Key result
Serum tryptophan identifies depression in CAD patients with moderate accuracy, achieving ~0.77 AUC.
Why the study?
Major depression is common in patients with CAD and is associated with adverse cardiovascular outcomes, but remains frequently underdiagnosed. Whether neuroactive tryptophan catabolites from the inflammation-activated kynurenine pathway can differentiate depressed from non-depressed CAD patients was evaluated.
Does serum tryptophan catabolite (TRYCAT) profiling accurately differentiate patients with major depression from non-depressed patients in a cohort with coronary artery disease?
Case-Control (n=135)
No
Does serum tryptophan catabolite (TRYCAT) profiling accurately differentiate patients with major depression from non-depressed patients in a cohort with coronary artery disease?
Patients with coronary artery disease and comorbid depression exhibit a distinct inflammatory tryptophan catabolite signature (lower tryptophan and neuroprotective kynurenic acid, elevated neurotoxic metabolites) that provides moderate diagnostic accuracy as an adjunctive screening tool for depression.
Answers are grounded in this paper and cite their sources.
Serum tryptophan shows moderate accuracy for depression in CAD; hypothesis-generating and requires prospective validation before any screening role.
Background: Major depression is common in patients with coronary artery disease (CAD) and it is associated with adverse cardiovascular outcomes, but remains frequently underdiagnosed. The kynurenine pathway (KP) of tryptophan metabolism, activated by chronic inflammation, produces neuroactive metabolites that may link CAD to depression. This study evaluated whether tryptophan catabolites (TRYCATs) can differentiate depressed from non-depressed CAD patients. Methods: A total of 135 participants were enrolled: 45 healthy controls, 38 CAD patients without depression, and 52 CAD patients with clinical depression. Serum levels of tryptophan, kynurenine, 3-hydroxykynurenine (3-HK), kynurenic acid (KYNA), quinolinic acid (QA), and anthranilic acid (AA) were measured. ROC curve analysis determined the diagnostic performance of each biomarker.Results: CAD patients with depression exhibited significantly lower tryptophan and KYNA, and higher kynurenine, 3-HK, QA, AA, and KYN/TRP ratio compared to both controls and non-depressed CAD patients (all p≤0.011). The KYNA/KYN ratio was markedly reduced in the depressed CAD group (p<0.001). White blood cell count and neutrophil-to-lymphocyte ratio were highest in the CAD with depression group. ROC analysis showed that tryptophan had the best discriminatory ability for differentiating depressed from non-depressed CAD patients, with an area under the curve of 0.77 (95% CI: 0.67–0.87, p<0.001) and a cut-off value of ≤45.07 µM (sensitivity 68.9%, specificity 66.4%). 3-HK (AUC=0.71) and KYNA (AUC=0.69) also showed moderate diagnostic performance. Conclusions: Depression in CAD patients is characterized by a distinct TRYCAT signature of reduced neuroprotective KYNA and elevated neurotoxic metabolites. Tryptophan, 3-HK, and KYNA demonstrate moderate diagnostic accuracy for identifying depression in CAD patients; although these biomarkers are not ready for standalone clinical use, they could serve as adjunctive screening tools.
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Al-Hadhrawi et al. (2026) conducted a case-control in Coronary artery disease with and without major depression (n=135). Serum tryptophan catabolites (TRYCATs) vs. Non-depressed CAD patients and healthy controls was evaluated on Diagnostic differentiation of depressed from non-depressed CAD patients using serum tryptophan levels (AUC 0.77, 95% CI 0.67-0.87, p=<0.001). Serum tryptophan differentiated depressed from non-depressed CAD patients with an AUC of 0.77 (95% CI 0.67-0.87, p<0.001), achieving 68.9% sensitivity and 66.4% specificity at <=45.07 uM.
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