Asymptomatic Hyperuricemia as a Potential Metabolic Risk Factor for Coronary Artery Calcification in Patients With Atrial Fibrillation or Heart Failure

Abstract

Purpose: To assess the role of asymptomatic hyperuricemia for the presence and severity of coronary arterial calcium (CAC) in adults with different cardiovascular (CV) pathology and its association with conventional CV risk factors. Material/Methods: Adults (n=81) of both genders were divided into controls: with moderate- to high risk without known CVD; AF-group: CVD-patients with paroxysmal or persistent atrial fibrillation in sinus rhythm, HF–group: heart failure subjects with preserved ejection fraction. A structured interview was performed at admittance for evaluation of the classical CVD risk factors. CAC score (CACS) was determined by multislice computed tomography. Routine laboratory parameters, including uric acid (UA), were extracted from medical documentation. Descriptive statistics, Mann-Whitney U-test, one-way ANOVA, chi-square test, Spearman's correlation, and multiple linear regression analysis were applied. The predictive power of serum UA was evaluated using receiver operating characteristic (ROC) analysis. Statistical significance was considered at p<0.05. Results: Serum UA was significantly higher in subjects with CACS=1-99AU (p=0.030), and with CACS≥100AU (p=0.067) vs. patients without CACS. Within the UA tertiles, highest CACS was found in the tertile with highest serum UA. UA revealed positive relation with CACS (r=0.35, p=0.002), age (r=0.25, p=0.027), body mass index (0.27, p=0.017), waist circumference (r=0.44, p<0.0001), triglycerides (r=0.29, p=0.001), and creatinine (r=0.54, p<0.0001). Multiple linear regression analysis revealed significant association between UA as dependent variable and waist circumference (β=0.63, p=0.061), serum triglycerides (β=0.37, p=0.028), creatinine levels (β=0.45, p<0.0001). Conclusions: Asymptomatic hyperuricaemia could be an important metabolic factor negatively affecting the chronic cardio-vascular pathology besides the conventional risk factors.

Uric acid effects on glutathione metabolism estimated by induction of glutamate-cysteine ligase, glutathione reductase and glutathione synthetase in mouse J744A.1 macrophage cell line

“…There are studies connecting UA levels with oxidative stress [3] and inflammation [4] . Many studies have demonstrated that elevated UA level in humans is an independent risk factor for hypertension [5] , diabetes [6] , cardiovascular disease [7] , endothelial dysfunction [8] , coronary artery calcification [9] , vascular damage [10] , obesity and metabolic syndrome. [11,12] Some reports reveal that physiological concentrations of uric acid could induce gene expression of macrophage-secreted inflammatory cytokines, such as monocyte chemoattractant protein-1 (MCP-1), and growth factors, such as platelet-derived growth factor.…”