Correlation between markers of calcification, serum uric acid and systemic inflammation in hypertensive patients

Introduction: Increased values of serum uric acid (SUA) levels may trigger hypertension and contribute to endothelial dysfunction, vascular damage and renal disease. The aim of the study was the correlation between SUA levels and markers of calcification: osteoprotegerina (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL), with markers of systemic inflammation: fibrinogen, C-reactiv protein (hsCRP) and parameters of subclinic atherosclerosis: carotid intima-media thickness (IMT) and aortic pulse-wave velocity (aortic PWV) in hypertensive patients (p) with or without coronary artery disease (CAD). Methods: 223 consecutive HTN patients were divided in 2 groups according to the presence of CAD: group 1(n = 140 p) with angiographically proven CAD (HTN + CAD) and group 2 (n = 83 p) without CAD (HTN – CAD). The hypertensive groups were compared to a control group consisting of 74 healthy subjects (CON). SUA levels were measured in all p. Serum levels of hsCRP, OPG and RANKL were determined by ELISA. The carotid intima-media thickness (carotid IMT) was measured by high resolution B-mode ultrasound imaging according to the Mannheim Consensus. Left ventricular wall thickness (LVWT) and ejection fraction (LVEF) were measured by echocardiography. Aortic pulse wave velocity (PWV) was determined using the Arteriograph device. The Pearson correlation test was used for interpretation of results. Results: In group 1 (HTN + CAD) high levels of SUA were found compared to group 2 (HTN) (p = 0.001, a = 0.01) and CON (p < 0.001, a = 0.001). SUA values were significantly correlated with the parameters of cardiac function: LVWT (r = 0.603, p < 0.001), LVEF (r = -0.580, p < 0.001), with inflammatory parameters hsCRP (r = 0.675, p < 0.001) and fibrinogen (r = 0.548, p < 0.001), with aortic PWV (r = 0.579, p < 0.001) and carotid IMT (r = 0.672, p < 0.001). A significantly positive correlation between SUA values and OPG (r = 0.637, p < 0.001) and a significantly negative correlation with RANKL (r = -0.287, p < 0.001) were observed. Conclusions: In hypertensive patients, coronary artery disease may enhance the inflammatory process and vascular calcification. It is correlated with endothelial dysfunction, its expression being elevated levels of SUA. Beside carotid IMT and aortic PWV, SUA and markers of vascular calcification may be useful in daily practice for the cardiovascular risk stratification in hypertensive patients.

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