Thor Ueland1, Axel Åkerblom2, Tatevik Ghukasyan3, Annika E Michelsen4, Richard C Becker5, Maria Bertilsson3, Andrzej Budaj6, Jan H Cornel7, Anders Himmelmann8, Stefan K James2, Agneta Siegbahn9, Robert F Storey10, Frederic Kontny11, Pål Aukrust12, Lars Wallentin2. 1. Research Institute of Internal Medicine, The National Hospital, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Norway; K.G. Jebsen - Thrombosis Research and Expertise Center (TREC), University of Tromsø, Tromsø, Norway. Electronic address: thor.ueland@medisin.uio.no. 2. Department of Medical Sciences, Cardiology, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. 3. Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden. 4. Research Institute of Internal Medicine, The National Hospital, University of Oslo, Oslo, Norway. 5. Division of Cardiovascular Health and Disease, Heart, Lung and Vascular Institute, University of Cincinnati College of Medicine, Cincinnati, OH, USA. 6. Postgraduate Medical School, Grochowski Hospital, Warsaw, Poland. 7. Department of Cardiology, Noordwest Ziekenhuisgroep, Alkmaar, the Netherlands. 8. AstraZeneca Research and Development, Gothenburg, Sweden. 9. Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden; Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. 10. Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, United Kingdom. 11. Stavanger University Hospital, Department of Cardiology, Stavanger, Norway; Drammen Heart Center, Drammen, Norway. 12. Research Institute of Internal Medicine, The National Hospital, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Norway; K.G. Jebsen - Thrombosis Research and Expertise Center (TREC), University of Tromsø, Tromsø, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Abstract
BACKGROUND AND AIMS: Activated leukocyte cell adhesion molecule (ALCAM) is upregulated during inflammation and involved in transmigration of leukocytes and T-cell activation. We hypothesized that ALCAM might be associated with recurrent events in patients with acute coronary syndromes (ACS). METHODS:ALCAM was measured in serum obtained on admission, at discharge, 1 month and 6 months in a subgroup of 5165 patients admitted with ACS and included in the PLATelet inhibition and patient Outcomes (PLATO) trial (NCT00391872). The association between ALCAM and the composite endpoint and its components, including cardiovascular (CV) death, non-procedural spontaneous myocardial infarction (MI) or stroke during 1-year follow-up, was assessed by Cox proportional hazards models with incremental addition of clinical risk factors and biomarkers (including high-sensitivity troponin T, N-terminal pro-B-type natriuretic peptide and growth differentiation factor-15). RESULTS: The median (Q1-Q3) concentration of ALCAM at admission was 97 (80-116) ng/mL. A 50% higher level of ALCAM on admission was associated with a hazard ratio (HR) of 1.16 (95% confidence interval [1.00-1.34] p = 0.043) for the composite endpoint in fully adjusted analysis, mainly driven by the association with CV death (HR 1.45 [1.16-1.82] p = 0.0012). CONCLUSIONS: In patients with ACS, admission level of ALCAM was independently associated with adverse outcome including CV death even after adjustment for established inflammatory and cardiac biomarkers.
RCT Entities:
BACKGROUND AND AIMS: Activated leukocyte cell adhesion molecule (ALCAM) is upregulated during inflammation and involved in transmigration of leukocytes and T-cell activation. We hypothesized that ALCAM might be associated with recurrent events in patients with acute coronary syndromes (ACS). METHODS:ALCAM was measured in serum obtained on admission, at discharge, 1 month and 6 months in a subgroup of 5165 patients admitted with ACS and included in the PLATelet inhibition and patient Outcomes (PLATO) trial (NCT00391872). The association between ALCAM and the composite endpoint and its components, including cardiovascular (CV) death, non-procedural spontaneous myocardial infarction (MI) or stroke during 1-year follow-up, was assessed by Cox proportional hazards models with incremental addition of clinical risk factors and biomarkers (including high-sensitivity troponin T, N-terminal pro-B-type natriuretic peptide and growth differentiation factor-15). RESULTS: The median (Q1-Q3) concentration of ALCAM at admission was 97 (80-116) ng/mL. A 50% higher level of ALCAM on admission was associated with a hazard ratio (HR) of 1.16 (95% confidence interval [1.00-1.34] p = 0.043) for the composite endpoint in fully adjusted analysis, mainly driven by the association with CV death (HR 1.45 [1.16-1.82] p = 0.0012). CONCLUSIONS: In patients with ACS, admission level of ALCAM was independently associated with adverse outcome including CV death even after adjustment for established inflammatory and cardiac biomarkers.
Authors: Helen He; Caroline M Olesen; Ana B Pavel; Maja-Lisa Clausen; Jianni Wu; Yeriel Estrada; Ning Zhang; Tove Agner; Emma Guttman-Yassky Journal: Front Immunol Date: 2020-08-06 Impact factor: 7.561