Unusual Polymorphic Ventricular Tachycardia Originating from the Pulmonary Artery
A 27-year-old male presented with an episode of syncope while playing soccer. During the episode of syncope, a pulse was detected and sphincter function was preserved. He had experienced pre-syncope three times during resting status over the most recent 2 months. He had no history of hypertension and diabetes mellitus. He had no family history of sudden cardiac death or syncope. Also, he did not take any medication.\nA physical examination revealed that blood pressure was 130/80 mm Hg and heart rate was 78 beat per minute. Other physical examinations were normal. Baseline electrocardiography (ECG) showed a sinus rhythm with frequent PVC and non-sustained polymporphic VT (). QT interval was 370 ms. PVC morphology, which triggers polymorphic VT is uniform and identical to that of isolated PVC. Initiation of polymorphic VT is not related to the fixed coupling interval. There was no QT interval prolongation, ST elevation on the precordial lead, and abnormal notch at QRS wave. Holter monitoring showed frequent PVC greater than 40% a day and frequent non-sustained polymorphic VT, and there was no diurnal variation in their occurrence (). He felt no specific symptoms during polymorphic VT. A laboratory blood study including serum electrolytes showed no abnormalities. An exercise test using a treadmill showed no changes of PVC and non-sustained polymorphic VT frequency. Isoproterenol infusion did not change in corrected QT interval and PVC frequency. There was no remarkable structural heart disease on the echocardiography except for borderline left ventricular dysfunction (left ventricular ejection fraction=52%). Coronary angiography involving right ventricular angiography was normal and coronary spasm was excluded using the provocation test with ergonovine. A cardiac MRI after catheter ablation also showed no remarkable finding involving the right ventricle.\nWe thought that isolated PVC triggered polymorphic VT and then ablation of the PVC could abolish the genesis of polymorphic VT. Using activation mapping with an adjustable Lasso catheter (Biosense Webster, Diamond Bar, CA, USA) via the SL1 sheath (St. Jude Medical, Daig Division, Minnetonka, MN, USA), which was positioned at the right ventricular outflow tract (RVOT), a discrete potential was detected at the pulmonary artery just above the pulmonary valve, the free wall side of RVOT (). The local potential preceded the QRS onset by 60 ms and showed relatively high amplitude and reversal of polarity (). Radiofrequency ablation was done just above the pulmonary valve with the temperature setting of 60℃. After radiofrequency delivery for 3.2 seconds, PVC was abolished. There was no PVC or non-sustained VT on the ECG and Holter ECG (). Symptoms of vague chest discomfort improved and there was no PVC free of medication after a 2 month follow up visit.