Systemic Glucocorticoids Are Associated With Mortality After Carotid Endarterectomy
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2015-10
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taverne
Abstract
Glucocorticoids (GCs) are widely used anti-inflammatory drugs well known to cause many adverse effects. Still, there is a dearth of data on the long-term cardiovascular effects of GCs in patients with established cardiovascular disease and the effect on atherosclerotic plaque composition. A total of 1894 patients who underwent carotid endarterectomy (CEA), of whom 40 patients received systemic GCs, were included in the Athero-Express Biobank. Atherosclerotic plaque samples and peripheral blood samples were obtained during CEA. Cardiovascular events during 3 years of follow-up were investigated using Cox regression modeling to adjust for possible confounding. Atherosclerotic plaque composition was examined using immunohistochemical staining. Use of GCs at inclusion was associated with markedly increased incidences of ischemic stroke (15.2% vs. 5.9%), composite events (48.5% vs. 26.9%), and cardiovascular death (21.2% vs. 5.7%), as well as an increased risk of cardiovascular death (hazards ratio 2.7, 95% confidence interval, 1.1-6.7) and all-cause death (hazards ratio 2.3, 95% confidence interval, 1.1-4.8) after 2.6 years of follow-up. None of the histological features of atherosclerotic plaques were significantly different in patients using GCs. After CEA, the use of systemic GCs is independently associated with an increased incidence of cardiovascular events and an increased risk of cardiovascular and all-cause death, but not atherosclerotic plaque composition.
Keywords
atherosclerosis, glucocorticoid, risk, cardiovascular, adverse effects, CARDIOVASCULAR EVENTS, RHEUMATOID-ARTHRITIS, EUROPEAN-SOCIETY, ADVERSE EVENTS, ATHEROSCLEROSIS, DISEASE, RISK, CORTICOSTEROIDS, PREVENTION, Taverne
Citation
Siemelink, M, den Ruijter, H, van der Valk, F, de Vries, J-P, de Borst, G J, Moll, F, Stroes, E & Pasterkamp, G 2015, 'Systemic Glucocorticoids Are Associated With Mortality After Carotid Endarterectomy', Journal of Cardiovascular Pharmacology, vol. 66, no. 4, pp. 392-398. https://doi.org/10.1097/FJC.0000000000000292