Abstract
BackgroundIndoleamine 2,3 dioxygenase (IDO), the rate-limiting enzyme in the kynurenine (Kyn) pathway of tryptophan (Trp) degradation, is modulated by inflammation, and is regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. Little is known about IDO activity in patients with active coronary artery disease (CAD).MethodsWe prospectively enrolled patients who were scheduled to undergo coronary angiography. Measurement of IDO, high-sensitivity troponin T (hs-TnT), and high-sensitivity C-reactive protein (hs-CRP) levels was performed at baseline, and IDO activity was monitored at the 6-month follow-up.ResultsThree hundred and five patients were enrolled. Ninety-eight patients (32.1%) presented with recent acute coronary syndrome (ACS). Significant difference in IDO, kynurenine, and hs-TnT between patients with and without significant CAD was observed. Baseline IDO activity, kynurenine level, and hs-TnT level were all significantly higher in significant CAD patients with 3-vessel, 2-vessel, and 1-vessel involvement than in those with insignificant CAD [(0.17, 0.13, and 0.16 vs. 0.03, respectively; p = 0.003), (5.89, 4.58, and 5.24 vs. 2.74 µM/g, respectively; p = 0.011), and (18.27, 12.22, and 12.86 vs. 10.89 mg/dL, respectively; p < 0.001)]. One-year mortality was 3.9%. When we compared between patients who survived and patients who died, we found a significantly lower prevalence of left main (LM) disease by coronary angiogram (6.1% vs. 33.3%, p = 0.007), and also a trend toward higher baseline kynurenine (5.07 vs. 0.79 µM/g, p = 0.082) and higher IDO (0.15 vs. 0.02, p = 0.081) in patients who survived.ConclusionImmunometabolic response mediated via IDO function was enhanced in patients with CAD, and correlated with the extent and severity of disease. Patients with LM disease had higher 1-year mortality. Lower level of IDO, as suggested by inadequate IDO response, demonstrated a trend toward predicting 1-year mortality.Trial registration TCTR Trial registration number TCTR20200626001. Date of registration 26 June 2020. “Retrospectively registered”.
Highlights
Cardiovascular diseases (CVDs) are the leading cause of mortality and disability worldwide
Acute coronary syndrome (ACS), which is one of the most common presentations of CVD, is triggered by inflammation that causes the rupture of an atherosclerotic lesion, which leads to Wongpraparut et al BMC Cardiovasc Disord (2021) 21:353 acute coronary thrombosis and cardiac death
Atherosclerosis is initiated by a maladaptive immune response that is triggered by accumulation and retention of lowdensity lipoprotein (LDL) in the subendothelial space of large- and medium-sized arteries, which leads to chronic vascular inflammation that is mediated by the activation of immune and vascular cells [1]
Summary
Cardiovascular diseases (CVDs) are the leading cause of mortality and disability worldwide. Acute coronary syndrome (ACS), which is one of the most common presentations of CVD, is triggered by inflammation that causes the rupture of an atherosclerotic lesion, which leads to Wongpraparut et al BMC Cardiovasc Disord (2021) 21:353 acute coronary thrombosis and cardiac death. Atherosclerosis is initiated by a maladaptive immune response that is triggered by accumulation and retention of lowdensity lipoprotein (LDL) in the subendothelial space of large- and medium-sized arteries, which leads to chronic vascular inflammation that is mediated by the activation of immune and vascular cells [1]. The combined effect of activated macrophages and T lymphocytes promotes disease progression. This interaction is present within the atherosclerotic lesion microenvironment with cytokine involvement. Little is known about IDO activity in patients with active coronary artery disease (CAD)
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