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Urinary Excretion of Kynurenine and Tryptophan, Cardiovascular Events, and Mortality After Elective Coronary Angiography
Study Questions:
What is the association of urine kynurenine to tryptophan ratio (KTR) levels to incident major coronary events (MCEs), acute myocardial infarction (AMI), and ischemic stroke and mortality in patients with suspected stable coronary artery disease (CAD)?
Methods:
A total of 3,224 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. Hazard ratios (HRs) were calculated using the Cox regression and are reported per (log-transformed) standard deviation increment and for quartile 4 versus quartile 1 of the urine KTR.
Results:
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] 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 ischemic stroke.
Conclusions:
The authors concluded that a novel urinary inflammation marker, KTR, is strongly associated with adverse prognosis in patients with suspected stable CAD.
Perspective:
This study reported that in a large cohort of patients referred for suspected stable CAD, levels of the urine KTR at baseline showed a strong dose–response relationship with incident MCE, AMI, and all-cause and cardiovascular disease mortality. Furthermore, extensive multivariable adjustment hardly attenuated the risk estimates, suggesting that its association with adverse prognosis was not likely mediated through classical cardiovascular disease risk factors. Given the striking dose–response relationship and specificity to acute atherosclerotic events, further investigation into the role of tryptophan catabolism and renal inflammation in atherogenesis and plaque rupture is indicated.
Keywords: Tryptophan, Inflammation, Stroke, Myocardial Infarction, Coronary Artery Disease, Plaque, Atherosclerotic, Phlebotomy, Risk Factors, Prognosis, Incidence, Biomarkers, Cardiovascular Diseases, Kynurenine
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