TY - JOUR
T1 - Analysis of biomarkers for risk of acute kidney injury after primary angioplasty for acute st-segment elevation myocardial infarction
T2 - Results of the HORIZONS-AMI trial
AU - Guerchicoff, Alejandra
AU - Stone, Gregg W.
AU - Mehran, Roxana
AU - Xu, Ke
AU - Nichols, Dru
AU - Claessen, Bimmer E.
AU - Guagliumi, Giulio
AU - Witzenbichler, Bernhard
AU - Henriques, Jośe P.S.
AU - Dangas, George D.
N1 - Publisher Copyright:
© 2014 Wiley Periodicals, Inc.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Objectives: Contrast-induced acute kidney injury (CI-AKI) may occur after percutaneous coronary intervention (PCI). Methods: We evaluated patients with ST-elevation myocardial infarction (STEMI) undergoing emergency PCI with serial biomarkers. Results: Of the 390 patients enrolled in the HORIZONS-AMI biomarker substudy, 56 (14.3%) developed AKI. In the AKI group, the levels of B-type natriuretic peptide were consistently higher than in the no-AKI group at baseline (P = 0.0327), hospital discharge (P =0.0002), 30-day follow-up (P = 0.0193), and 1-year follow-up (P = 0.031). At hospital discharge, the AKI group had elevated biomarkers compared to the no-AKI group: D-dimer (P = 0.0066), C-reactive protein (P = 0.0468), endothelial cell-selective adhesion molecule (P = 0.0169), adiponectin (P = 0.0346), and von Willebrand factor (P = 0.0168); there was also a trend toward higher cystatin C (P = 0.0585) in the AKI group. Similar correlations between biomarker panel increase and the development of CI-AKI were consistent at baseline, 30-day, and 1-year follow-up. Chemokine (C-C motif) ligand 23 showed an opposite pattern with an increase at all time points in the no-AKI compared to the AKI group. Conclusions: The risk of CI-AKI after primary PCI for STEMI may be associated with hemostatic imbalances, activation of procoagulants, decreased endogenous anticoagulants, enhanced inflammation, platelet activation, or decreased fibrinolytic activity.
AB - Objectives: Contrast-induced acute kidney injury (CI-AKI) may occur after percutaneous coronary intervention (PCI). Methods: We evaluated patients with ST-elevation myocardial infarction (STEMI) undergoing emergency PCI with serial biomarkers. Results: Of the 390 patients enrolled in the HORIZONS-AMI biomarker substudy, 56 (14.3%) developed AKI. In the AKI group, the levels of B-type natriuretic peptide were consistently higher than in the no-AKI group at baseline (P = 0.0327), hospital discharge (P =0.0002), 30-day follow-up (P = 0.0193), and 1-year follow-up (P = 0.031). At hospital discharge, the AKI group had elevated biomarkers compared to the no-AKI group: D-dimer (P = 0.0066), C-reactive protein (P = 0.0468), endothelial cell-selective adhesion molecule (P = 0.0169), adiponectin (P = 0.0346), and von Willebrand factor (P = 0.0168); there was also a trend toward higher cystatin C (P = 0.0585) in the AKI group. Similar correlations between biomarker panel increase and the development of CI-AKI were consistent at baseline, 30-day, and 1-year follow-up. Chemokine (C-C motif) ligand 23 showed an opposite pattern with an increase at all time points in the no-AKI compared to the AKI group. Conclusions: The risk of CI-AKI after primary PCI for STEMI may be associated with hemostatic imbalances, activation of procoagulants, decreased endogenous anticoagulants, enhanced inflammation, platelet activation, or decreased fibrinolytic activity.
KW - Acute kidney injury
KW - Angioplasty
KW - Biomarkers
KW - STEMI
UR - http://www.scopus.com/inward/record.url?scp=84923046615&partnerID=8YFLogxK
U2 - 10.1002/ccd.25620
DO - 10.1002/ccd.25620
M3 - Article
C2 - 25130788
AN - SCOPUS:84923046615
SN - 1522-1946
VL - 85
SP - 335
EP - 342
JO - Catheterization and Cardiovascular Interventions
JF - Catheterization and Cardiovascular Interventions
IS - 3
ER -