title: Outcomes after planned invasive or conservative treatment strategy in patients with non-ST-elevation acute coronary syndrome and a normal value of high sensitivity troponin at randomisation: A Platelet Inhibition and Patient Outcomes (PLATO) trial biomarker substudy.
abstract: OBJECTIVE
  Current guidelines for patients with non-ST-elevation acute coronary syndrome (NSTE-ACS) recommend early invasive treatment in intermediate-to-high risk patients based on medical history, electrocardiogram (ECG) and elevated troponin. Patients with normal levels of cardiac troponin measured with a high-sensitivity method (cTnT-hs) might not benefit from early invasive procedures.
  
  
  RESULTS
  In this Prospective Randomized Platelet Inhibition and Patient Outcomes (PLATO) blood-core substudy, 1232 patients presented with NSTE-ACS had a high sensitivity cardiac troponin T (cTnT-hs) level <99thpercentile (<14 ng/l) at randomisation. The outcomes in relation to a planned invasive ( n=473) vs planned conservative treatment ( n=759), were evaluated by adjusted Cox proportional hazard analyses. In patients with a normal cTnT-hs at randomisation, regardless of randomised treatment, a planned invasive vs conservative treatment was associated with a 2.3-fold higher risk (7.3% vs 3.4%, p=0.0028) for cardiovascular (CV) death or myocardial infarction (MI), driven by higher rates of procedure-related MI (3.4% vs 0.1%), while there were no differences in rates of CV death (1.3% vs 1.3%, p=0.72) or spontaneous MI (3.0% vs 2.1%, p=0.28). There were significantly more major bleeds (hazard ratio (HR) 2.98, p<0.0001), mainly due to coronary artery bypass graft (CABG)-related (HR 4.05, p<0.0001) and non-CABG procedural-related major bleeding events (HR 5.31, p=0.0175), however there were no differences in non-procedure-related major bleeding (1.5% vs 1.9%, p=0.45). Findings were consistent for patients with a normal cTnI-hs at randomisation.
  
  
  CONCLUSIONS
  In patients with NSTE-ACS and normal cTnT-hs, a planned early invasive treatment strategy was associated with increased rates of procedure-related MI and bleeding but no differences in long-term spontaneous MI, non-procedure-related bleeding or mortality.
authors.affiliation: 1 Medizinische Klinik, Universitätsklinikum Heidelberg, Germany.
authors.forename: Evangelos
authors.initials: E
authors.lastname: Giannitsis
authors.affiliation: 2 Department of Medical Sciences, Uppsala University, Sweden.|3 Uppsala Clinical Research Center, Uppsala University, Sweden.
authors.forename: Lars
authors.initials: L
authors.lastname: Wallentin
authors.affiliation: 2 Department of Medical Sciences, Uppsala University, Sweden.|3 Uppsala Clinical Research Center, Uppsala University, Sweden.
authors.forename: Stefan K
authors.initials: SK
authors.lastname: James
authors.affiliation: 3 Uppsala Clinical Research Center, Uppsala University, Sweden.
authors.forename: Maria
authors.initials: M
authors.lastname: Bertilsson
authors.affiliation: 2 Department of Medical Sciences, Uppsala University, Sweden.|3 Uppsala Clinical Research Center, Uppsala University, Sweden.
authors.forename: Agneta
authors.initials: A
authors.lastname: Siegbahn
authors.affiliation: 4 Department of Cardiovascular Science, University of Sheffield, UK.
authors.forename: Robert F
authors.initials: RF
authors.lastname: Storey
authors.affiliation: 5 Medical Department, Hospital Unit West, Herning/Holstebro, Denmark.
authors.forename: Steen
authors.initials: S
authors.lastname: Husted
authors.affiliation: 6 Cardiovascular Division, Brigham and Women's Hospital, USA.|7 Harvard Clinical Research Institute, USA.
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
authors.affiliation: 8 Canadian VIGOUR Centre, University of Alberta, Canada.
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.affiliation: 9 INSERM-Unité 1148, France.|10 Assistance Publique-Hôpitaux de Paris, Hôpital Bichat, France.|11 Université Paris-Diderot, Sorbonne-Paris Cité, France.|12 National Heart and Lung Institute, Imperial College London, UK.|13 Institute of Cardiovascular Medicine and Science, Royal Brompton Hospital, UK.
authors.forename: Philippe G
authors.initials: PG
authors.lastname: Steg
authors.affiliation: 1 Medizinische Klinik, Universitätsklinikum Heidelberg, Germany.
authors.forename: Hugo A
authors.initials: HA
authors.lastname: Katus
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis / Q000628:therapy*; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D000072700:Conservative Treatment / Q000379:methods*; D017023:Coronary Angiography / Q000379:methods; D004311:Double-Blind Method; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D009204:Myocardial Revascularization / Q000379:methods*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D017410:Practice Guidelines as Topic; D011446:Prospective Studies; D012016:Reference Values; D020107:Troponin T / Q000097:blood*
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D020107:Troponin T
keywords: Acute coronary syndrome; biological markers; blood platelets; myocardial infarction