Dipyridamole suppresses catecholamine- and Ca++ influx-sensitive ventricular arrhythmias
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Updated: Nov 3, 2026

Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia
Published on: December 22, 2023
Y Kobayashi1, A Miyata, K Chiyoda
1Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
Abstract:
To study the mechanism of ventricular arrhythmias, the effect of dipyridamole (DIP; 300 mg/day), an adenosine transport inhibitor, on ventricular premature contractions (VPCs) was assessed in 12 patients who showed VPCs (21312 +/- 12314/day) on Holter ECG in a controlled setting. The effects were compared with those of verapamil (240 mg/day) and bisoprolol (5 mg/day). DIP suppressed more than one-half the VPCs in 5 patients. The mean degree of reduction in these DIP-responders was 75 +/- 18%. Both verapamil and bisoprolol inhibited VPCs in all of the DIP-responders (verapamil: 71 +/- 15%, bisoprolol: 88 +/- 16%). Two of the 5 DIP-responders had sustained ventricular tachycardias (VT) that were terminated by intravenous DIP, ATP, acetylcholine, verapamil, and propranolol. In contrast, verapamil did not inhibit VPCs in any of the DIP-nonresponders. Bisoprolol also did not suppress VPCs in 3 of 6 DIP-non responders. heart rate was unaffected by DIP, but was suppressed by both verapamil and bisoprolol. In addition, DIP increased the serum concentration of adenosine (control 16.3 +/- 17.1 vs 22.3 +/- 19.0 pmol/ml after DIP, p < 0.05). The inhibitory effect of DIP may involve suppression of Ca+2 current through an extracellular increase in adenosine.
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