title: Personalised antiplatelet therapy in stent thrombosis: observations from the Clopidogrel Resistance in Stent Thrombosis (CREST) registry.
abstract: OBJECTIVE
  Previous studies have demonstrated significant heterogeneity in responses to antiplatelet therapy (APT), and high residual platelet reactivity is associated with the risk of ischaemic events, including stent thrombosis (ST). The prevalence of APT hyporesponsiveness in a 'real world' registry of ST patients and the feasibility of personalising APT are reported.
  
  
  METHODS
  39 consecutive patients admitted to a single regional cardiothoracic centre with definite ST were prospectively evaluated.
  
  
  METHODS
  Response to aspirin and clopidogrel was measured following discharge using short thrombelastography (TEG), a rapid, well validated near patient platelet function test. Treatment modification in hyporesponders comprised an increase in aspirin dose and/or changing clopidogrel to prasugrel or ticagrelor. Short TEG was repeated following treatment modification to ensure an adequate response had been achieved.
  
  
  RESULTS
  12 (31%) patients had an adequate response to both aspirin and clopidogrel, 16 (41%) were hyporesponsive to clopidogrel alone, one (3%) was hyporesponsive to aspirin alone and 10 (26%) were hyporesponsive to both aspirin and clopidogrel. Following treatment modification, an adequate response to aspirin and P2Y12 agent was achieved in 10 (91%) and 22 (85%) patients, respectively. None has presented with a further ST episode.
  
  
  CONCLUSIONS
  There is a high prevalence of hyporesponsiveness to APT in patients with ST. Improved APT efficacy can be achieved by tailored therapy. Short TEG is a plausible platelet function test that can be used to deliver point of care personalised APT.
authors.affiliation: Wessex Cardiothoracic Unit, University Hospital Southampton NHS Foundation Trust, Southampton, UK.
authors.forename: Nalyaka
authors.initials: N
authors.lastname: Sambu
authors.forename: Ashwin
authors.initials: A
authors.lastname: Radhakrishnan
authors.forename: Hazel
authors.initials: H
authors.lastname: Dent
authors.forename: Alison Louise
authors.initials: AL
authors.lastname: Calver
authors.forename: Simon
authors.initials: S
authors.lastname: Corbett
authors.forename: Huon
authors.initials: H
authors.lastname: Gray
authors.forename: Iain A
authors.initials: IA
authors.lastname: Simpson
authors.forename: Nick
authors.initials: N
authors.lastname: Curzen
mesh_terms: D000368:Aged; D001241:Aspirin / Q000008:administration & dosage / Q000627:therapeutic use; D000077144:Clopidogrel; D003328:Coronary Thrombosis / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006083:Graft Occlusion, Vascular / Q000097:blood / Q000188:drug therapy* / Q000453:epidemiology; D006801:Humans; D008297:Male; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000627:therapeutic use*; D015995:Prevalence; D011446:Prospective Studies; D012042:Registries; D013916:Thrombelastography; D013988:Ticlopidine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000627:therapeutic use; D016896:Treatment Outcome; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin