Case report
This report was approved by the Ethical Committee of Xuzhou Central
Hospital and the patient signed informed consent willingly to support
this study. The 38-year-old female patient was implanted with St. Jude
dual-chamber pacemaker (Victory XL DR 5816) 3 years ago in Cardiac
Diagnosis and treatment Center of Xuzhou Central Hospital after
diagnosed with viral myocarditis, sinus bradycardia, and
atrioventricular block II. After palpitation for 1 month, the patient
came for re-diagnosis and we conducted pacemaker program control and
24-hour dynamic ECG tracking.
Details of pacemaker program control: operating mode, DDD; Basic
frequency,60 times/min; the rest frequency was 45 times/min; PAV, 275ms;
SAV, 250ms; AP accounted for 13% of total heart beats, and
VP accounted for 9.1% of total
heart beats.
A pace on PVC option by this specific pacemaker: upon the occurrence of
PVC event, the PVARP interval of 480ms will be on. The first 150ms of
PVARP is ARP and the latter 330ms is RRP. If P wave is sensed within the
RRP, it is called retrograde P wave and AP will be released at 330ms
behind this retrograde P wave (Figure 4).
Normal sinus rhythm. DDD, VAT and AAI modes. AP accounted for 15% of
the total heart beats, VP 9.0%, frequent PVC 3.2% and occasional PVC
73.3%.
Through ECG interrogation, pacemaker has aberrant responses to
occasional PVC: PVC was marked in Figure 1 and 2, where ① and ④ pointed
at. After PVC, sinus P wave was
transmitted to ventricle and PVC recurred at ②. At the end of T wave
after this PVC, spontaneous P wave was seen clearly. However, this P
wave didn’t trigger VP of the pacemaker and it took 720ms from this PVC
to the next AP, shorter than VA interval.
At ② , the retrograde P wave occurred within the RRP(330ms period marked
in the Figure 1) after PVC, defined as AR event. Due to A pace on PVC,
the pacemaker could sense the retrograde P wave and release AP at 330ms
after AR without triggering VP.
③⑤ displayed a different response from ②. P wave after PVC occurred
within the ARP (the former 150ms in the PVARP interval) and couldn’t be
sensed by the pacemaker, which consequently resulted in the AP release
during the VA interval. This happened at 04.03 am at the rest status
with heart beats 45 times/min, VV interval 1340ms, PAV 275ms and VA
1065ms. ECG showed the patient had occasional PVC or VPB with three
typical patterns as below: sinus P wave was transmitted to ventricle, a
pace on PVC response by the pacemaker and AP was triggered during VA
interval after PVC.
Furthermore, a double pulse appeared after PVC(⑥, Figure 3) and the
interval was 275ms. The first pulse was AP. The QRS wave after PVC
occurred within the PAVB interval and remained undetected. Thereafter,
VP was released at 275ms after the AP and occurred in the VVP of sinus
QRS. Besides, this AP was 330ms after the AR event and the P wave was
over 280ms later than the QRS wave.
AP-VP sequence was also detected after PVC ⑦ and the interval was 120ms.
The first pulse was AP and was overlapped with the spontaneous sinus QRS
wave, which occurred within CDW and thus triggered the VSS function,
forming an AP-VS-VP sequence. The pacemaker could not tell whether the
signal was crosstalk or spontaneous and released an early VP to avoid
asystole. The AR event was 330ms earlier than the AP and the former QRS
wave was over 280ms earlier than this AR event due to a pace on PVC
option. The ECG results disclosed the combined outcomes of both
functions of a pace on PVC and VSS of the pacemaker. Therefore, after
the ECG interrogation, we turned off A pace on PVC option and asked the
patient to take 47.5mg Metoprolol Succinate Sustained-release Tablets
once every day. 1 month later, the follow-up results showed that
arrhythmia was alleviated significantly (Figure 5).