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RESEARCH PRODUCT
Plaque and blood vulnerability in ST segment elevation myocardial infarction patients: association between lesion morphology using intravascular ultrasound radiofrequency analysis and circulating biomarkers.
Karlis TrusinskisDace JuhnevicaAndrejs ĒRglisKarlis Strengesubject
MaleAcute coronary syndromemedicine.medical_specialtyTime FactorsMyocardial InfarctionCoronary AngiographyCulpritLesionchemistry.chemical_compoundNecrosisPercutaneous Coronary InterventionPredictive Value of TestsInternal medicineIntravascular ultrasoundPlasminogen Activator Inhibitor 1medicineST segmentHumansMyocardial infarctionProspective StudiesUltrasonography InterventionalAgedmedicine.diagnostic_testbusiness.industryGeneral MedicineMiddle Agedmedicine.diseaseIntercellular Adhesion Molecule-1Coronary VesselsFibrosisPlaque Atheroscleroticmedicine.anatomical_structureTreatment OutcomechemistryPlasminogen activator inhibitor-1CardiologyFemalemedicine.symptomCardiology and Cardiovascular MedicinebusinessBiomarkersArterydescription
AIM 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. METHODS AND 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. CONCLUSION Nonculprit plaque vulnerability characteristics were associated with elevated plasma biomarkers for sICAM-1 and plasminogen activator inhibitor 1.
year | journal | country | edition | language |
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2013-11-22 | Coronary artery disease |