Table 2.
More potent effect of ranolazine (Ran) to reduce atrial fibrillation (AF) inducibility and depress sodium channel-dependent parameters in heart failure (HF) vs. vagal non-HF models of AF
| AF Model | ΔVmax | ΔVmax 500-300 ms | ΔERP | Δ PRR | ΔS1 –S1 | Reduction of AF/AFl inducibility |
|---|---|---|---|---|---|---|
| Ran 5 μM in HF Model | −18%* | −32%* | +49 ms† (+39%) | +40 ms† | +109 ms† (+81%) | 70% |
| Ran 5 μM in Vagal Non-HF Model | −4% | −9% | +20 ms (38%) | + 11 ms | +38 ms (+68%) | 29% |
| Ran 10 μM in Vagal Non-HF Model | −7% | −15% | +57 ms (+98%) | +47 ms | +108 ms (+148%) | 80% |
Shown are changes of average values. Data from non-HF atria are from Burashnikov et al.4, 11 S1-S1 = the shortest S1-S1 pacing interval permitting a 1:1 activation. Pacing cycle length (CL) = 500 ms (except for the shortest S1–S1). Vagal non-HF Model = control atria exposed to acetylcholine (1.0 μM). Vmax 500-300 ms = maximum rate of rise of the action potential upstroke (Vmax) changes in % following acceleration of pacing rate from a CL of 500 to 300 ms.
p<0.05 vs Ran 5 μM and μM 10 in Vagal non-HF model.
p<0.05 vs Ran 5 μM in Vagal non-HF model (unpaired t-test).
N=10 for each. ERP, effective refractory period; PRR, post-repolarization refractoriness.