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Published on: February 26, 2013
Ivabradine reduced ventricular rate in patients with non-paroxysmal atrial fibrillation
Wanwarang Wongcharoen1, Adisai Ruttanaphol1, Siriluck Gunaparn1
1Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Insights
Ivabradine effectively reduced ventricular rate in patients with non-paroxysmal atrial fibrillation (AF). This study suggests ivabradine as a potential treatment for improving ventricular control in AF patients.
Area of Science:
- Cardiology
- Pharmacology
- Electrophysiology
Background:
- If channels are present in the atrioventricular (AV) node, not just the sinus node.
- Animal studies indicate If inhibitors reduce AV node conduction during atrial fibrillation (AF).
Purpose of the Study:
- To investigate the effect of ivabradine on ventricular rate control in patients diagnosed with non-paroxysmal AF.
- To evaluate ivabradine's efficacy as an addition to standard therapy for AF management.
Main Methods:
- A prospective, randomized, double-blind, placebo-controlled study was conducted.
- Adult patients with non-paroxysmal AF received either 5mg of ivabradine twice daily or a placebo for one month.
- The primary endpoint was assessed by comparing the mean ventricular rate via 24-hour Holter monitoring from baseline to one month.
Main Results:
- Ivabradine significantly decreased the mean ventricular rate from 86.0±10.9 to 79.2±9.6 beats/min (p<0.001).
- The placebo group showed no significant change in ventricular rate (84.3±11.2 vs. 82.9±9.9 beats/min, p=0.469).
- The rate reduction achieved with ivabradine was significantly greater than with placebo (6.9±6.3 vs. 1.4±6.0 beats/min, p=0.024), with no observed adverse effects.
Conclusions:
- Ivabradine demonstrated a significant reduction in ventricular rate in patients with non-paroxysmal AF compared to placebo.
- Ivabradine presents a potential therapeutic option for enhancing ventricular rate control in AF patients.
- Larger studies are recommended to confirm these findings due to the study's small sample size.
Background:
It has been shown that If channels can be found in AV node, apart from the sinus node. Previous animal studies showed that If inhibitor resulted in the rate-dependent reduction in AV node conduction during atrial fibrillation (AF). Therefore, we aimed to examine the effect of ivabradine on ventricular rate in patients with non-paroxysmal AF.
Method:
This study was a prospective randomized, double blind, placebo-controlled study. Ivabradine, 5mg twice a day (n=21), or placebo (n=11) was administered for 1month to adult patients with non-paroxysmal AF, in addition to standard therapy. The primary end point was the change in mean ventricular rate between baseline and 1month, as assessed by 24-hour Holter.
Results:
The baseline characteristics did not differ between ivabradine and placebo groups (mean age was 59.7±13.3years, male 62.5%). Mean 24-hour ventricular rate at baseline was comparable between 2 groups. We found that ivabradine significantly decreased mean ventricular rate from 86.0±10.9beats/min to 79.2±9.6beats/min (p<0.001). In contrast, no significant change in ventricular rate was observed in placebo group (84.3±11.2 vs. 82.9±9.9beats/min, p=0.469). The effect of ivabradine on rate reduction was significantly greater than placebo (6.9±6.3 vs. 1.4±6.0beats/min, p=0.024). No drug-related adverse effects were observed in both groups.
Conclusion:
We demonstrated that ivabradine significantly decreased ventricular rate during AF compared to placebo. Therefore, ivabradine can be a potential treatment to improve ventricular control in patients with non-paroxysmal AF. Due to the small sample size, larger studies are needed to confirm this effect of ivabradine.
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