Antiarrhythmic efficacy of dipyridamole in treatment of reperfusion arrhythmias: Evidence for cAMP-mediated triggered activity as a mechanism responsible for reperfusion arrhythmias

Academic Article

Abstract

  • Background - Intracellular calcium overload is believed to play an important role in development of reperfusior arrhythmias. Dipyridamole, an inhibitor of cellular uptake of adenosine, may prevent or terminate reperfusior arrhythmias by reducing intracellular calcium overload. Methods and 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 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 reperfusioninduced AIVR and VT.
  • Authors

    Published In

  • Circulation  Journal
  • Digital Object Identifier (doi)

    Author List

  • Yoshida Y; Hirai M; Yamada T; Tsuji Y; Kondo T; Inden Y; Akahoshi M; Murakami Y; Tsuda M; Tsuboi N
  • Start Page

  • 624
  • End Page

  • 630
  • Volume

  • 101
  • Issue

  • 6