Slow ventricular tachycardia located in the epicardium of the left ventricular base and characterized by effects of adenosine triphosphate, nicorandil and verapamil.
A 31-year-old male with slow ventricular tachycardia (VT) developed a nonsustained VT with prolongation of the JT intervals after injection of contrast medium and saline into the marginal vein of the coronary sinus. The earliest activation site of the VT existed in the epicardium of the left ventricular base. Adenosine triphosphate prevented induction of VT and prolongation of JT intervals. Ventricular premature contractions showing the same morphology as the VT were also inhibited by nicorandil and verapamil. The mechanism of the VT was suggested to be abnormal automaticity due to an increase in the Ca++ current into cells after prolongation of the action potential duration induced by hypothermia.
Kobayashi
Y
Y
Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
Miyata
A
A
Tanno
K
K
Kikushima
S
S
Baba
T
T
Katagiri
T
T
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008297:Male; D020108:Nicorandil / Q000494:pharmacology*; D010496:Pericardium / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology*; D018879:Ventricular Premature Complexes / Q000188:drug therapy; D014700:Verapamil / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D020108:Nicorandil; D000255:Adenosine Triphosphate; D014700:Verapamil