A pilot study evaluating the role of ivabradine for rate control in patients with rheumatic atrial fibrillation.

OBJECTIVES

Ivabradine may have a role in rate control of atrial fibrillation (AF) due to effects on HCN channels in AV node. We studied role of Ivabradine in rate control of rheumatic AF.

METHODS

80 patients, rheumatic AF, HR > 100 bpm (age 47 ± 11 yrs, AF duration 6.8 ± 2.9 years, rate 131 ± 16 bpm) on maximally tolerated ββ or CCB's, randomized to Ivabradine or escalated ββ/CCB. Ivabradine started @ 2.5 mg BD; increased to 5 mg BD if inadequate response at 1 week (failure to decrease HR < 10% vs baseline). After Holter at 1 month, dose escalated to 7.5 mg BD if needed.

RESULTS

Ivabradine resulted in significantly lower HR (81 ± 10 vs 99 ± 9) at 3 months and 6 months (79 ± 8 vs 94 ± 8, p < 0.001). Absolute reduction in HR: 56 ± 15 vs 31 ± 14 bpm and % change in HR: 41 ± 7 vs 24 ± 9%, both p < 0.00001). At 6 months, Ivabradine group had. 1Significantly lower NT Pro BNP (1168 vs 1314 pg/ml), higher 6 min walk distance (410 ± 47 vs 349 ± 54 m, all p < 0.001) 2Better symptom class (EHRA score 1: asymptomatic 84% vs 40%), improvement >1 EHRA class; baseline 60% vs 17% 3Better LA Strain (22.8 ± 2.8% vs 20.6 ± 2.5%) Ivabradine was well tolerated and there was no drug withdrawal.

CONCLUSION

Our data suggest that Ivabradine can be an option for rate control in rheumatic AF.