title: Abnormal coronary flow velocity reserve after coronary intervention is associated with cardiac marker elevation.
abstract: BACKGROUND
  Residual reduction of relative coronary flow velocity reserve (rCVR) after successful coronary intervention has been related to microvascular impairment. However, the incidence of cardiac enzyme elevation as a surrogate marker of an underlying embolic myocardial injury in these cases has not been studied.
  
  
  RESULTS
  A series of 55 consecutive patients with successful coronary stenting, periprocedural intracoronary Doppler analysis, and determination of creatine kinase (CK; upper limit of normal [ULN] for women 70 IU/L, for men 80 IU/L) and cardiac troponin T (cTnT; bedside test, threshold 0.1 ng/mL) before and 6, 12, and 24 hours after intervention were studied. Postprocedural rCVR was the only intracoronary Doppler parameter that independently correlated with cTnT (r=-0.498, P<0.001) and CK outcome (r=-0.406, P=0.002). Receiver operating characteristic analysis identified a postprocedural rCVR of 0.78 as the best discriminating value, with a sensitivity of 83.3% and 69.2% and a specificity of 79.1% and 76.2% for detection of cTnT and CK elevation, respectively. Stratified according to this cutoff value, the incidence of cTnT elevation was 52.6% in patients with (n=19) and 5.6% in patients without (n=36) a postprocedural rCVR <0.78 (P<0.001), associated with a CK elevation >1 times the ULN in 36.8% and 5.6% (P=0.005) of patients, respectively.
  
  
  CONCLUSIONS
  Cardiac marker elevation can frequently be found after coronary procedures that are associated with a persistent reduction of rCVR, indicating procedural embolization of atherothrombotic debris with microvascular impairment and myocardial injury as a potential underlying mechanism.
authors.affiliation: Department of Cardiology, University Clinic Essen, Essen, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Herrmann
authors.forename: M
authors.initials: M
authors.lastname: Haude
authors.forename: A
authors.initials: A
authors.lastname: Lerman
authors.forename: R
authors.initials: R
authors.lastname: Schulz
authors.forename: L
authors.initials: L
authors.lastname: Volbracht
authors.forename: J
authors.initials: J
authors.lastname: Ge
authors.forename: A
authors.initials: A
authors.lastname: Schmermund
authors.forename: H
authors.initials: H
authors.lastname: Wieneke
authors.forename: C
authors.initials: C
authors.lastname: von Birgelen
authors.forename: H
authors.initials: H
authors.lastname: Eggebrecht
authors.forename: D
authors.initials: D
authors.lastname: Baumgart
authors.forename: G
authors.initials: G
authors.lastname: Heusch
authors.forename: R
authors.initials: R
authors.lastname: Erbel
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000032:analysis; D017023:Coronary Angiography; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy; D003402:Creatine Kinase / Q000378:metabolism; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D011446:Prospective Studies; D015607:Stents; D020107:Troponin T / Q000378:metabolism
chemical_list: D015415:Biomarkers; D020107:Troponin T; D003402:Creatine Kinase