title: Frequency, clinical and angiographic characteristics, and outcomes of high-risk non-ST-segment elevation acute coronary syndromes patients with left circumflex culprit lesions.
abstract: BACKGROUND
  The relationship between culprit vessel, infarct size, and outcomes in non-ST-segment elevation acute coronary syndromes (NSTE ACS) is unclear. In some reports, the left circumflex artery (LCX) was more often the culprit at angiography than the right coronary artery (RCA) or left anterior descending artery (LAD), and infarcts were larger with LCX culprits.
  
  
  METHODS
  We determined culprit vessel frequency and initial patency (TIMI flow grade), median fold elevation of peak troponin above the upper limit of normal, and outcomes (30-day death or myocardial infarction [MI] and 1-year mortality) by culprit vessel in high-risk NSTE ACS patients in the EARLY ACS trial.
  
  
  RESULTS
  Of 9406 patients, 2066 (22.0%) had angiographic core laboratory data. We evaluated 1774 patients for whom the culprit artery was not the left main, a bypass graft, or branch vessel. The culprit was the LCX in 560 (31.6%), LAD in 653 (36.8%), and RCA in 561 (31.6%) patients. There were fewer women (24.1%) and more prior MI (25.5%) among patients with a culprit LCX compared with those with a culprit LAD or RCA. Patients with LCX (21.2%) and RCA (27.5%) culprits more often had an occluded artery (TIMI 0/1) than did those with LAD (11.3%). Peak troponin elevation was significantly higher for LCX than RCA or LAD culprits. LCX culprit vessels were not associated with worse 30-day or 1-year outcomes in adjusted models.
  
  
  CONCLUSIONS
  Among patients with NSTE ACS, the frequencies of LCX, LAD, and RCA culprits were similar. Although LCX lesions were associated with higher peak troponin levels, there was no difference in short- or intermediate-term outcomes by culprit artery.
authors.affiliation: Division of Cardiology and Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Sharif A
authors.initials: SA
authors.lastname: Halim
authors.affiliation: Division of Cardiology and Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Robert M
authors.initials: RM
authors.lastname: Clare
authors.affiliation: Division of Cardiology and Duke Clinical Research Institute, Durham, NC, USA. Electronic address: kristin.newby@duke.edu.
authors.forename: L Kristin
authors.initials: LK
authors.lastname: Newby
authors.affiliation: Division of Cardiology and Duke Clinical Research Institute, Durham, NC, USA.
authors.forename: Yuliya
authors.initials: Y
authors.lastname: Lokhnygina
authors.affiliation: Tufts University School of Medicine, Baystate Medical Center, Springfield, MA, USA.
authors.forename: Marc J
authors.initials: MJ
authors.lastname: Schweiger
authors.affiliation: Division of Cardiology, Hospital 'De Weezenlanden', Isala Klinieken, Zwolle, The Netherlands.
authors.forename: Arnoud W
authors.initials: AW
authors.lastname: Hof
authors.affiliation: Department of Medicine, New York University School of Medicine, New York, NY, USA.
authors.forename: Judith S
authors.initials: JS
authors.lastname: Hochman
authors.affiliation: Uppsala University Hospital, Cardiology, Uppsala, Sweden.
authors.forename: Stefan K
authors.initials: SK
authors.lastname: James
authors.affiliation: Green Lane Cardiovascular Service, Auckland, New Zealand.
authors.forename: Harvey D
authors.initials: HD
authors.lastname: White
authors.affiliation: Third Faculty of Medicine, Charles University, Prague, Czech Republic.
authors.forename: Petr
authors.initials: P
authors.lastname: Widimsky
authors.affiliation: Department of Cardiology, Hospital Clinic, Barcelona, Spain.
authors.forename: Amadeo
authors.initials: A
authors.lastname: Betriu
authors.affiliation: University Hospital of Freiburg, Freiburg, Germany.
authors.forename: Christoph
authors.initials: C
authors.lastname: Bode
authors.affiliation: TIMI Study Group, Brigham and Women's Hospital, Boston, MA, USA.
authors.forename: Robert P
authors.initials: RP
authors.lastname: Giugliano
authors.affiliation: Department of Medicine, Stanford University, Stanford, CA, USA.
authors.forename: Robert A
authors.initials: RA
authors.lastname: Harrington
authors.affiliation: Herzzentrum Ludwigshafen, Germany.
authors.forename: Uwe
authors.initials: U
authors.lastname: Zeymer
mesh_terms: D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging / Q000453:epidemiology* / Q000628:therapy; D000368:Aged; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000000981:diagnostic imaging* / Q000601:surgery; D004562:Electrocardiography; D000077542:Eptifibatide; D005060:Europe / Q000453:epidemiology; D005260:Female; D006801:Humans; D015994:Incidence; D007262:Infusions, Intravenous; D008297:Male; D009520:New Zealand / Q000453:epidemiology; D010455:Peptides / Q000008:administration & dosage*; D062645:Percutaneous Coronary Intervention / Q000379:methods*; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors; D011379:Prognosis; D012307:Risk Factors; D015996:Survival Rate / Q000639:trends; D013997:Time Factors; D016896:Treatment Outcome; D014481:United States / Q000453:epidemiology
chemical_list: D010455:Peptides; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D000077542:Eptifibatide
keywords: Acute coronary syndromes; Infarct size; Left circumflex artery