title: Lack of Evidence for Deterioration in Endothelial Function Following Ticagrelor Treatment Cessation.
abstract: Ticagrelor may exert pleiotropic actions, beyond platelet inhibition, which are possibly adenosine-mediated. It has been suggested that in patients with coronary artery disease (CAD) ticagrelor may influence endothelial function.
  
  
  
  We aimed to assess the possibility of endothelial function deterioration following ticagrelor treatment cessation.
  
  
  
  This was a prospective, observational study, in stable CAD patients with prior percutaneous coronary intervention (PCI) for acute coronary syndrome manifested 1 year earlier, under ticagrelor maintenance dose (90 mg bid) and due to discontinue ticagrelor. Endothelial function was assessed by Peripheral Arterial Tonometry (EndoPat 2000 system, Itamar Medical, Caesarea, Israel) immediately after receiving the last tablet of ticagrelor (Day 0) and at Day 2 and Day 5 post-ticagrelor cessation. Reactive hyperaemia index (RHI) was calculated by automated software and endothelial dysfunction (ED) was defined as a RHI <1.67.
  
  
  
  We identified 30 eligible patients with endothelial function assessment pre- and post-ticagrelor cessation (86.7% men, 13.3% with diabetes and 33.3% current smokers; mean age: 63.6±11.5 years). The study's primary endpoint of RHI at Day 5 did not differ significantly compared with RHI at Day 0, 1.69 (1.45-2.23) vs 1.81 (1.59-2.13). ED rate did not differ significantly between Day 5 and Day 0, 40 vs 33.3%, p=0.8, respectively. No differences in RHI or ED rate were observed between Day 2 and Day 0, 1.64 (1.54-2.04) vs 1.8 1(1.59-2.13), p=0.3 and 53.3 vs 33.3%, p=0.2, respectively. In stable CAD patients there is no evidence of deterioration in endothelial function after discontinuing ticagrelor.
authors.forename: Ioanna
authors.initials: I
authors.lastname: Xanthopoulou
authors.forename: Chrysoula
authors.initials: C
authors.lastname: Vogiatzi
authors.forename: Theodora
authors.initials: T
authors.lastname: Bampouri
authors.forename: Athina
authors.initials: A
authors.lastname: Chasapi
authors.forename: Ilianna
authors.initials: I
authors.lastname: Bei
authors.forename: Periklis
authors.initials: P
authors.lastname: Davlouros
authors.forename: George
authors.initials: G
authors.lastname: Hahalis
authors.affiliation: Patras University Hospital, Department of Cardiology, 26500, Patras, Greece. dalex@med.upatras.gr.
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Alexopoulos
mesh_terms: D054058:Acute Coronary Syndrome / Q000503:physiopathology / Q000628:therapy*; D000241:Adenosine / Q000008:administration & dosage / Q000009:adverse effects / Q000031:analogs & derivatives*; D000368:Aged; D004334:Drug Administration Schedule; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D019317:Evidence-Based Medicine; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D008365:Manometry; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage* / Q000009:adverse effects; D011446:Prospective Studies; D058921:Purinergic P2Y Receptor Antagonists / Q000008:administration & dosage* / Q000009:adverse effects; D000077486:Ticagrelor; D013997:Time Factors; D016896:Treatment Outcome; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D010975:Platelet Aggregation Inhibitors; D058921:Purinergic P2Y Receptor Antagonists; D000077486:Ticagrelor; D000241:Adenosine