Tachycardiomyopathy Induced by Ventricular Premature Complexes: Complete Recovery after Radiofrequency Catheter Ablation
A 32-year-old male patient visited the emergency room and presented with resting dyspnea and palpitations. He had suffered from intermittent palpitations and dyspnea (class II) for more than 10 years. He had undergone a radiofrequency catheter ablation procedure 10 years ago for these frequent VPCs without success at another hospital. He had received intensive heart failure medications including beta-blockers, angiotensin-converting enzyme inhibitors and spironolactone from a local hospital during the last two years.\nA physical examination revealed jugular vein engorgement and slightly rapid and irregular heart sounds. His vital signs were as follows: a blood pressure of 110/70 mmHg, a pulse rate of 88 beats/min and a respiration rate of 21 breaths/min. The standard 12-lead electrocardiography (ECG) revealed frequent VPCs. The right ventricular outflow tract was suspected as being the origin of this condition due to the negative deflection of the VPCs in lead V1, the positive deflection in leads II, III and aVF, and the QRS transition in lead V4 (). The chest X-ray revealed cardiomegaly and increased broncho-vascular markings. The echocardiography demonstrated dilatation of the left ventricle (LV) and a decreased LV contractile function (LV end-diastolic dimension: 66 mm, LV end-diastolic volume: 211 mL and an ejection fraction: 34%) (). A 24 hour ambulatory ECG showed very frequent VPCs; there were 22,256 isolated VPCs and 16,081 couplets out of 123,139 total heart beats (31%) during 22 hours.\nAn electrophysiological study and radiofrequency catheter ablation were performed after obtaining an informed written consent on the following day after hospital admission. A 6 Fr. Quadripolar electrode catheter was positioned in the right ventricular (RV) apex. A 7 Fr. deflectable quadripolar ablation catheter (Boston Scientific EP Technologies, Natick, Massachusetts) with a 4-mm-tip electrode was introduced percutaneously into the RV using an 8 Fr. SR0 sheath (Daig®). The origin of the spontaneous VPCs was determined based on the 12-lead-surface ECG and it was further located with the mapping catheter that was placed into the RV outflow tract. The triggering focus of the VPCs was located in the high anteroseptal region ().\nThe electrograms recorded from the ablation catheter were very tiny in the area that was mapped, and this was probably due to the scar formation created by the previous unsuccessful radiofrequency catheter ablation. The onset of the bipolar electrogram of the spontaneous VPCs recorded by the ablation catheter was 38 ms earlier than that of the surface ECG, and the unipolar electrogram had abrupt negative deflections without an initial positive component at the site we chose for ablation (). Radiofrequency energy was delivered for 60 seconds with a preset temperature of 60℃ and power limit of 40 W. The VPCs disappeared within 5 seconds after reaching a tissue-electrode temperature of 50℃. A booster application of energy was delivered to four sites around the successfully ablated focus for 30 seconds each.\nA 24 hour ambulatory ECG taken the same day as the radiofrequency catheter ablation procedure recorded only a few atrial premature complexes without any VPCs. The medications that has been administered for heart failure before the treatment were continued thereafter. No VPCs were observed throughout a series of ECGs that were recorded during the 6 months following his discharge. The LV dimensions and function returned to normal, as determined by the 6 month follow-up echocardiography: the LV end-diastolic dimension was 51 mm and the ejection fraction was 55% ().