Background and purposeXanthine oxidoreductase (XOR), which catalyzes purine catabolism, has two interconvertible forms, xanthine dehydrogenase and xanthine oxidase, the latter of which produces superoxide during uric acid (UA) synthesis. An association between plasma XOR activity and cardiovascular and renal outcomes has been previously suggested. We investigated the potential association between cardiac parameters and plasma XOR activity among cardiology patients.Methods and resultsPlasma XOR activity was measured by [13C2,15N2]xanthine coupled with liquid chromatography/triplequadrupole mass spectrometry. Among 270 patients who were not taking UA-lowering drugs, XOR activity was associated with body mass index (BMI), alanine aminotransferase (ALT), HbA1c and renal function. Although XOR activity was not associated with serum UA overall, patients with chronic kidney disease (CKD), those with higher XOR activity had higher serum UA among patients without CKD. Compared with patients with the lowest XOR activity quartile, those with higher three XOR activity quartiles more frequently had left ventricular hypertrophy. In addition, plasma XOR activity showed a U-shaped association with low left ventricular ejection fraction (LVEF) and increased plasma B-type natriuretic peptide (BNP) levels, and these associations were independent of age, gender, BMI, ALT, HbA1C, serum UA, and CKD stages.ConclusionsAmong cardiac patients, left ventricular hypertrophy, low LVEF, and increased BNP were significantly associated with plasma XOR activity independent of various confounding factors. Whether pharmaceutical modification of plasma XOR activity might inhibit cardiac remodeling and improve cardiovascular outcome should be investigated in future studies.

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SummaryThe role of pentraxin 3 (PTX3) has been implicated in the process of plaque vulnerability. However, few studies have addressed the direct relationship between plaque morphology and plasma PTX3. We evaluated the relationship between coronary vulnerable plaque, assessed by optical coherence tomography (OCT), and plasma PTX3 in patients with coronary artery disease (CAD).OCT was used to determine plaque vulnerability in 51 patients with non-ST segment elevation acute coronary syndrome (NSTE-ACS; n = 17) and stable angina (SA; n = 34). Both highly-sensitive C-reactive protein and systemic plasma PTX3 were measured.Based on the OCT findings, patients were divided into 3 groups; a fibrous plaque (n = 18), thick-cap fibroatheroma (ThCFA) (n = 19), and thin-cap fibroatheroma (TCFA) (n = 14) groups. ThCFA was defined as a lipid-rich plaque (lipid content in ≥ 2 quadrant) covered with ≥ 65 μm thick fibrous cap, and TCFA was that with < 65 μm. There were no differences in patient characteristics between the 3 groups except for the presence of ACS and eicosapentaenoic acid levels. TCFA was more frequently observed with plaque rupture and intraluminal thrombus compared with the other 2 groups. Plasma PTX3 levels were higher in the TCFA group compared with the fibrous plaque and ThCFA groups, and showed weak correlation with cap thickness.Plasma PTX3 level was associated with plaque vulnerability assessed by OCT in patients with CAD. (Int Heart J 2016; 57: 18-24)

Aim: Previous studies have revealed that blockade of the renin angiotensin system attenuates plaque vulnerability and reduces cardiovascular events; however, few studies have compared the effects of an angiotensin-converting enzyme inhibitor (ACEI) with an angiotensin receptor blocker (ARB) and evaluated combination therapy. The objective of this study was to compare the efficacy and mechanisms of plaque stabilization by ACEI or ARB and to determine the effects of combination therapy. Methods: Twenty-eight male Japanese white rabbits were fed a high-cholesterol diet after balloon injury of the carotid arteries, then separated into ACEI (n = 7; imidapril 0.5 mg/kg/day), ARB (n = 7; TA606 4.5 mg/kg/day), combination (n=7; imidapril 0.5 mg/kg/day＋TA606 4.5 mg/kg/day), and vehicle (n = 7) groups.