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 theater). We hypothesized that (1) risk factors and clinical course differ between ''Immediate'' and ''Delayed'' MCS; and (2) 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-center 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≥ 0.2 mcg/kg/min for ''Delayed'' MCS were 71% and 81%. Sensitivity and specificity of DPP of ≥40 mmHg for No MCS were 83% and 74%. The discriminatory value of systemic vascular resistance for ''Delayed'' MCS was poor.

Conclusion: Risk factors and 1-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.