Brain death leads to abnormal contractile properties of the human donor right ventricle.

Abstract

Experimental and clinical data suggest that brain death predominantly affects the right ventricle. We aimed to investigate right ventricle function after brain death and during clinical transplantation with load-independent methods. Patients with and without brain death were enrolled. A total of 33 consecutive heart donors (5 live, "domino" donors) and 10 patients undergoing coronary surgery (coronary artery bypass graft controls) were studied with pressure-volume loops in the right ventricle. Contractile reserve was measured with dopamine stimulation. Brain-dead donors had a higher mean cardiac index than coronary artery bypass graft controls (3.3 vs 2.8 L/min/m2), but impaired load-independent indices. Despite increased right ventricle stroke volume, the ejection fraction and slope of the end-systolic pressure-volume relationship were significantly reduced in brain-dead donors compared with controls. Diastolic abnormalities were also manifest as increased end-diastolic volume index and prolonged Tau (P < .05). Dopamine improved cardiac output, but without influencing end-systolic pressure-volume relationship, or Tau, and at the expense of further increased right ventricle end-diastolic volume. Before explantation, a significantly higher diastolic volume was also seen in hearts that developed postoperative dysfunction compared with organs without this complication (114.4 vs 77.2 mL/m2, P = .02). Brain death leads to right ventricle dysfunction, which may go undetected with conventional techniques. Right ventricle dilatation could represent an early marker of failure. Refinement of selection criteria to include load-independent indices of performance may be desirable to help expand the donor pool.