Abstract 17679: A Randomized Pilot Trial of Intra-arrest Cyclosporine and Methylprednisolone for Attenuation of Post-arrest Myocardial Dysfunction
Introduction: Myocardial dysfunction is common after cardiac arrest and may result from the systemic inflammatory response syndrome. It is unknown if immunosuppressants can prevent myocardial dysfunction post cardiac arrest.
Hypothesis: Intra-arrest cyclosporine (CCY) and methylprednisolone (MP) will preserve cardiac output (CO), left ventricular ejection fraction (LVEF) and mean arterial pressure (MAP) after return of spontaneous circulation (ROSC).
Methods: We performed a randomized, blinded placebo-controlled pilot. Ten female swine, 25-30kg, were anesthetized with fentanyl and midazolam. We placed femoral arterial and venous sheaths and introduced an arterial Millar pressure transducer and a continuous CO catheter (Edwards LifeScience) into the pulmonary artery. Ventricular fibrillation was induced by transthoracic shock and allowed to continue for 8min after which we began ACLS and administered either 10 mg/kg CCY + 40mg MP or placebo. Animals with ROSC were supported for 12h using norepinephrine as a vasopressor as needed. We performed echocardiography at baseline, and 1, 2, 6 and 12h post-ROSC to measure LVEF and fractional shortening (FS). Our primary outcomes were CO, FS, LVEF and MAP. We analyzed repeated measures data using generalized estimating equations with robust standard errors and down-sampled continuously measured data to 5min epochs.
Results: Eight animals had ROSC after 7.1±2.6 min of CPR with 1.8±0.6 doses of epinephrine and 2.0±1.3 shocks. Animals receiving CCY+MP had lower post-arrest CO (mean 3.2 vs 4.0L/min, p<0.02) and higher MAP (mean 97 vs 87mmHg, p<0.001) compared to placebo . There was no difference in echocardiographic findings or vasopressor use between arms.
Conclusions: Intra-arrest cyclosporine and methylprednisolone worsen post-arrest cardiac output without an appreciable change in echocardiographic parameters but cause a modest increase in mean arterial pressure and may therefore be of little clinical utility after ventricular fibrillation cardiac arrest.
Author Disclosures: M. Chonde: Research Grant; Significant; UPMC Heart and Vascular Institute Fellows Research Grant. K.L. Flickinger: None. M. Sundermann: None. A. Koller: None. D. Salcido: None. C. Dezfulian: Research Grant; Significant; NIH support through K08NS069817. J. Menegazzi: None. J. Elmer: Research Grant; Significant; NIH support through: 5K12HL109068.
- © 2016 by American Heart Association, Inc.