Lars E Laugsand1, Bjørn O Åsvold2, Lars J Vatten3, Imre Janszky4, Carl Platou5, Annika E Michelsen6, Fizza Arain7, Jan K Damås8, Pål Aukrust9, Thor Ueland10. 1. Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N- 7491 Trondheim, Norway; Department of Cardiology, St.Olavs Hospital, Trondheim, Norway. Electronic address: lars.e.laugsand@ntnu.no. 2. Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N- 7491 Trondheim, Norway; Department of Endocrinology, St. Olavs Hospital, Trondheim, Norway. 3. Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N- 7491 Trondheim, Norway. 4. Department of Public Health, Faculty of Medicine, Norwegian University of Science and Technology, N- 7491 Trondheim, Norway; Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden. 5. Department of Internal Medicine, Levanger Hospital, Nord-Trøndelag Health Trust, Norway. 6. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. 7. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Department of Cardiology, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway. 8. Centre of Molecular Inflammation Research, Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway; Department of Infectious Diseases, St. Olavs Hospital, Trondheim, Norway. 9. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway; K. G. Jebsen Thrombosis Research and Expertise Center, University of Tromsø, Tromsø, Norway. 10. Research Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Inflammatory Research Center, University of Oslo, Oslo, Norway; K. G. Jebsen Thrombosis Research and Expertise Center, University of Tromsø, Tromsø, Norway.
Abstract
BACKGROUND AND AIMS: CXCL16 is an interferon-γ-regulated chemokine and scavenger receptor for oxidized low-density lipoprotein that is expressed in atherosclerotic lesions. High soluble CXCL16 levels during acute cardiovascular events may indicate impaired long-term prognosis, but it is not known if CXCL16 is associated with the risk of developing cardiovascular disease in healthy individuals. We aimed to assess whether soluble CXCL16 is associated with risk of myocardial infarction (MI) in a nested case-control study within a large population-based cohort. METHODS: We conducted a case-control study nested within the population-based HUNT2 cohort in Norway. A total of 58,761 men and women free of known cardiovascular disease were followed for a first myocardial infarction (MI), and during 11.3 years of follow-up, 1587 incident MIs were registered. These cases were compared to 3959 age- and sex-matched controls. RESULTS: Among MI cases, the median CXCL16 concentration was 9.9 ng/ml (interquartile range 7.2-12.6) compared to 9.6 ng/ml (interquartile range 6.9-12.3) among controls (p < 0.001). Although the difference in median value between cases and controls was small, MI risk was twice as high (OR, 2.08; 95% CI: 1.74-2.50) among participants in the highest quartile compared to participants in the lowest quartile of CXCL16 after adjustment for age and sex. Additional adjustment for serum lipids, body mass index, smoking habits, diabetes mellitus, serum creatinine, and high-sensitivity C-reactive protein attenuated the excess risk by about half, yielding an odds ratio of 1.46 (95% CI: 1.19-1.79). CONCLUSION: Soluble CXCL16 may provide novel information in clinical cardiovascular risk assessment, but its importance needs to be verified in other prospective population studies.
BACKGROUND AND AIMS: CXCL16 is an interferon-γ-regulated chemokine and scavenger receptor for oxidized low-density lipoprotein that is expressed in atherosclerotic lesions. High soluble CXCL16 levels during acute cardiovascular events may indicate impaired long-term prognosis, but it is not known if CXCL16 is associated with the risk of developing cardiovascular disease in healthy individuals. We aimed to assess whether soluble CXCL16 is associated with risk of myocardial infarction (MI) in a nested case-control study within a large population-based cohort. METHODS: We conducted a case-control study nested within the population-based HUNT2 cohort in Norway. A total of 58,761 men and women free of known cardiovascular disease were followed for a first myocardial infarction (MI), and during 11.3 years of follow-up, 1587 incident MIs were registered. These cases were compared to 3959 age- and sex-matched controls. RESULTS: Among MI cases, the median CXCL16 concentration was 9.9 ng/ml (interquartile range 7.2-12.6) compared to 9.6 ng/ml (interquartile range 6.9-12.3) among controls (p < 0.001). Although the difference in median value between cases and controls was small, MI risk was twice as high (OR, 2.08; 95% CI: 1.74-2.50) among participants in the highest quartile compared to participants in the lowest quartile of CXCL16 after adjustment for age and sex. Additional adjustment for serum lipids, body mass index, smoking habits, diabetes mellitus, serum creatinine, and high-sensitivity C-reactive protein attenuated the excess risk by about half, yielding an odds ratio of 1.46 (95% CI: 1.19-1.79). CONCLUSION: Soluble CXCL16 may provide novel information in clinical cardiovascular risk assessment, but its importance needs to be verified in other prospective population studies.
Authors: L Turgunova; B Baidildina; Y Laryushina; B Koichubekov; A Turmukhambetova; L Akhmaltdinova Journal: Cardiol Res Pract Date: 2020-06-23 Impact factor: 1.866
Authors: Gary A Cuthbert; Faheem Shaik; Michael A Harrison; Sreenivasan Ponnambalam; Shervanthi Homer-Vanniasinkam Journal: Cells Date: 2020-11-10 Impact factor: 6.600