Increased platelet reactivity after heart transplantation

Abstract

BackgroundThe role of antiplatelet therapy following heart transplantation (HT) is unclear. Ex-vivo studies suggest increased platelet hyperaggregability after HT. Recent studies suggest that early aspirin therapy is associated with improved survival and lower rates of cardiac allograft vasculopathy (CAV). We examined: (1) the prevalence of increased platelet reactivity on aspirin and clopidogrel post-HT, (2) platelet reactivity post-clopidogrel treatment in aspirin-resistant patients, and (3) the relationship between platelet reactivity and outcomes. MethodsHT patients on aspirin and/or clopidogrel who underwent coronary angiography in 2015–2018 were assessed using the VerifyNow aspirin and/or P2Y12 assay. High on-treatment platelet reactivity (HPR) to aspirin and clopidogrel were defined by aspirin reaction unit (ARU) > 550 and P2Y12 reaction unit (PRU) > 208. Patients with HPR to aspirin were switched to clopidogrel for 7 days, then reassessed with the P2Y12 assay. ResultsPlatelet reactivity was assessed in 76 patients at 4.6 (IQR 2.2-9.4) median years post-HT. ARU was assessed in 71 patients and PRU in 16 patients. Median ARU was 471 (IQR 419-537) and PRU 186 (IQR 120-244). The prevalence of HPR to aspirin and clopidogrel were 18% and 37%, respectively, which is comparable to patients with coronary artery disease. 45% of patients with HPR to aspirin also had HPR to clopidogrel. There was no difference in aspirin HPR prevalence between patients with and without CAV. ConclusionsThere is increased platelet reactivity despite treatment with aspirin or clopidogrel following HT. Further evaluation may determine whether increased platelet reactivity is associated with adverse outcomes including the development of CAV.