Key result
Intrapericardial ranolazine significantly increased atrial effective refractory period (from 129 to 186 ms, P<0.01) and atrial fibrillation threshold (from 4.8 to 28 mA, P<0.03) in an intact porcine model.
Why the study?
Does intrapericardial ranolazine increase atrial and ventricular refractory periods and fibrillation thresholds in closed-chest anesthetized pigs?
Does intrapericardial ranolazine increase atrial and ventricular refractory periods and fibrillation thresholds in closed-chest anesthetized pigs?
p-value: p=<0.01
Intrapericardial ranolazine exhibits potent atrial antiarrhythmic actions by increasing refractoriness and fibrillation threshold in a porcine model without altering blood pressure.
Supports targeted AF therapy via pericardial delivery; extends systemic ranolazine data to localized administration in RCTs.
INTRODUCTION: Extensive experimental studies and clinical evidence (Metabolic Efficiency with Ranzolazine for Less Ischemia in Non-ST-Elevation Acute Coronary Syndrome Thrombolysis in Myocardial Infarction-36 [MERLIN TIMI-36] trial) indicate potential antiarrhythmic efficacy of the antianginal agent ranolazine. Delivery of agents into the pericardial space allows high local concentrations to be maintained in close proximity to myocardial tissue while systemic effects are minimized. METHODS AND RESULTS: The effects of intrapericardial (IPC) administration of ranolazine (50-mg bolus) on right atrial and right ventricular effective refractory periods (ERP), atrial fibrillation threshold, and ventricular fibrillation threshold were determined in 17 closed-chest anesthetized pigs. IPC ranolazine increased atrial ERP in a time-dependent manner from 129 +/- 5.14 to 186 +/- 9.78 ms (P < 0.01, N = 7) but did not significantly affect ventricular ERP (from 188.3 +/- 4.6 to 201 +/- 4.3 ms (NS, N = 6). IPC ranolazine increased atrial fibrillation threshold from 4.8 +/- 0.8 to 28 +/- 2.3 mA (P < 0.03, N = 6) and ventricular fibrillation threshold (from 24 +/- 3.56 baseline to 29.33 +/- 2.04 mA at 10-20 minutes, P < 0.03, N = 6). No significant change in mean arterial pressure was observed (from 92.8 +/- 7.1 to 74.8 +/- 7.5 mm Hg, P < 0.125, N = 5, at 7 minutes). CONCLUSIONS: IPC ranolazine exhibits striking atrial antiarrhythmic actions as evidenced by increases in refractoriness and in fibrillation inducibility without significantly altering mean arterial blood pressure. Ranolazine's effects on the atria appear to be more potent than those on the ventricles.
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Carvas et al. (2010) studied Atrial fibrillation (n=17). Intrapericardial ranolazine vs. Baseline was evaluated on Atrial effective refractory period and atrial fibrillation threshold (p=<0.01). Intrapericardial ranolazine significantly increased atrial effective refractory period (from 129 to 186 ms, P<0.01) and atrial fibrillation threshold (from 4.8 to 28 mA, P<0.03) in an intact porcine model.
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