Case Report
Eighteen years old female presented to our arrhythmia outpatient clinic with palpitation for past 12 months. Her symptoms were milder before but worsened during last weeks. She has been diagnosed with frequent premature ventricular contractions (PVC) and treated before with oral beta-blocker, isoptin, flecainide and amiodarone. The patient was referred to our center for catheter ablation after observing no improvement in her symptoms and failing in the suppression of PVC’s.
Her medical and family history was unremarkable. Lab tests revealed normal complete blood count, cardiac troponins, biochemistry and thyroid hormone panel. 12-lead standard electrocardiography (ECG) revealed sinus rhythm with ventricular bigeminy (Figure 1A). PVC’s had inferior axis with R wave larger in DIII compared to DII, early precordial transition at V3 and slurring in the initial segment of the QRS which were suggestive of LVS and epicardial origin9. Transthoracic echocardiography (TTE) demonstrated normal left and right ventricular functions and no signs of any structural heart disease. Holter recording was performed for quantifying the burden of PVC’s and revealed 96000 PVC’s over 72 hours (Figure 2A). The patient was planned to undergo catheter ablation with 3D mapping system (EnSite Precision, Abbott, MN, USA). The mapping and ablation was performed by using 3.5-mm tip irrigated catheter. First, septal side of the right ventricular outflow tract (RVOT) region was mapped. No early ventricular signal could be recorded from these regions. We then assessed the coronary cusps and the left ventricle (LV) endocardial region below the left coronary cusp. However, we could not find early ventricular electrograms to proceed with ablation. Lastly, great cardiac vein (GCV)/anterior interventricular vein was mapped (Figure 3). An area with 26 ms pre-QRS signal (-26 ms) was found and pace mapping showed satisfactory match. Ablation was performed to this area after demonstrating more than 5 mm distance from coronary arteries. The power was set to 30 W with a maximum temperature 45 C° and aiming for a minimum 10 Ω drop in impedance. The power was titrated with 5 W up to 50 W in case impedance did not drop at least 5 Ω within the first 10 seconds. Although PVC’s were transiently suppressed, they ensued following the cessation of the ablation. The procedure was ended after failing to achieve the suppression of PVC’s.
In the morning after the procedure that patient was still complaining of palpitations and her ECG showed frequent PVC’s. After considering various medications that were used by the patient previously, we started ivabradine 5 mg BID after counseling with the patient about the potential side effects of the drug. Two days later her complains improved significantly, the mean heart rate was 84 bpm and no side effects were observed. The dose was increased to 7.5 mg BID and the patient was discharged from the hospital with a planned outpatient clinical visit a week later. In the clinical visit she reported no palpitations, her ECG showed normal sinus rhythm with a mean heart rate 79 bpm (Figure 1B) and no PVC’s. Seventy-two hour Holter recording demonstrated 12000 PVC’s burden (Figure 2B), which was significantly lower compared to the one that was recorded prior to ivabradine treatment. Considering patient was asymptomatic, we did not increase the ivabradine dose to 10 mg BID for further suppressing PVC’s. Serial clinical visits were planned for the evaluation of PVC burden and LV functions.