CONGRESS ABSTRACT

Even if coronary vasospasm (CV) is considered a rare phenomenon in heart transplant (HT) recipients, during routine coronary angiography asymptomatic CV may be observed. We report the case of a 30-year-old male who underwent HT in 2007 for dilatative cardiomyopathy. He was maintained on tacrolimus and mycophenolate mofetil and had no significant rejection or coronary allograft vasculopathy (CAV) demonstration. In December 2020 patient presented with cardiac arrest preceded by angina. Coronary angiography demonstrated diffuse spasm of the right coronary artery (RCA) with resolution after intracoronary nitrate administration. An endomyocardial biopsy (EBM) revealed no signs of cellular rejection whilst cardiac magnetic resonance showed signs of acute rejection (Fig.1). Moreover, two major histocompatibility complex (MHC) Class 2 donor-specific antibodies (DSAs) were positive with a high title. Treatment for antibody-mediated rejection (AMR) was initiated with steroids and plasmapheresis, followed by immunoglobulin infusion. Cardiac defibrillator was implanted before discharge. In August 2021, patient experienced a second cardiac arrest.  Left heart catheterization found diffuse CV and after nitrates administration, proximal critical stenosis of RCA was pointed out and treated with stent insertion (Fig. 2-3). EMB and DSAs assessment were both negative. The patient was discharged after medical therapy optimization for CV prevention including the switch from mycophenolate to everolimus. After two more episodes of ACS with angiography finding of CV we decided to empirically treat the patient with weekly photopheresis sessions. Despite aggressive AMR management, a third ACC occurred in March 2022. The patient was finally reintroduced to the HT waiting list. Most CV episodes run without any symptoms due to the denervated heart post-transplant so probably re-innervation occurred in our patient. Calcium channel blockers, nitrates, and beta-blockers failed in CV prevention, suggesting ineffectiveness in HT recipients because of a different pathogenetic mechanism when compared to healthy subjects. Furthermore, documentation of coronary disease progression after the second ACC supports the hypothesis that CV could be the first manifestation of CAV. An intriguing hypothesis would be the presence of pathological vasoreactivity in the donor's heart, ascribable to an “inherited” endothelial dysfunction that could last be exacerbated by multiple factors, including AMR