期刊
EUROPEAN HEART JOURNAL
卷 34, 期 34, 页码 2689-+出版社
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/eht264
关键词
Coronary artery disease; Risk prediction; Urinary biomarker; Kynurenine; Tryptophan; Inflammation
资金
- Norwegian Foundation for Health and Rehabilitation
- Norwegian Heart and Lung Patient Organization
- Norwegian Ministry of Health and Care Services
- Western Norway Regional Health Authority
- Foundation to promote research into functional vitamin B12-deficiency
- Department of Heart Disease, Haukeland University Hospital, Norway
Aims Kynurenine is a potent endothelium-derived vasodilator. Its synthesis from tryptophan is stimulated by interferon g and may represent an important compensatory pathway for the regulation of vascular function in inflammatory conditions. We assessed associations of urine kynurenine to tryptophan ratio (KTR) levels to incident major coronary events (MCEs), acute myocardial infarction (AMI), and ischaemic stroke and mortality in patients with suspected stable coronary artery disease (CAD). Methods and results A total of 3224 patients (mean age 62 years, 69% men) underwent urine and blood sampling prior to elective coronary angiography and were subsequently followed up for median 55 months. A total of 8.4% experienced an MCE, 7.8% suffered an AMI, and 7.6% died. In age-and gender-adjusted analyses, the hazard ratios [HRs; 95% confidence intervals (CI)] of MCE, AMI, and all-cause mortality were 1.43 (1.29-1.59), 1.44 (1.29-1.59), and 1.38 (1.23-1.54) per standard deviation increment of the (log-transformed) urinary KTR, respectively. These estimates were only minimally attenuated after adjustment for potential confounders. The addition of the urine KTR to a model of conventional risk factors significantly improved goodness of fit, discrimination, and risk classification for these clinical endpoints. No association was seen between the urine KTR and the risk of incident ischaemic stroke. Conclusion A novel urinary inflammation marker, KTR, is strongly associated with adverse prognosis in patients with suspected stable CAD. Underlying pathomechanisms should be further elucidated.
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