Utility of Cardiovascular Magnetic Resonance Imaging in Non-HLA Mediated Cardiac Allograft Dysfunction

Abstract

<h3>Introduction</h3> Cardiac MRI (cMRI) with late gadolinium enhancement may be beneficial in guiding medical therapy in non-HLA mediated allograft dysfunction in heart transplant recipients (HTR). Cardiac MRI utilizing pre/post-contrast T1/T2 mapping and myocardial delayed enhancement imaging were performed in two HTRs with non-HLA mediated allograft dysfunction. <h3>Case Report</h3> Patient A and B were adult males transplanted for non-ischemic cardiomyopathy with compatible crossmatches at the time of transplant. Patient A received basiliximab induction while patient B received no induction. Both were maintained on tacrolimus, mycophenolate, and prednisone. On surveillance echocardiogram (ECHO) at 90-days post-transplant, a decreased ejection fraction (45%) was noted in both patients. Subsequent biopsies, donor specific antibodies, and MICA antibodies were negative. Biopsy immunofluorescence C4d staining was 90% in patient A and negative in patient B (Table 1). Patient A's cMRI demonstrated mildly increased T1 and T2 values that when combined with the clinical history, was suggestive of acute rejection. He subsequently received treatment with plasmapheresis, immunoglobulin, and rituximab. A repeat cMRI at 1-month post-treatment demonstrated normalization of T1 and T2 values. In contrast, patient B had generally normal T1 and T2 values on initial cMRI, indicating likely absence of acute rejection. Given cMRI findings, combined with a possible alternative etiology of mitochondrial disease contributing to decreased cardiac function, rejection treatment was not pursued and instead, sirolimus was initiated to slow disease progression. Follow-up biopsies and ECHOs in both patients indicate stable allograft function with slight improvements in ejection fraction. <h3>Summary</h3> In the absence of typical rejection findings, aspects of cMRI measurement may have favorable clinical utility and help guide medical management of early post-transplant non-HLA mediated allograft dysfunction.