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.
Keywords: Atrial fibrillation; Ivabradine; Rate control; Rheumatic heart disease.
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