Abstract
<h3>Introduction</h3> Accelerated cardiac allograft vasculopathy (CAV) is an uncommon ominous finding after heart transplantation (HTx), with unclear pathophysiology and poor prognosis. We present a case of accelerated CAV in a heart recipient with recurrent acute pancreatitis. <h3>Case Report</h3> A 38 year-old male with non-ischemic dilated cardiomyopathy, on INTERMACS 3 profile, was transplanted with a 23 year-old donor heart. Post-operatively, acute ischemic pancreatitis ensued with recurrent relapses requiring readmissions. Maintenance immunosuppression was suboptimal due to concerns regarding pancreatic toxicity, and 4 episodes of high-grade acute cellular rejection occurred in the 1st year. By 9 months post-transplant, coronary angiography showed severe multivessel CAV (Figure 1A and 1B). In order to delay its progression, bortezomib was initiated due to presumed humoral response triggers. Staged PCI was planned; however, the patient died suddenly before the procedure was attempted. <h3>Summary</h3> Aggressive accelerated CAV developing early post HTx is rare and almost invariably associated with dismal prognosis. Inflammatory and/or humoral responses may play an important role in such forms of very fast-developing disease, which may course with an acute, predominant component of vasculitis. Herein, pro-inflammatory state set up by recurrent pancreatitis may have contributed to the clinical picture (Figure 1C).Increased biomarkers, as pro-inflammatory cytokines and fibroblast growth factors, have been linked to advanced CAV. Likewise, pancreatitis pathogenesis is related to cytokine activation with remarkable systemic inflammatory response. A high-grade inflammatory state secondary to recurrent acute pancreatitis may have been a major trigger for early, severe CAV development in this case. Understanding predictors of increased risk for severe accelerated CAV may facilitate the institution of close surveillance and targeted therapies for this challenging scenario.
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