A 66-year-old Han Chinese male was admitted after several VT attacks over the course of 1 month. The patient was diagnosed with rheumatic heart disease and impaired left ventricular ejection fraction (LVEF) of 42% in a functional New York Heart Association stage III, suffering from VT/VF and atrial fibrillation. He underwent surgery of the mitral valve and an aortic valve replacement 10 years ago. Electrolytic measurements showed sodium, calcium, and potassium values were within the normal range. He was treated with aldosterone antagonist, angiotensin converting enzyme inhibitor, lidocaine, β-blocker, and amiodarone, but VT recurred despite the optimized drug treatment. Additional doses of antiarrhythmic drugs were administered but unsuccessful. The patient was placed on amiodarone 200 mg orally once a day and metoprolol 25 mg orally four times a day. Attempts to reduce the frequency of VT using optimized antiarrhythmic drugs failed. VT could only be terminated by external cardioversion. The patient satisfied the requirement for ICD therapy according to the criteria of the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT), [5] so a single chamber ICD (Model 1231–40, St. Jude Medical Cardiac Rhythm Management, USA) was implanted with lead in the right ventricular (RV) apex after symptom stabilization (Fig. 1a). During the implantation, electrical specifications were confirmed, including the R-wave of 9.0 mV, the slew rate of 1.7 V/s, the impedance of 574 Ohm, and pacing threshold of 0.6 V/0.5 ms.
Two days later, the patient was abruptly awakened by an episode of VT/VF. The initial administration of the ATP therapy through the ICD was unsuccessful. VF was finally terminated by a 36 J ICD shock. Frequent ICD shocks were associated with anxiety and intolerance of ICD therapy. The patient was thin and weak. ATP and Low energy cardioversion (15/25 J) were successfully used to relieve the patient’s pain, anxiety and possible myocardial injury (Fig. 2-a, b, c). Overall, the patient experienced 155 episodes of VT/VF and received a total of 27 shocks after the first implantation of ICD. The most severe attack was 34 VT/VF episodes within 24 h. Rarely, a 36.0 J shock at last reverted VT, which was not terminated by ATP burst and a 15.0 J/25 J shock (Fig. 2-d). Frequent ICD discharges depleted the battery life considerably. His treatment was aggressively escalated. Catheter ablation was contraindicated because of the patient’s metal valve and multiple original VTs. Renal artery denervation was recommended but refused. Attempts to reduce the frequency of VT only using antiarrhythmic drugs, such as lidocaine, were unsuccessful. The combination of ATP and intravenous esmolol seemed to reduce, but did not fully eliminate the episodes of VT.
After repeated discharge of the device for 8 weeks, the capture threshold was gradually increased. Initial threshold of device interrogation was respectively 2.37 V/0.5 ms, 2.75 V/0.5 ms, and 3.75 V/1.0 ms in 2, 4 and 9 weeks post- implantation (Additional file 1). Thorax X-ray at 9 weeks post-implant did not show apparent dislocation of the lead (Fig. 1b). Considering the patient’s reliance on the pacemaker, we decided to reposition the RV lead to better match the ventricular myocardium in the threshold field as a final alternative (Fig. 1c). Fortunately, this remedy did lower the pacing threshold. Lead measurements showed the ventricular sensing at 11.3 mV, a pacing threshold of 1.4 V/0.5 ms, and an impedance of 730 Ohms. The further clinical course of the patient was uncomplicated and he was discharged in good clinical status after the surgery. Recent device interrogation respectively showed a ventricular sensing of 8.9 mV, 7.9 mV and 9.1 mV, a pacing threshold of 1.75 V/0.5 ms, 1.5 V/1.0 ms and 1.5 V/1.0 ms at 13, 20, 24 months post-implantation follow-up (Additional file 1). Amiodarone 200 mg qd and metoprolol 25 mg q6h were given to enhance the efficacy of anti-arrhythmias. The patient’s pacing threshold and ventricular arrhythmias have carefully being monitored in the long term. Until now, the shock never occurred again and ATP burst significantly decreased.