Severe Early Graft Dysfunction Post-Heart Transplantation: Two Clinical Trajectories and Diastolic Perfusion Pressure as a Predictor of Mechanical Circulatory Support.

Abstract

BACKGROUND Severe early graft dysfunction (EGD) is defined by mechanical circulatory support (MCS) <24 hours of heart transplantation (HT). We classified severe EGD based on timing of post-HT MCS: 'Immediate' intra-operative vs 'Delayed' post-operative MCS (after admission into intensive care unit (ICU) from operating theatre). We hypothesised that (i) risk factors and clinical course differ between 'Immediate' and 'Delayed' MCS; and (ii) diastolic perfusion pressure (DPP=diastolic blood pressure-central venous pressure) and Norepinephrine equivalents (NE=sum of vasopressor doses), as measures of vasoplegia are related to 'Delayed' MCS. METHODS Two-centre study of 216 consecutive patients who underwent HT. Recipient, donor, vasopressor doses and hemodynamic data at T0 and T6 (on admission and 6 hours after admission into ICU) were collected. RESULTS Of the 216 patients, 67 patients had severe EGD ('Immediate' MCS: n=43, 'Delayed' MCS: n=24). The likelihood of 'immediate' MCS but not 'delayed' MCS increased with increasing warm ischemic and cardiopulmonary bypass times on multinomial regression analysis with 'no MCS' as the referent group. One-year mortality was highest in 'Immediate' MCS vs 'no MCS' and 'delayed' MCS (34.9% vs 3.4% and 8% respectively, P<0.001). Of the patients who had no immediate post-transplant MCS, DPP and NE at T6 were independently associated with subsequent 'delayed' MCS'. Sensitivity and specificity of NE ≥0.2mcg/kg/min for 'Delayed' MCS were 71% and 81%. Sensitivity and specificity of DPP of ≥40mmHg for No MCS were 83% and 74%. The discriminatory value of systemic vascular resistance for 'Delayed' MCS was poor. CONCLUSION Risk factors and one-year survival differed significantly between 'Immediate' and 'Delayed' post-HT MCS. The latter is related to lower DPP and higher NE, which is consistent with vasoplegia as the dominant pathophysiology.