Acute myocardial infarction (MI) is associated with an inflammatory response that may lead and/or worsen adverse left ventricular (LV) remodeling. Among inflammation markers is Indoleamine 2,3-dioxygenase (IDO), which production is induced upon inflammation. IDO catalyzes the transformation of tryptophane into kynurenine.

We tested plasma IDO activity as a predictor of LV remodeling post-MI.

The PREGICA cohort recruited prospectively patients with first MI. Blood samples, echocardiography and cardiac MRI were obtained at day 4 and at 6months. To be included, the number of akinetic LV wall segments had to be≥3 at day 4. IDO activity was the ratio between kynurenine and tryptophane measured by high-pressure liquid chromatography coupled with fluorimetric detection. Remodelers were identified as patients with a variation of end-diastolic left ventricular volume (EDLVV) between day 4 and 6 months post-MI≥20%.

Among the 292patients studied (mean age 57y, mean necrosis size 26% on MRI), the median increase in EDLVV was 16.7% and 137 (47%) were classified as remodelers. At day 4, IDO activity was significantly higher in remodelers (8.2±4.2% vs. 5.3±2.5% and 8.7±5.7% vs. 5.6±4.4%, p<0.001) and remained higher at 6 months post-MI. IDO activity at day 4 was highly predictive of LV remodeling (AUC=87% [95% CI 83–91%]);IDO threshold of 5.8 resulted in specificity=81%, sensitivity=89%, negative predictive value=89%, positive predictive value=80%. In contrast, plasma levels of NT-proBNP, ST2, Galectin 3 or CRP at day 4 were poorly predictive. In multivariate analysis including other predictive variables at day 4 (primary angioplasty, EDLVV, LVEF, necrosis size), increase in IDO activity was significantly associated with LV remodeling (OR 1.21 [95%CI 1.11–1.33]).

IDO activity appears as a promising biomarker for the prediction of LV remodeling after MI. Its specific role in post-MI remodeling pathways requires further investigation.