LAUSR

INTRODUCTION Arginase inhibition increases plasma citrulline, citrulline / ornithine ratio (C / O), and reduces plasma ornithine, ornithine / arginine ratio (O / A) in animal model of myocardial infarction (MI). OBJECTIVES We hypothesize that the presence of thin-cap fibroatheroma (TCFA) in the culprit lesion and increased non-culprit intima-media thickness of an infarct-related artery (IRA) are associated with an altered balance of arginine metabolites. PATIENTS AND METHODS Arginine and its metabolites were measured using liquid chromatography and tandem mass spectrometry in 100 consecutive MI patients upon admission and at 6-month follow-up. TCFA and adjacent to culprit proximal and distal 10-mm segments were assessed with optical coherence tomography in acute phase. As controls served 25 patients without coronary lesions in angiography. RESULTS The C / O increased 5.33 times (P <0.001), while the O / A decreased 2.53 times (P <0.001) at 6-month follow-up compared with acute MI phase. Patients with (n = 75) versus without (n = 25) TCFA had lower C / O by 29% (P = 0.003) while the mean intima-media diameter of adjacent non-culprit region correlated with follow-up O / A (R = 0.337, P = 0.003). By multivariable analysis, a higher acute phase C / O was associated with a lower risk of TCFA presence (odds ratio 0.978, 95% confidence interval 0.962-0.994, P = 0.006) whereas higher follow-up O / A correlated with larger intima-media diameter of adjacent segments (beta-coefficient 0.227, 95% confidence interval for beta-coefficient 0.045-0.409, P = 0.018). CONCLUSIONS The enhanced arginase activity over nitric oxide synthase following ischemia was associated with the presence of TCFA in the culprit lesion, while similar metabolic shift in chronic phase correlated with a higher thickness of intima-media in the adjacent non-culprit IRA segments.