Effect of Atrial Natriuretic Peptide on Electrical Defibrillation Efficacy

ANP and Defibrillation. Introduction: In vitro studies have suggested that human atrial natriuretic peptide (ANP) modulates the electrophysiologic properties of myocardial cells. This study assessed whether ANP could influence defibrillation efficacy. Methods and Results: In 35 anesthetized dogs, the transcardiac defibrillation threshold (DFT) as well as hemodynamic and electrophysiologic variables were determined before and during treatment with ANP (n = 11), hydralazine (n = 11), or saline (n = 13). ANP (1.5 μg/kg + 0.2 μg/kg per min) increased the plasma concentration of cyclic GMP (a second messenger for ANP) and significantly decreased aortic blood pressure (mean 100 ± 11 mmHg to 83 ± 15 mmHg). ANP also prolonged ventricular repolarization (effective refractory period 157 ± 7 msec to 165 ± 11 msec) and markedly reduced DFT (5.4 ± 1.2 J to 3.8 ± 0.7 J [P < 0.01]) without changing pulmonary artery pressure or sinus cycle length. Neither saline nor hydralazine (1.5 mg/kg) had a significant effect on DFT (saline 4.7 ± 2.1 J to 4.6 ± 2.4 J; hydralazine 4.3 ± 2.0 J to 4.2 ± 1.9 J), although hydralazine caused pronounced hypotension (mean aortic pressure 103 ± 9 mmHg to 74 ± 13 mmHg). Conclusion: These results suggest that ANP increases defibrillation efficacy, and that this effect is not necessarily shared by other vasodilating agents.