Abstract
Coronary artery disease (CAD) is one of the leading cause of mortality worldwide. Several risk factors including unhealthy lifestyle, genetic background, obesity, diabetes, hypercholesterolemia, hypertension, smoking, age, etc. contribute to the development of coronary atherosclerosis and subsequent coronary artery disease. Inflammation plays an important role in coronary artery disease development and progression. Pro-inflammatory signals promote the degradation of tryptophan via the kynurenine pathway resulting in the formation of several immunomodulatory metabolites. An unbalanced kynurenic pathway has been implicated in the pathomechanisms of various diseases including CAD. Significant improvements in detection methods in the last decades may allow simultaneous measurement of multiple metabolites of the kynurenine pathway and such a thorough analysis of the kynurenine pathway may be a valuable tool for risk stratification and determination of CAD prognosis. Nevertheless, imbalance in the activities of different branches of the kynurenine pathway may require careful interpretation. In this review, we aim to summarize clinical evidence supporting a possible use of kynurenine pathway metabolites as clinical biomarkers in various manifestations of CAD.
Highlights
Coronary artery disease (CAD), sometimes called ischemic heart disease or coronary heart disease, is one of the leading cause of disability and death worldwide
Taken together, disturbed kynurenine pathway (KP) is associated with atherosclerosis, and increased blood KYN/Trp ratio and decreased Trp seem to correlate with the severity of atherosclerosis, thereby KYN/Trp ratio and Trp may correlate with coronary atherosclerosis as well
kynurenic acid (KYNA) seems to be neuroprotective against ischemic brain damage caused by global or focal cerebral hypoperfusion [138,139,140,141], but probably the effect of endogenously raised KYNA is blunted by several factors or the production rate of KYNA was not enough to overcome the neurotoxic effects, which would explain the lack of correlation between increased level of KYNA and good prognosis in studies conducted by Ristango et al Another prospective cohort study investigating the possible relationships between the activation of KP and the mortality of cardiac arrest patients revealed that both increased KYN concentration and KYN/Trp ratio is significantly associated with in-hospital mortality (Table 4) [110]
Summary
Coronary artery disease (CAD), sometimes called ischemic heart disease or coronary heart disease, is one of the leading cause of disability and death worldwide. According to the latest ESC guidelines, chronic coronary syndrome includes i) stable coronary artery diseases such as stable angina, coronary spasm or microvascular angina, ii) new onset heart failure or left ventricular dysfunction with suspected CAD and iii) stabilized conditions after recent revascularization or within the 1st year after ACS events [3]. All these conditions share similar pathophysiology in which inflammation plays a role [5] and many inflammatory biomarkers (e.g. C-reactive protein (CRP), interleukin(IL)-6, myeloperoxidase, soluble CD40 ligand, etc.) may have a potential role for predicting CAD or assessing the severity of CAD [6]. Here we review the literature on the potential use of KP metabolites as clinical biomarkers in CAD and evaluate the currently available detection methods
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
