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.