Abstract 15646: Pathological Assessment of Primary Graft Dysfunction Does Not Suggest a Prominent Role for an Adaptive Immune Response

Abstract

Introduction: Primary graft dysfunction (PGD) is a major cause of mortality following heart transplant (HT). Pathological characteristics of PGD have not been well characterized. We sought to describe the clinical and pathological characteristics of patients who died or were re-transplanted due to PGD. Methods: We identified a cohort of 161 HT recipients between 3/7/2012 to 12/31/17 who developed PGD. Of these, 40 patients had severe PGD, and 16 died in the first month post-transplant. Autopsy or explant pathology was available in 6 patients, which was compared to pathology from the first endomyocardial biopsy in 24 patients with severe PGD that survived. Results: Of the 6 patients for whom pathology was available, mean age was 54, four were male and five were white. Half had non-ischemic dilated cardiomyopathy. Two were sensitized. Five patients had severe PGD and one patient had moderate PGD. There were five deaths and one re-transplant. On pathologic examination, most patients (4/6) had broad areas of myocardial necrosis with diffuse vascular thrombosis. Two patients had focal areas of myocardial necrosis. In no cases was there evidence of cellular rejection (ACR) or antibody-mediated rejection (AMR). In the 24 survivors of severe PGD, median age was 54 , twenty were male and half were white. Five were sensitized. On pathologic examination, ischemic changes were found in 10 patients (42%). While there was no significant ACR, 7/24 (30%) of cases showed evidence of either AMR 1 or AMR 2. Conclusions: In patients succumbing to moderate or severe PGD, PGD was associated with diffuse myocardial necrosis and vascular thrombi. In survivors of severe PGD, the most prominent finding was diffuse ischemic changes on routine heart biopsy. In both, there was no evidence of cellular rejection, however there was significant incidence of AMR, possibly induced by ischemic changes. These findings suggest that severe PGD may have an ischemic component characterized by vascular thrombosis.