Late-Breaking Clinical Trial Abstracts

Background: The most common complication associated with prolonged duration cardiopulmonary bypass (CPB) is acute kidney injury (AKI), which markedly increases the mortality rate. Rationale: Prolonged CPB causes hemolysis with high levels of circulating plasma hemoglobin (Hb). Plasma Hb scavenges Nitric Oxide (NO) via the dioxygenation reaction, depleting endogenous NO and causing vasoconstriction, proximal renal tubular injury and AKI. Hypothesis: Exposure to NO during and after CPB protects the kidney, by three possible mechanisms: 1. Selective vasodilation of the pulmonary circulation leading to increased cardiac output and renal perfusion. 2. Reduction of ischemia-reperfusion renal injury and 3. Oxidation of plasma Hb to metHb, which cannot scavenge NO. Study Design: A single center, prospective, randomized, double blind controlled trial comparing treatment with 80 part per million (ppm) NO (NO group) versus N2 (N2 group). Study gas was given via the gas exchanger during CPB and by inhalation for 24h post-operatively in adults. Study Population: 217 consenting adults with normal kidney function undergoing elective multiple valve replacement surgery with CPB. Study Objective: To determine whether NO reduces AKI (primary outcome), and other major complications immediately post-surgery, at 30 days, and 90 days (secondary outcomes). AKI was defined as either an increase of serum creatinine by 50% within 7 days after surgery, or an increase of serum creatinine by 0.3 mg/dl within 48 hrs. Preliminary results: are summarized in the tables 1, 2, 3 and 4. Conclusions: I) Administration of 80ppm NO for 24 hours was safe. Blood metHb was always below 10%. II) NO decreased the incidence of AKI from 63% to 50% (p=0.04, primary endpoint achieved).