title: Antiarrhythmic efficacy of dipyridamole in treatment of reperfusion arrhythmias : evidence for cAMP-mediated triggered activity as a mechanism responsible for reperfusion arrhythmias.
abstract: BACKGROUND
  Intracellular calcium overload is believed to play an important role in development of reperfusion arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusion arrhythmias by reducing intracellular calcium overload.
  
  
  RESULTS
  First, we tested for a preventive effect of dipyridamole. Sixty-one patients who underwent primary PTCA for treatment of acute anterior wall myocardial infarction were enrolled in this prospective study. Patients were divided into dipyridamole (DP) and nondipyridamole (non-DP) groups. The 2 groups had similar baseline characteristics. In the DP group, dipyridamole 0.5 mg/kg was infused intravenously for 3 minutes immediately before reperfusion during primary PTCA. Arrhythmias after reperfusion were analyzed from continuous ECG recordings. None of the patients in the DP group (n=23) had accelerated idioventricular rhythms (AIVR) or ventricular tachycardia (VT). In contrast, 7 (18.4%) had AIVR and 3 (7.9%) had VT in the non-DP group (n=38; P<0.01). Second, we tested for a termination effect of dipyridamole. Dipyridamole 0.5 mg/kg was infused intravenously while continuous ECG recordings were obtained in 9 patients who had either sustained AIVR (n=7) or sustained VT (n=2) after reperfusion of occluded coronary artery. Arrhythmias were terminated in all patients.
  
  
  CONCLUSIONS
  These results indicate that administration of dipyridamole can prevent and terminate reperfusion arrhythmias such as AIVR and VT. cAMP-mediated triggered activity may, at least in part, be responsible for reperfusion-induced AIVR and VT.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, University of Nagoya School of Medicine, Nagoya, Japan. ykyoshi@wb3.so-net.ne.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Yoshida
authors.forename: M
authors.initials: M
authors.lastname: Hirai
authors.forename: T
authors.initials: T
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Tsuji
authors.forename: T
authors.initials: T
authors.lastname: Kondo
authors.forename: Y
authors.initials: Y
authors.lastname: Inden
authors.forename: M
authors.initials: M
authors.lastname: Akahoshi
authors.forename: Y
authors.initials: Y
authors.lastname: Murakami
authors.forename: M
authors.initials: M
authors.lastname: Tsuda
authors.forename: N
authors.initials: N
authors.lastname: Tsuboi
authors.forename: H
authors.initials: H
authors.lastname: Hirayama
authors.forename: M
authors.initials: M
authors.lastname: Okamoto
authors.forename: T
authors.initials: T
authors.lastname: Ito
authors.forename: H
authors.initials: H
authors.lastname: Saito
authors.forename: J
authors.initials: J
authors.lastname: Toyama
mesh_terms: D000241:Adenosine / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D001145:Arrhythmias, Cardiac / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D000242:Cyclic AMP / Q000378:metabolism; D004176:Dipyridamole / Q000008:administration & dosage*; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology / Q000601:surgery; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D011446:Prospective Studies; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000008:administration & dosage*
chemical_list: D014665:Vasodilator Agents; D004176:Dipyridamole; D000242:Cyclic AMP; D000241:Adenosine