Abstract 12547: Time-Course Influence of Brain Death on Cardiac Function and Its Impact on Posttransplant Graft Function

Abstract

Introduction: Heart transplantation became the most effective treatment for end-stage heart failure. Donors after brain death are currently the only reliable source for cardiac transplants. However, hemodynamic instability and cardiac dysfunction have been demonstrated in brain-dead donors and this could therefore also affect posttransplant graft function. Hypothesis: Our aims were to evaluate in rats the time-course cardiac influence of brain death and we tested the hypothesis that brain death impairs graft left ventricular function. Methods: Lewis rats were either maintained brain death for 5h by inflation of a subdurally placed balloon catheter (n=7) or subjected to sham-operation (control group, n=9). We continuously assessed cardiac function during 5 h. Then, hearts were excised, stored in cold preservation solution for 1 h, and heterotopically transplanted. We evaluated graft function 1.5 h after transplantation. Results: Brain death was associated with decreased left ventricular contractility (ejection fraction: 37±6% vs. 57±5%; dP/dt max : 4770±197 mmHg/s vs. 7604 ±348 mmHg/s; dP/dt max -EDV: 60±7 mmHg/s vs. 74±2 mmHg/s; E max : 2.4±0.1 mmHg/μl vs. 4.4±0.3 mmHg/μl; PRSW: 47±9 mmHg vs. 78±3 mmHg; p<0.05) and relaxation (dP/dt min: -6638±722 mmHg/s vs. -11285±539 mmHg/s; Tau: 12.6±0.7 ms vs.10.5±0.4 ms; EDPVR: 0.33±0.14 mmHg/μl vs. 0.09±0.03 mmHg/μl, p<0.05) 45 min after its initiation and for the rest of 5 h compared to controls. Moreover, after transplantation, graft systolic and diastolic functions were impaired in the brain-dead group compared to controls (reflected by decreased left ventricular systolic and developed pressures, dP/dt max and dP/dt min , and prolonged Tau). Conclusions: In conclusion, we have a well detailed characterized in vivo rat model to examine the influence of brain death on ventricular dysfunction using a microconductance catheter technology via pressure-volume analysis. These results demonstrate that brain death increases the susceptibility of donor heart to ischemia/reperfusion injury after transplantation.