title: Elevations in troponin I after percutaneous coronary interventions are associated with abnormal tissue-level perfusion in high-risk patients with non-ST-segment-elevation acute coronary syndromes.
abstract: BACKGROUND
  In the setting of non-ST-segment-elevation (NSTE) acute coronary syndromes (ACS), the pathophysiological mechanisms underlying post-percutaneous coronary intervention (PCI) cardiac troponin I (cTnI) elevation remain unclear.
  
  
  RESULTS
  We evaluated the relationship between troponin elevation and tissue-level perfusion using the TIMI flow grade, corrected TIMI frame count, TIMI myocardial perfusion grade (TMPG), and myocardial contrast enhancement by intracoronary myocardial contrast echocardiography (MCE) before and immediately after PCI performed within 24 to 48 hours of hospital admission in 42 high-risk (angina at rest, unequivocal ST-segment depression, and cTnI elevation) patients with NSTE-ACS. All patients were treated with glycoprotein IIb/IIIa inhibitors (27 with tirofiban and 15 with abciximab) and had successful PCI. Fourteen patients had a postprocedural cTnI elevation, whereas 28 did not. TMPG 0/1 after PCI was observed more frequently in patients with postprocedural cTnI elevation (43% versus 7%; P<0.02). cTnI levels were higher among patients with TMPG 0/1 versus patients with TMPG 2/3 (5.3+/-2.7 versus 1.5+/-1.3 ng/mL; P<0.0001). Patients with postprocedural cTnI elevation also presented a significantly lower number of perfused segments at MCE (59% versus 81%; P=0.02) as well as a lower MCE score index (0.65+/-0.38 versus 0.89+/-0.21; P<0.02).
  
  
  CONCLUSIONS
  Postprocedural cTnI elevation in high-risk patients with NSTE-ACS is associated with an abnormal tissue-level perfusion.
authors.affiliation: Division of Cardiology, S. Donato Hospital, Via P. Nenni n. 22, 52100 Arezzo, Italy. leonardobolognese@hotmail.com
authors.forename: Leonardo
authors.initials: L
authors.lastname: Bolognese
authors.forename: Kenneth
authors.initials: K
authors.lastname: Ducci
authors.forename: Paolo
authors.initials: P
authors.lastname: Angioli
authors.forename: Giovanni
authors.initials: G
authors.lastname: Falsini
authors.forename: Francesco
authors.initials: F
authors.lastname: Liistro
authors.forename: Silvia
authors.initials: S
authors.lastname: Baldassarre
authors.forename: Antonio
authors.initials: A
authors.lastname: Burali
mesh_terms: D000077284:Abciximab; D000208:Acute Disease; D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D015415:Biomarkers; D000077144:Clopidogrel; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D003326:Coronary Circulation; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000097:blood*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011446:Prospective Studies; D012306:Risk; D013988:Ticlopidine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D000077466:Tirofiban; D019210:Troponin I / Q000097:blood*; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D014463:Ultrasonography
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019210:Troponin I; D014443:Tyrosine; D000077144:Clopidogrel; D000077466:Tirofiban; D013988:Ticlopidine; D001241:Aspirin; D000077284:Abciximab