Incessant ventricular tachycardia and long-standing ectopic beats lead to tachycardia-induced cardiomyopathy. Catheter ablation eliminates ventricular tachycardia and reverses left ventricular (LV) dysfunction. 201-Thallium ((201)Tl) scintigraphy demonstrates perfusion defects with ischemic cardiomyopathy. Reversible perfusion defects are observed even in non-ischemic cardiomyopathy, related to regional flow or metabolism derangements. 123-I-metaiodobezylguanidine ((123)I-MIBG) scintigraphy delineates regional cardiac sympathetic denervation and heterogeneity. We demonstrated the progression of tachycardia-induced cardiomyopathy in a patient with idiopathic LV outflow tract tachycardia using (201)Tl and (123)I-MIBG scintigraphic findings. Regional defects were reversed predominantly in the basal interventricular septal wall in (201)Tl scintigraphy and (123)I-MIBG scintigraphic findings. This report suggests that incessant ventricular tachycardia or long-standing ventricular ectopic beats may develop adverse myocardial remodeling and sympathetic neurological remodeling. Treatment with catheter ablation for tachycardia-induced cardiomyopathy can reverse sympathetic neurological remodeling as well as myocardial structural remodeling.

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A 74-year-old man presented with palpitation and 12-lead ECG exhibited atrial premature contraction (APC) at general check-up. Holter ECG demonstrated narrow QRS tachycardia with a rate of 160/min and more than 31,000/day atrial premature beats. The P wave morphology of atrial premature beats showed negative in II, III, aVF and biphasic in V1. Venography was performed and disclosed persistent left superior vena cava (LSVC) draining into the right atrium via the markedly dilated coronary sinus (CS). Electrogram recordings from LSVC and CS were obtained with an electrode catheter via the left subclavian vein. At the level where a ventricular potential disappeared, the intra-LSVC potentials began to show a discrete second sharp potential after local left atrial signals. Double potentials were obtained within the LSVC from the lower left atrium (LA) to the higher LA. A proximal-to-distal activation sequence of the second components was observed. The interval between the 1st and 2nd component ranged from 8 to 22 msec between the proximal LSVC and distal LSVC. The double potentials resulted in fusion at the lower part of the LSVC, indicating the presence of an electrical connection between the LSVC and lower LA. The thoracic veins play an important role in the genesis and maintenance of atrial arrhythmias. 1)The left superior vena cava (LSVC) is the embryological precursor of the ligament of Marshall (LOM), which contains multiple electrical connections to the left atrium (LA). The electrical connection has also been implicated as an arrhythmogenic substrate of reentry in atrial tachy-arrhythmias. 2-4) Case ReportA 74-year-old man presented with palpitation and 12-lead ECG exhibited atrial premature contraction at general check-up. Holter ECG demonstrated narrow QRS tachycardia with a rate of 160/min and more than 31,000/day atrial premature beats. He was admitted for electrophysiologic study and radiofrequency ablation for the atrial tachycardia (AT).