Ivabradine effectively prevents heart rate increase, however, has no effect on cardiac arrhythmias during dobutamine infusion: a comparative study with beta-blocker therapy

Abstract

Purpose: Ivabradine is a novel Heart Rate (HR) lowering agent acting by inhibiting the If current. Dobutamine (DOB) does increase HR and cardiac arrhythmias. We compared the effects of ivabradine with β blocker therapy on the increase in HR and the incidence of ventricular arrhythmias during DOB infusion. Methods: 69 patients with decompensated heart failure requiring inotropic support and LVEF <35% were included in this study. All patients underwent holter recording for 6 h before DOB and then, DOB was administered at incremental doses of 5, 10 and 15 μgr/kg/min, with 6-h steps. Holter monitoring was continued during DOB infusion. Ivabradine 7.5 mg was given at the initiation of DOB and readministered at 12 h of DOB in 26 patients not receiving β blocker (ivabradine group). 15 patients under β blocker (β blocker group) and 28 patients not taking β blocker (control group) did not receive ivabradine during DOB. Results: HR gradually and significantly increased at each step of DOB infusion in both control (81±11, 90±16, 97±14 and 101±16 respectively, p=0.001) and β blocker groups (75±13, 82±13, 86±14 and 88±13 respectively, p=0.001), while no significant increase in HR was observed in ivabradine group (82±17, 82±15, 85±14 and 83±12 respectively, p=0.439). The median number of Ventricular Premature Contractions (VPCs) and total ventricular arrhythmia significantly increased in ivabradine (p<0.001 and p<0.015) and control groups (p<0.01 and p<0.018). However, in β blocker group, no significant increase was found in VPCs and total ventricular arrhythmias (Table). The incidence of non-sustained ventricular tachycardia did not significantly change in three groups. View this table: Table 1. Cardiac arrhythmias during dobutamine Conclusions: Ivabradine effectively prevents HR increase, however, it has no effect on ventricular arrhythmias during DOB therapy. In contrast, β blocker therapy fails to blunt DOB-induced increase in HR, but it prevents DOB-induced increase in ventricular arrhythmias.