Slow Ventricular Tachycardia Located in the Epicardium of the Left Ventricular Base and Characterized by Effects of Adenosine Triphosphate, Nicorandil and Verapamil

Abstract

A 31-year-old male had slow VT during an operation to repair a jaw fracture. He was referred to our clinic for closer examination. Physical examination and chest X-ray were both normal. The baseline of the ECG showed an incomplete right bundle branch block (RBBB). A Holter monitor showed 158 episodes of 3 or more consecutive ventricular premature contractions (VPCs) of which the longest VT lasted about 5 min with a slow rate of 75-95 beats/min (Fig 1). Exercise testing did not induce VT and no changes were shown in the ST and T waves.Cardiac catheterization revealed normal coronary arteries and normal intracardiac pressures. Left ventriculography showed a normal ejection fraction (61.5%), although the septum, anterolateral wall, and posterolateral wall were hypokinetic. Endomyocardial biopsy revealed mild hypertrophic myocardial cells with mild degeneration. Electrophysiological StudyInformed written consent was obtained before the electrophysiological study. Clinical VT could not be induced by programmed atrial and ventricular stimulation even under isoproterenol provocation, but a nonclinical polyJapanese Circulation Journal Vol.62, December 1998 morphic VT was induced. When contrast medium was injected into the marginal vein of the coronary sinus (CS), which was located at the LV base, slow VT showing a RBBB pattern was induced with warm-up phenomenon (Fig 2, left panel; Fig 3, upper panel). However, the injection of contrast medium into the apical marginal vein of the CS could not induce VT (Fig 2, right panel). The slow VT induction by contrast medium was reproducible, and VT was also induced by injection of physiological saline solution into the vein (Fig 3, middle panel). Electrogram recording from the distal tip of the CS catheter preceded the QRS by -31 ms (Fig 3, lower panel). These findings strongly suggested that the focus of the VT was located in the epicardium of the posterior wall in the LV base. We then tried to evaluate the efficacy of ATP on the VT using injections of mixtures of ATP (5 mg) with saline, and ATP with contrast medium (Fig 4). As shown in Fig 4, both mixtures prevented induction of the VT. Table 1 shows the JT intervals in lead II at VT induction and prevention. The mean values of 3-7 RR and JT intervals were calculated at 400 mm/s of paper speed in the control state, just before VT induction, and around 10 s after ATP injection. JT intervals were prolonged just before VT induction by injection of saline and contrast medium. ATP prevented the prolongation of JT intervals. Drug InterventionsOn separate days we assessed the efficacy of a K + channel opener, nicorandil, and a Ca ++ antagonist, verapamil. Electrocardiograms were recorded for more than 30 min and we confirmed frequent VPCs with the same morphology as the VT. Nicorandil (12 mg) was infused intravenously over 3 min and the electrocardiograms were observed for 40 min. As shown in lines 1 and 2 of Fig 5, 81 VPC were observed in 10 min in the control state. As shown in lines 5-8, after around 10 mg of nicorandil, VPCs were ...