What Can We Do if Recommended Medical Therapy and Catheter Ablation for Frequent Premature Ventricular Contractions Fail

A 44-year-old man without structural heart disease and with symptomatic frequent premature ventricular contractions (PVCs) was referred to our clinic in 2009. He had family history of sudden cardiac death (SCD). It was a normal study by ECHO with preserved left ventricular (LV) systolic function. The 24 h Holter monitoring registered up to 31,000 monomorphic frequent PVCs. For risk stratification we evaluated his cholesterol level, which was in the normal range, and performed exercise testing, during which the frequency of PVCs decreased. All other laboratory data, including thyroid hormones, were in normal ranges. Having in consideration current recommendations, we started therapy with a b-blocker titrated to the maximal therapeutic dose (bisoprolol 10 mg/day). On repeated Holter monitoring there was no decrease in PVC count and the patient continued to be symptomatic. Using a 12-lead ECG, it was suggested that origin of the PVCs was outflow tract (Figure 1). The morphology of PVCs suggested an outflow tract origin as QRS complexes were strongly positive in the inferior leads (II, III, aVF) and strongly negative in aVL and aVR. Transition of QRS in precordial leads in this case was at the ‘‘border zone’’, between V2 and V3. So, right ventricular outflow tract (RVOT) ventricular tachycardia (VT) was suggested. As medical therapy was not effective for this patient, he was referred for an electrophysiologic (EP) study. During EP study, activation and pace mapping had been performed in the RVOT. The earliest activation site was in the RVOT posterior segment of the septal wall. Although fixed pace mapping was not identical on 12lead ECG, we put a couple of lesions in the posterior segment of RVOT and there was no result. Then, we performed left ventricular outflow tract (LVOT) activation and pace mapping and contrast imaging of sinus Valsalva and coronary arteries. The earliest activation site was the left coronary cusp close to the left main coronary artery. In the same site, pace mapping was identical on 12-lead ECG. And by the activation map it was preceding the target QRS by about 20 ms (Figure 2a,b). We refused to put lesions at this site because of proximity to the left main coronary artery. Following this, we started thinking about use of alternative drugs or drug combinations and started with sotalol. As there was no change in the patient’s symptoms within 2 weeks of therapy, we did not uptitrate the dose to more than 160 mg/day. Flecainide is not a registered drug in Armenia, so we could not use it. The patient refused treatment with amiodarone because of the possible adverse effects of long-term therapy. Before starting any drug combination, we decided to start IC class of Vaughan Williams classification of antiarrhythmic agentspropafenone (450 mg/day). On this drug, the patient became asymptomatic. During The authors report no conflicts of interest for the published content. Manuscript received April 26, 2011, final version accepted May 20, 2011. Address correspondence to: Hermine R. Poghosyan, MD, 14 Titogradyan Street, Building 14, Left Wing, 4 Floor, Yerevan, Armenia, 0087. E-mail: herminep@mail.ru The Journal of Innovations in Cardiac Rhythm Management, 2 (2011), 408–411