Circulatory load during hypoxia impairs post-transplant myocardial functional recovery in donation after cardiac death.

BACKGROUND

Circulatory load during hypoxia is unavoidable in donation after cardiac death (DCD) hearts, but it causes severe myocardial damage. The impact of circulatory load on donor heart function has not been investigated. The purpose of this study was to evaluate its effect on post-transplant functional recovery of DCD hearts.

METHODS

Twelve donor pigs (20 kg) were used. Cardiac arrest was induced by asphyxiation (turning off the ventilator) in the load group (n = 6) and by exsanguination (dividing the vena cava) in the unload group (n = 6). Left ventricle end-diastolic volume (LDEDV) and end-systolic pressure (LVESP) were monitored until cardiac arrest. Orthotopic transplantation was performed after 30-minute warm ischemia following cardiac arrest. After weaning from cardiopulmonary bypass, left ventricular end-diastolic pressure-volume ratio (LV Emax) and creatine kinase (CK-MB) were measured while on 0.1 microg/kg/min epinephrine.

RESULTS

During the agonal period, the maximum LVEDV and LVESP in the load group were 132 +/- 1% of baseline at 10 minutes and 148 +/- 16% of baseline at 4 minutes, respectively. Recovery rates of post-transplant cardiac function in the load group were worse than in the unload group (LV Emax: 64 +/- 8 vs 84 +/- 5%, p < 0.05). Levels of post-transplant CK-MB in the load group were higher than in the unload group (639 +/- 119 vs 308 +/- 70 IU/liter, p < 0.05).

CONCLUSIONS

Cardiac arrest with circulatory load by asphyxiation caused more myocardial damage than unloaded arrest. This difference between the modes of death should be considered when evaluating the DCD hearts for clinical application.