We report on a patient with ischaemic cardiomyopathy who had received an implantable cardioverter-defibrillator for recurrent ventricular tachycardia (VT). He also developed paroxysmal atrial fibrillation (AF) which led to therapy with dronedarone. As demonstrated by the device memory, the drug not only suppressed AF but also completely suppressed VT.
Patients with advanced structural heart disease often suffer from atrial fibrillation (AF) and from ventricular arrhythmias. Although implantable cardioverter-defibrillator (ICD) therapy and catheter ablation are often used to treat ventricular tachycardia (VT), some patients continue to have frequent VT episodes triggering ICD therapy. Frequent ICD shocks, however, result in significant impairment of quality of life and may further impair left ventricular function. Thus, many patients continue to need antiarrhythmic drug therapy. We report here on such a patient who was intolerant to amiodarone and was subsequently treated with dronedarone.
A 69-year-old male suffered from inferior myocardial infarction in 2008 and underwent coronary bypass grafting. His left ventricular function was 45% at the time of hospital discharge. Four weeks after discharge, he was readmitted for sustained monomorphic VT (120–170 bpm). He underwent endocardial VT mapping and ablation. There were, however, frequent subsequent VT recurrences for which therapy with amiodarone was started. After a cumulative dose of 10 g, there was significant QT prolongation (QTc 555 ms) necessitating discontinuation of amiodarone. Subsequently, he underwent epicardial VT ablation and was rendered non-inducible. A dual-chamber ICD was implanted (St Jude Medical Atlas II+ DR V-268) directly after the VT ablation. The ICD was interrogated at close intervals at least every 3 months or when clinically indicated. Approximately 2 weeks after implantation, in January 2009, the patient started to receive ICD therapy for recurrent frequent VT episodes. All VT episodes were haemodynamically tolerated with rates around 150–170 bpm. Exercise could be detected as a possible trigger for the VT. Our patient suffered from 3 to >299 VT episodes per month (Figure 1), of which more than 90% were terminated by antitachycardia pacing. Standard SVT discrimination was programmed in the ICD for the diagnosis of VT and every available episode was checked by an experienced electrophysiologist. At the 12-month follow-up, more than 299 VT episodes were in the counter of the ICD memory. In terms of EGM storage, however, ICD memory is limited to 60 VT episodes. As all of the 60 EGMs showed the same VT and were adequate detections, we assumed that all of the other episodes with a similar cycle length were adequate detections as well. In parallel, the patient started in May 2009 to suffer from highly symptomatic paroxysmal AF. Some of these AF episodes resulted in inappropriate ICD therapy. EGM recordings were available and verified in all cases by experienced electrophysiologists. Upon approval of dronedarone for treatment of paroxysmal AF in Germany in January 2010, the patient was started on dronedarone 400 mg bid. As demonstrated in the device memory (Figure 1), dronedarone therapy yielded in a significant reduction in AF episodes and more impressively, in complete freedom from recurrent episodes of VT over the next 6 months. Unlike amiodarone, treatment with dronedarone did not prolong the QT interval (QTc 495 ms before, 485 ms during treatment). Furthermore, there was no significant change in LVEF 6 months after start of dronedarone.
Number of ventricular tachycardia episodes (green bars) and time in atrial fibrillation/months (red bars) since implantation of the implantable cardioverter-defibrillator. Note the complete suppression of both, atrial fibrillation and ventricular tachycardia, shortly after initiation of dronedarone therapy.
Dronedarone is a new multichannel blocking antiarrhythmic drug which has been shown to be effective for rhythm and rate control in patients with AF.1 In addition, the compound has been demonstrated to reduce cardiovascular events such as cardiovascular hospitalization or death in a large randomized trial.2 Dronedarone is approved for therapy of non-permanent AF in many jurisdictions. Preclinical studies have indicated that the drug has not only antiarrhythmic effects on the atrial but also on the ventricular myocardium.3 Although dronedarone has not been specifically tested in patients with sustained VT, there is evidence for a beneficial effect on electrical vulnerability of the ventricles in humans. Specifically, the ATHENA study2 demonstrated a reduction in arrhythmic death in patients receiving dronedarone compared to controls.2 In accordance with this observation, the present case illustrates a strong effect in preventing episodes of recurrent VT. Another important observation in our patient is the fact that dronedarone did not cause a clinically significant prolongation of the QT interval whereas amiodarone had to be discontinued.
Conflict of interest: S.H.H. has received consulting fees from Sanofi Aventis, Cardiovie, ARYx Therapeutics, and Bristol-Myers Squibb, research grants from Sanofi-Aventis and St. Jude Medical, and lecture fees from Sanofi-Aventis, St. Jude Medical, Bristol-Myers Squibb. G.Z.D. has received lecture fees from Sanofi-Aventis and St. Jude Medical. A.F. reports no conflict of interest.
. Effects of a new amiodarone-like agent, SR 33589, in comparison to amiodarone, D,L-sotalol, and lignocaine, on ischemia-induced ventricular arrhythmias in anesthetized pigs. J Cardiovasc Pharmacol 1995;26:570-6.