title: Plaque and blood vulnerability in ST segment elevation myocardial infarction patients: association between lesion morphology using intravascular ultrasound radiofrequency analysis and circulating biomarkers.
abstract: OBJECTIVE
  The purpose of the study was to evaluate associations between iMap intravascular ultrasound tissue characterization of culprit and nonculprit lesions in infarct-related artery and plasma biomarkers during ST segment elevation myocardial infarction (STEMI) and at 10-month follow-up.
  
  
  RESULTS
  Sixty-three STEMI patients at the time of index hospitalization and 10-month follow-up underwent coronary angiography and intravascular ultrasound with iMap tissue characterization of the culprit artery. Proximal and culprit segments were analyzed. A higher percentage of necrotic tissue in the nonculprit segment was found in patients in the top soluble intercellular adhesion molecule 1 (sICAM-1) quartile compared with the other three quartiles (34.3±10.9 vs. 26.3±11.6%, P=0.041) in the acute setting. At 10-month follow-up the top quartile of sICAM-1 in both the acute and stable setting was associated with a lower percentage of fibrotic tissue, but a higher percentage of lipidic and necrotic tissue in the nonculprit segment. In the top quartile of plasminogen activator inhibitor 1 during STEMI, a lower percentage of fibrotic tissue (53.0±13.9 vs. 63.0±13.3%, P=0.014), higher percentage of lipidic tissue (11.7±3.1 vs. 9.4±2.4%, P=0.004), and higher percentage of necrotic tissue (33.4±11.6 vs. 25.7±11.3%, P=0.025) were found in the nonculprit segment.
  
  
  CONCLUSIONS
  Nonculprit plaque vulnerability characteristics were associated with elevated plasma biomarkers for sICAM-1 and plasminogen activator inhibitor 1.
authors.affiliation: aLatvian Centre of Cardiology, Pauls Stradins Clinical University Hospital bFaculty of Medicine, Riga Stradins University cFaculty of Medicine, University of Latvia, Riga, Latvia.
authors.forename: Karlis
authors.initials: K
authors.lastname: Trusinskis
authors.forename: Dace
authors.initials: D
authors.lastname: Juhnevica
authors.forename: Karlis
authors.initials: K
authors.lastname: Strenge
authors.forename: Andrejs
authors.initials: A
authors.lastname: Erglis
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography; D003331:Coronary Vessels / Q000000981:diagnostic imaging*; D005260:Female; D005355:Fibrosis; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000628:therapy; D009336:Necrosis; D062645:Percutaneous Coronary Intervention; D058226:Plaque, Atherosclerotic; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D011237:Predictive Value of Tests; D011446:Prospective Studies; D013997:Time Factors; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
chemical_list: D015415:Biomarkers; C573420:ICAM1 protein, human; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D018799:Intercellular Adhesion Molecule-1