title: Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study.
abstract: OBJECTIVE
  The purpose of this study was to assess whether: 1) very small increases in troponin T, measured by a new highly sensitive cardiac troponin T (hs-cTnT), may reflect ischemia without necrosis; and 2) serial changes can discriminate ischemia from other causes of cardiac troponin T (cTnT) release.
  
  
  BACKGROUND
  A new hs-cTnT assay offers greater sensitivity than current assays.
  
  
  METHODS
  Nineteen patients referred for diagnostic catheterization underwent cannulation of the coronary sinus (CS). Serial CS and peripheral plasma samples were obtained at multiple time points during and after incremental rapid atrial pacing. cTnT was quantified using both a standard and a pre-commercial highly sensitive assay. Ischemia was determined by the presence of significant coronary artery disease (CAD) and myocardial lactate release with pacing.
  
  
  RESULTS
  cTnT concentrations in CS blood increased from a median of 6.8 pg/ml prior to pacing to 15.6 pg/ml 60 min after termination of rapid atrial pacing (p < 0.0001), changes that were mirrored at 180 min in peripheral blood (5.1 to 11.8 pg/ml, p < 0.0001). Although peripheral cTnT concentrations tended to be higher at 180 min following pacing for patients with CAD and lactate elution (n = 7) when compared with those without either marker (n = 5) (25.0 pg/ml vs. 10.2 pg/ml, p = 0.10), relative (1.7-fold vs. 5.2-fold) and absolute (6.8 pg/ml vs. 8.8 pg/ml, p = 0.50) changes were not different between groups.
  
  
  CONCLUSIONS
  Brief periods of ischemia, without frank infarction, cause low-level cTnT release, and small increases are common after periods of increased myocardial work, even among patients without objective evidence of myocardial ischemia or obstructive CAD. Additional research is needed before hs-cTnT assays are widely adopted in the management of subjects with chest pain syndromes.
authors.affiliation: Department of Medicine, Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas 75230-9047, USA. aslan.turer@utsouthwestern.edu
authors.forename: Aslan T
authors.initials: AT
authors.lastname: Turer
authors.forename: Tayo A
authors.initials: TA
authors.lastname: Addo
authors.forename: Justin L
authors.initials: JL
authors.lastname: Martin
authors.forename: Marc S
authors.initials: MS
authors.lastname: Sabatine
authors.forename: Gregory D
authors.initials: GD
authors.lastname: Lewis
authors.forename: Robert E
authors.initials: RE
authors.lastname: Gerszten
authors.forename: Ellen C
authors.initials: EC
authors.lastname: Keeley
authors.forename: Joaquin E
authors.initials: JE
authors.lastname: Cigarroa
authors.forename: Richard A
authors.initials: RA
authors.lastname: Lange
authors.forename: L David
authors.initials: LD
authors.lastname: Hillis
authors.forename: James A
authors.initials: JA
authors.lastname: de Lemos
mesh_terms: D000328:Adult; D000787:Angina Pectoris / Q000097:blood / Q000628:therapy*; D001681:Biological Assay / Q000379:methods*; D015415:Biomarkers / Q000097:blood; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects* / Q000379:methods; D003324:Coronary Artery Disease / Q000097:blood / Q000175:diagnosis; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000209:etiology; D012189:Retrospective Studies; D018570:Risk Assessment; D012494:Sampling Studies; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D020107:Troponin T / Q000032:analysis / Q000097:blood*
chemical_list: D015415:Biomarkers; D020107:Troponin T