSP and AS without VP appeared regularly (Figure-2: ②). Because of
the regular occurrence of ventricular pacing missing, the patient’s
palpitation became worse.And the increase in the proportion of right
ventricular apical pacing may worsen cardiac function. Finally, our
solution is to reduce the dosage of beta blocker, set ICD pacing rate of
55 times / min, MVP on, VSP on, and suggested the strategy of catheter
ablation of PVC.
The main reason for the delay of ventricular electrode perception is the
slow conduction through the scar zone of posterior inferior left
ventricle and interventricular septum due to the old myocardial
infarction(Figure-3). The second reason is the deterioration of
conduction system itself(senile degeneration, old myocardial infarction
involving conduction system, ventricular septal conduction time
delay).The latter was confirmed by the significant atrioventricular
block after increasing the dose of beta blocker.