This report describes the case of an active 64-year-old man with an implantable cardioverter-defibrillator (ICD) who received several ICD shocks while exercising.The review of this clinical event highlights the need for high-energy devices since there is often variation in energy required to terminate tachyarrhythmias.
A 64-year-old man was referred to our practice in November 2010 due to a history of ventricular tachycardia (VT), ischemic cardiomyopathy, and an ejection fraction of 30%. On November 30, 2010, the patient underwent implantation of a 40 joule (J) high output dual chamber ICD system (Fortify model 2231-40Q, St. Jude Medical, St. Paul, MN; CapSureFix® atrial lead, model 4076, Medtronic, Minneapolis, MN; and Durata single coil ventricular lead, model 7122Q, St. Jude Medical). The atrial and ventricular leads were placed in the right atrial appendage and right ventricular apex, respectively, and connected to the ICD placed in the left pectoral region. Lead testing showed normal function (atrial capture threshold of 0.5V at 0.5ms, P wave sensing at 5mV, and an impedance of 650 ohms; ventricular capture threshold of 0.5V at 0.5ms, R wave sensing at 12mV, and an impedance of 630 ohms). Defibrillation threshold (DFT) testing was completed using the Shock-on-T induction method, revealing a DFT of less than or equal to 15J and a high voltage impedance of 78 ohms. The device was programmed in a two-zone configuration (VT: 160–199 bpm. ATP x 5, 36J, 40J x 3; VF: >200 bpm. 36J, 40J x 5).
Prior to the following event, the patient was seen for device follow-up on five separate occasions. During this time, the device function was deemed normal and a total of 28 VT episodes were recorded. Twenty-seven of the episodes were either non-sustained or successfully terminated by anti-tachycardia pacing (ATP), while one was terminated with a 36J shock after ATP was unsuccessful at conversion.
At the time of the following event, the patient’s medications were carvedilol, aspirin, warfarin, niacin, ramipril, and vytorin. Amiodarone was discontinued in February 2011 due to its possible exacerbation of the frequency of VT episodes.
While the patient was participating in a 10K walk on April 2, 2011, he experienced near syncope and two subsequent ICD shocks. Upon admission to the emergency department, the patient denied chest pain and shortness of breath. He inadvertently failed to take his beta blocker dose that morning. Upon device interrogation, stored electrograms revealed that the patient had three episodes of VT. The first was at a rate of 187 bpm for which the device delivered four sequences of ATP to terminate the rhythm (Figure 1). After a very brief return to sinus, the rhythm reaccelerated to a rate of 193 bpm. Three bursts of ATP failed to convert the VT and the rhythm continued to accelerate into the VF zone. The first shock was delivered at 36J but failed to convert the arrhythmia (Figure 2). After redetection, a 40J shock successfully terminated the ventricular arrhythmia (Figure 3).
Lead testing showed normal function (atrial capture threshold of 0.5V at 0.5ms, P wave sensing at 5mV, and an impedance of 440 ohms; ventricular capture threshold of 0.75V at 0.5ms, R wave sensing at 12mV, and an impedance of 630 ohms). The high voltage impedance was 82 ohms.
The patient underwent left heart catheterization, which revealed patent ducts. The patient also underwent DFT testing. Using the DC Fibber™ (St. Jude Medical) induction method, VF was induced and successfully converted with a single 20J shock. Upon return to our practice, the patient was started on mexiletine and repeat defibrillation testing was done, revealing a DFT of less than or equal to 15J.
The 40-joule delivered shock that finally converted the VT was at least double his defibrillation threshold at implant and two separate DFT tests conducted after this episode. The failure of 36J to terminate this patient’s tachyarrhythmia is unusual given these DFT results. One possibility is that it was a random failure as the ability of an ICD to defibrillate is probabilistic in nature. Strickberger et al1 reported that the likelihood of defibrillation at a delivered energy equal to the defibrillation threshold is 70 ± 27%. At an absolute safety margin of 7J, the probability increases to 96%.1 In the present case report, 36 joules failed to convert the tachyarrhythmia. Considering this 21J safety margin, the probability of the failure being random is highly unlikely.
One may also speculate that the energy required to terminate spontaneous tachyarrhythmias may be greater than that required to terminate induced tachyarrhythmias. However, Gold et al2 reported that with a safety margin of 4 to 6 J above DFT, the conversion success for spontaneous arrhythmias >200 bpm was 97.3%,2 making this theory also unlikely.
An area that is less understood is the effect of exercise or autonomic tone on the ability to defibrillate. In order to simulate the effects of moderate exercise on DFTs at the time of implant, Kalus et al3 studied the impact of catecholamines on defibrillation threshold in 50 patients. Compared to baseline, norepinephrine reduced DFT by 22.6% while epinephrine and placebo had no significant impact.3 While this information is helpful in quantifying the impact of elevated plasma concentrations of catecholamines on the DFT, it’s difficult to draw any major conclusions about exercise and DFT. To our knowledge, impact of exercise on DFT has not been reported. This type of study would be difficult to conduct since most patients with ICDs are not physically active and spontaneous tachyarrhythmias during exercise are rare.
One plausible explanation for the failure of the first shock in this case may be the duration of arrhythmia. Previous studies have shown that defibrillation efficacy decreases with increasing VF duration.4,5 In the present case report, the patient was in the tachyarrhythmia for 39 seconds prior to the first shock due to the use of a high number of intervals to detect (30) and the use of three bursts of ATP.
Highlighting the complexity of potential shock failure and success, this case report provides evidence to the importance of a high output device even in the setting of low DFTs at implant. The energy required to defibrillate can vary due to myriad reasons. Device manufacturers continue to make ICDs smaller while increasing the delivered energy capabilities. When the prevention of sudden cardiac death is the goal in ICD therapy, it is difficult to make a case for not implanting a high-energy device.
- Strickberger S, Daoud E, Davidson T, et al. Probability of successful defibrillation at multiples of the defibrillation energy requirement in patients with an implantable defibrillator. Circulation 1997;96:1217–1223.
- Gold MR, Higgins S, Klein R, et al. Efficacy and temporal efficacy of reduced safety margins for ventricular defibrillation: Primary results from the Low Energy Safety Study (LESS). Circulation 2002;105:2043–2048.
- Kalus J, White M, Caron M. The impact of catecholamines on defibrillation threshold in patients with implanted cardioverter defibrillators. Pacing Clin Electrophysiol 2005;28:1147–1156.
- Gradaus R, Bode-Shnurbus L, Weber M, et al. Effect of ventricular fibrillation duration on the defibrillation threshold in humans. Pacing Clin Electrophysiol 2002;25:14–19.
- Windecker S, Ideker R, Plumb V. The influence of ventricular fibrillation duration on defibrillation efficacy using biphasic waveforms in humans. J Am Coll Cardiol 1999;33:33–38
- Pelosi F Jr, Oral H, Kim MH, et al. Effect of chronic amiodarone therapy on defibrillation energy requirements in humans. J Cardiovasc Electrophysiol 2000;11:736–740.
Disclosure: Dr. Hsu is the principle investigator for the ENVISION study at Mid Carolina Cardiology and a co-investigator on the SJ4 Post Approval Study and the DEFEAT- PE trial, all sponsored by St. Jude Medical. Chad Beaver and Anne Giguere are employees of St. Jude Medical.
Editor’s Note: This article underwent peer review by one or more members of EP Lab Digest’s editorial board.