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).