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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 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.
AuthorsY Kobayashi, A Miyata, K Tanno, S Kikushima, T Baba, T Katagiri
JournalJapanese circulation journal (Jpn Circ J) Vol. 62 Issue 12 Pg. 947-51 (Dec 1998) ISSN: 0047-1828 [Print] Japan
PMID9890211 (Publication Type: Case Reports, Journal Article)
Chemical References
  • Anti-Arrhythmia Agents
  • Nicorandil
  • Adenosine Triphosphate
  • Verapamil
Topics
  • Adenosine Triphosphate (pharmacology)
  • Adult
  • Anti-Arrhythmia Agents (pharmacology)
  • Heart Ventricles (physiopathology)
  • Humans
  • Male
  • Nicorandil (pharmacology)
  • Pericardium (physiopathology)
  • Tachycardia, Ventricular (drug therapy, physiopathology)
  • Ventricular Premature Complexes (drug therapy)
  • Verapamil (pharmacology)

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