Endothelial Dysfunction In Essential Hypertension Research Articles

The circulating level of miR-122 is a potential risk factor for endothelial dysfunction in young patients with essential hypertension.

MicroRNAs are key molecules involved in the regulation of endothelial function. They are important risk factors and biomarkers for the development of hypertension related to endothelial dysfunction. However, the gene expression patterns associated with hypertension development related to endothelial dysfunction have not been fully elucidated. We conducted a case-control study of 65 patients with essential hypertension (EH) and 61 controls without EH. Plasma levels of miR-122 and its target protein high-affinity cationic amino acid transporter 1 (CAT-1) were measured by qRT-PCR and ELISA, respectively. miR-122 expression in plasma of patients with EH was significantly higher than that of the control group (p = 0.001), while CAT-1 expression in patients with EH was significantly lower than that in the control group (p = 0.018). miR-122 expression in plasma of young patients with EH was significantly higher than that in young people without EH (p = 0.0004), and CAT-1 expression in plasma of young patients with EH was also significantly lower than that of the control group (p = 0.002). CAT-1 expression in the plasma of young participants was significantly higher than that of individuals aged ≥40 years (p = 0.003), whereas miR-122 expression was significantly lower (p = 0.001). We showed that among patients with EH, the high expression of miR-122 contributed to endothelial dysfunction by suppressing the expression of the CAT-1 protein, which led to a decrease in CAT-1 expression in plasma. Therefore, high expression of miR-122 appears to be a risk factor for endothelial dysfunction in EH, especially in younger patients.

Association of YKL-40 with endothelial dysfunction in patients with essential hypertension

Human cartilage glycoprotein 39 (YKL-40) is related with presence and extent of atherosclerosis, which can be a new biomarker of inflammation and endothelial dysfunction. The relationship between YKL-40 and endothelial dysfunction in patients with essential hypertension (EH) has not been intensively investigated. The relationship between serum level of YKL-40 and endothelial dysfunction was evaluated in 60 EH subjects and 50 normal control (NEH) subjects. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of YKL-40. Brachial artery flow-mediated vasodilation (FMD) was used to measure endothelial-dependent nitric oxide-mediated vasodilatory capacity as the function of endothelial index. This study demonstrated that YKL-40 expression was significantly increased ( p < 0.05) in EH subjects compared with NEH subjects. The FMD was significantly impaired in EH subjects compared with NEH subjects. YKL-40 was not only negatively correlated with FMD, but also with carotid artery intima-media thickness (IMT). Multiple liner regression analysis identified that YKL-40 was independent of FMD development. The level of YKL-40 was elevated in EH patients and inversely related with FMD and may be independent of endothelial dysfunction in EH.

Features of endothelial dysfunction in essential hypertension

This review was described in detail the mechanisms of endothelial dysfunction development in patients with essential hypertension, lists the risk factors leading to endothelial dysfunction, diagnostic markers of endothelial dysfunction, and gives an idea of endothelial progenitor cells that can regenerate damaged endothelium. The data of the authors’ own studies were presented evaluating the severity of endothelial dysfunction with the help of such markers as sPECAM-1. The authors were conducted studies of endothelial progenitor cells in patients with different stages and degrees of arterial hypertension.

A6326 Correlation between neutrophil / lymphocyte ratio and endothelial dysfunction in essential hypertension

A6326 Correlation between neutrophil / lymphocyte ratio and endothelial dysfunction in essential hypertension

The role of asymmetric dimethylarginine in the development of arterial
 hypertension.

The results of numerous studies of recent decades confirm the crucial role of vascular endothelium in regulating vascular homeostasis. A plethora of recent studies have shed light on the clinical significance of endothelial dysfunction in essential hypertension. Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide synthase inhibitor. At present, it is considered as a generally recognized marker of endothelial dysfunction by most researchers. In vitro experiments showed that ADMA inhibits endothelium-dependent arterial relaxation, increases the level of indicators characterizing the degree of oxidative stress in endothelial cells, enhances the synthesis of the superoxide anion radical by endothelial cells. The molecular mechanisms described above, activated with an increase in the concentration of ADMA, cause various disturbances in the function of the cardiovascular system, which gave grounds to consider the level of ADMA as a criterion and risk factor for the development of cardiovascular diseases. Thus, ADMA plays a key role in the development and progression of CVD associated with a spectrum of diseases and pathological conditions characterized by a disturbance in NO production. Despite clinical and experimental confirmation of the relationship between the increase in ADMA in plasma and the development of cardiovascular events, the unambiguous etiopathogenetic role of ADMA in CVD requires further research. In order to accurately answer the question of whether ADMA is an etiological factor or a biological marker of CVD, additional analysis is needed to study the biochemical, genetic and pharmacological aspects of ADMA metabolism, the results of which are presented in this article.

ENDOTHELIAL DYSFUNCTION IN ESSENTIAL HYPERTENSION IN ADOLESCENTS (CLINICAL AND EXPERIMENTAL STUDY)

Objective. The aim of the study was to evaluate endothelial dysfunction based on the blood concentration of endothelin 1 (ET‑1), nitric oxide (NO), serotonin (5‑HT) in essential hypertension (EHTN) in adolescents and in experimental animal models. Design and methods. The work was carried out in two stages. The clinical part was preceded by the investigation of experimental models of arterial hypertension (HTN). Twenty five immature male SHR rats aged 6–7 weeks and 10 immature male Wistar–Kyoto rats aged 6–7 weeks (control group) were examined. The clinical part of the study included 70 untreated male adolescents (mean age 15,63 ± 0,26 years), among them 24 people had a labile form of EHTN (LHTN), 30 had stable form of EHTN (SHTN), the control group included 16 subjects. All participants underwent 24-hour blood pressure monitoring. The plasma concentration of EN-1 (ET‑1) was determined by enzyme immunoassay, total concentration of stable metabolites of NO, 5‑HT in serum and platelets was measured. Results. The serum levels of ET-1 and 5-HT were higher in HTN groups than in the control group, and in adolescents with SHTN levels of both indices were higher compared to those with LHTN (p < 0,0001). Serotonin level in platelets in HTN groups was lower than in the control group (p < 0,0001). Compared to the control group, NO levels were higher in adolescents with LHTN, but lower in patients with SHTN (p < 0,0001). The changes in the level of ET‑1, 5‑HT and NO in plasma, serum and blood platelets in the experimental animal model were similar to those found in patients with labile and stable HTN. Conclusions. NO, ET‑1 and 5‑HT are early sensitive markers of endothelial dysfunction in EHTN in adolescent males, as well as in the experimental SHR rat model.

Endothelial dysfunction in patients with hypertension and peripheral artery disease

Aim. To assess endothelial function in patients with hypertension and peripheral artery disease.Methods. The study included 100 patients with an established diagnosis of essential hypertension. Ultrasonic duplex scanning of brachiocephalic arteries and lower limb arteries was performed. The functional state of the endothelium was evaluated using postocclusive reactive hyperemia test by D.S. Celermajer.Results. Atherosclerotic plaques in the carotid arteries were found in 71% of patients, in the lower limb arteries - in 60%. The combined affection of both vascular beds was diagnosed in 51% of patients. Endothelial dysfunction was found in 64% of patients. In patients with carotid arterial system atherosclerosis, brachial artery dilation response was 6.1%, while in those with intact carotid arteries - 4.7% (p=0.041). The value of the brachial artery dilation response in patients with atherosclerotic lesions of lower extremities arteries was 5.9%. In the subgroup of patients with intact lower limbs arteries, the increase in brachial artery diameter was 9.60% an average (p=0.04). Among 51 people with affection of both vascular systems the brachial artery diameter increase was 5.4%, while in comparison, in the subgroup consisting of 49 patients without combined carotid and lower limb arteries lesions, - 9.9% (p=0.003). According to the results of the correlation analysis, the relation between endothelial dysfunction and the maximum percentage of stenosis of the carotid arteries and lower limb arteries at the level of tibial segment was revealed.Conclusion. In patients with hypertension and peripheral artery disease, decrease in dilation response in endothelium-dependent vasodilation test was registered regardless of the localization of atherosclerotic lesions; endothelial dysfunction in essential hypertension was associated with the highest percentage of stenosis of the carotid arteries and lower limb arteries at the level of tibial segment.

Endothelial dysfunction in human essential hypertension.

Although the endothelium has a number of important functions, the term endothelial dysfunction is commonly used to describe impairment in its vasodilatory capacity. It is increasingly recognized that this is related to hypertension, although whether it predates essential hypertension or is a consequence of it is still unknown. In this review, we explore the mechanisms of endothelial dysfunction in essential hypertension, its prognostic significance and methods of pharmacological reversal.

Clinical Significance of Endothelial Dysfunction in Essential Hypertension.

The endothelium is recognized as a major determinant of vascular physiology and pathophysiology. Over the last few decades, a plethora of studies have implicated endothelial dysfunction in the progression of atherosclerosis and the subclinical target organ damage observed in essential hypertension. However, the clinical significance of diagnosing endothelial dysfunction in patients with essential hypertension remains under investigation. Although a number of vascular and non-vascular markers of endothelial dysfunction have been proposed, there is an ongoing quest for a marker in the clinical setting that is optimal, inexpensive, and reproducible. In addition, endothelial dysfunction emerges as a promising therapeutic target of agents that are readily available in clinical practice. In this context, a better understanding of its role in essential hypertension becomes of great importance. Here, we aim to investigate the clinical significance of endothelial dysfunction in essential hypertension by accumulating novel data on (a) early diagnosis using robust markers with prognostic value in cardiovascular risk prediction, (b) the association of endothelial dysfunction with subclinical vascular organ damage, and (c) potential therapeutic targets.

Relationship Between Inflammation and Endothelial Dysfunction in Essential Hypertension

Background: A proposed pathogenic link between inflammation and hypertension is possibly through endothelial dysfunction. Objective: To study the relationship between inflammation and endothelial dysfunction in essential hypertension Methods: In a cross-sectional prospective study, 102 patients with essential hypertension underwent endothelial function evaluation at rest and after reactive hyperaemia by high-resolution B-mode ultrasound images in right upper arm after a written, informed consent. Glucose, lipid profile, creatinine, hsCRP (Diagnostics Biochem Canada Inc.), IL-6 (BD OptEIA™) and TNF- α (BD OptEIA™) were estimated in a 12 hours overnight fasting blood sample. Results: 102 patients (mean age 45 ± 8years, duration of hypertension 3.89 ± 0.43 years, and antihypertensive treatment in 91% and statins in 39.2%) were studied. The mean flow mediated vasodilatation (FMD) of the brachial artery was 12.2 ± 8.0%. 39 (38.2%) of patients had an abnormal FMD (a change of less than 10% in the diameter of the vessel wall). No correlation was found between FMD and duration of hypertension, systolic or diastolic blood pressure, body mass index, waist circumference or lipid profile using Spearman's test of correlation. hsCRP (75 patients), TNF-α levels (75 patients) and IL-6 levels (64 patients) were 69.5 ± 67.4 mg/L,125 ± 252pg/ml and 527 ± 1253pg/ml respectively. No correlation was found between any of the inflammatory markers and brachial FMD. Conclusions: A significant inflammation was observed in well controlled hypertensive patients. However there was no correlation between endothelial dysfunction and the degree of inflammation. Absence of target organ damage, younger age, shorter duration of hypertension and treatment could be the factors responsible for the same.

Epoxyeicosatrienoic Acids Contribute With Altered Nitric Oxide and Endothelin-1 Pathways to Conduit Artery Endothelial Dysfunction in Essential Hypertension

We sought to clarify, using functional and biological approaches, the role of epoxyeicosatrienoic acids, nitric oxide (NO)/reactive oxygen species balance, and endothelin-1 in conduit artery endothelial dysfunction during essential hypertension. Radial artery diameter and mean wall shear stress were determined in 28 untreated patients with essential hypertension and 30 normotensive control subjects during endothelium-dependent flow-mediated dilatation induced by hand skin heating. The role of epoxyeicosatrienoic acids and NO was assessed with the brachial infusion of inhibitors of cytochrome P450 epoxygenases (fluconazole) and NO synthase (N(G)-monomethyl-l-arginine [L-NMMA]). Compared with controls, hypertensive patients exhibited a decreased flow-mediated dilatation in response to postischemic hyperemia as well as to heating, as shown by the lesser slope of their diameter-shear stress relationship. In controls, heating-induced flow-mediated dilatation was reduced by fluconazole, L-NMMA, and, to a larger extent, by L-NMMA+fluconazole. In patients, flow-mediated dilatation was not affected by fluconazole and was reduced by L-NMMA and L-NMMA+fluconazole to a lesser extent than in controls. Furthermore, local plasma epoxyeicosatrienoic acids increased during heating in controls (an effect diminished by fluconazole) but not in patients. Plasma nitrite, an indicator of NO availability, increased during heating in controls (an effect abolished by L-NMMA) and, to a lesser extent, in patients, whereas, inversely, reactive oxygen species increased more in patients (an effect diminished by L-NMMA). Plasma endothelin-1 decreased during heating in controls but not in patients. These results show that an impaired role of epoxyeicosatrienoic acids contributes, together with an alteration in NO/reactive oxygen species balance and endothelin-1 pathway, to conduit artery endothelial dysfunction in essential hypertension. https://www.eudract.ema.europa.eu. Unique identifier: RCB2007-A001-10-53.

Hypertension and Endothelial Dysfunction: Therapeutic Approach

A large body of evidence indicates that patients with essential hypertension are characterized by endothelial dysfunction mediated by an impaired NO availability secondary to oxidative stress production. A dysfunctioning endothelium is an early marker of the development of atherosclerotic changes and can also contribute to cardiovascular events. Vascular reactivity tests represent the most widely used methods in the clinical assessment of endothelial function. In the last two decades, many studies have evaluated the endothelium in hypertensive patients, using different techniques. Several methodologies were developed to study microcirculation (resistance arteries and arterioles) and macrocirculation (conduit arteries), both in coronary and peripheral vascular districts. This review will describe the most relevant available techniques in the research on endothelial dysfunction in essential hypertension, their advantages and limitations, focusing on available data on endothelial dysfunction and on the effect of treatment. Endothelial dysfunction in the coronary and peripheral circulation of hypertensive patients are associated with hypertensive target organ damage and it is predictive of cardiovascular events. Several non-pharmacological approaches, including physical exercise and dietary interventions, can ameliorate endothelial function in hypertensive patients. Despite blood pressure reduction per se is not effective, some antihypertensive drugs can improve endothelial dysfunction, particularly calcium channel antagonist in the microcirculation, ACE-inhibitors and AT1-receptor antagonists mostly in conduit arteries. Some beneficial effects were also exerted by nebivolol and statins. Future studies are needed to confirm whether the improvement in endothelial dysfunction is associated to better cardiovascular prognosis in hypertension.

How to Evaluate Microvascular Organ Damage in Hypertension

Patients with essential hypertension are characterized by endothelial dysfunction and impaired nitric oxide availability secondary to oxidative stress production. A dysfunctioning endothelium is an early marker of the development of atherosclerotic changes and can also contribute to cardiovascular events. The autocrine/paracrine activity of endothelial cells makes it very difficult to investigate endothelial function in clinical research. Vascular reactivity tests represent the most widely used methods of clinical assessment of endothelial function. The aim of these tests is to activate or block endothelial cell function while measuring consequent changes in vascular tone in selected vascular districts. Many studies have evaluated the endothelium in hypertensive patients, using different techniques. Several methodologies were developed to study microcirculation (resistance arteries and arterioles), both in coronary and peripheral vascular districts. In particular, peripheral microcirculation can be evaluated in functionally isolated vascular districts such as the peripheral muscle (usually forearm), the subcutaneous tissue, or the skin. This article focuses on the most relevant available techniques in the research on endothelial dysfunction in essential hypertension, in particular their advantages and major limitations. The coronary microcirculation can be evaluated by measuring coronary blood flow with Doppler flow wire and quantitative angiography during the intracoronary infusion of endothelial agonists. The isolated and perfused forearm technique is the most often used approach in the assessment of endothelial function in peripheral muscle microcirculation. The subcutaneous small resistance arteries can be studied using the Mulvany myograph device, an in vitro, ex vivo technique. Finally, the use of the laser digital Doppler technique provides a non-invasive approach to the evaluation of the skin microcirculation. Each technique employed to assess endothelial function has specific limitations that hinder its applicability in large-scale screening. In addition, studies assessing the degree of correlation among measures of endothelial function, as evaluated in different vascular beds, have demonstrated a poor relationship and, while statistically significant, the findings are of no clinical relevance. Therefore, no one technique can be considered a surrogate for another. At the present time, the optimal methodology for investigating the multifaceted aspects of endothelial dysfunction is still under debate. Only the growing concordant results from different reproducible and reliable methods exploring endothelial function with different stimuli will support and strengthen experimental findings, thus providing conclusive answers in this area of research.

An impaired role of epoxyeicosatrienoic acids contributes with altered NO and endothelin-1 pathways to conduit artery endothelial dysfunction in essential hypertension

An impaired role of epoxyeicosatrienoic acids contributes with altered NO and endothelin-1 pathways to conduit artery endothelial dysfunction in essential hypertension

Noninvasive assessment of endothelial dysfunction in essential hypertension: Comparison of the forearm microvascular reactivity with flow-mediated dilatation of the brachial artery

Endothelial dysfunction is detectable both in the forearm skin microcirculation by laser Doppler flowmetry and in the brachial artery by Duplex Ultrasound. The aim of the study was to evaluate whether endothelium-dependent vasodilation in the forearm microcirculation is related to endothelium-dependent flow mediated dilation (FMD) of the brachial artery. In 22 treated male essential hypertensive patients (EHT) who had impaired FMD of the brachial artery, and in 11 male normotensive subjects (NT) we measured first the postocclusive reactive hyperemic response (PORH), then the effect of two doses of acetylcholine (ACh) and sodium nitroprusside (SNP) on the forearm skin microcirculation. FMD resulted from forearm reactive hyperemia induced by 5 minutes of ischaemia and the vasodilation induced by sublingual nitroglycerine (GTN) were also measured. Responses were calculated as the maximal percent increase above baseline. PORH and the responses to ACh were significantly (p < 0.05, p <0.01) reduced in EHT (272 ± 180, 177 ± 194, 463 ± 302) as compared to NT (409 ± 123, 470 ± 467, 805 ± 603). Response to SNP was similar. FMD was significantly (p < 0.001) reduced in EHT as compared to NT (3.98 ± 2.2 vs 9.3 ± 2.88), while response to GTN was similar. There was no significant relationship (p = n.s.) either between maximal response to ACh and FMD (r = 0.28), or between PORH and FMD (r = −0.01). Endothelial dysfunction was detectable with both methods in EHT. Our results show that endothelium-dependent vasodilation in forearm microcirculation is not related to FMD of the brachial artery. This can be explained by the differences in vascular beds and mechanism involved in the hyperemic response.

Olmesartan improves endothelial function in hypertensive patients: link with extracellular superoxide dismutase

Endothelial dysfunction in essential hypertension is an independent predictor for future cardiovascular events. Although inhibition of the renin-angiotensin system (RAS) reportedly improves endothelial function through its effects on oxidative stress and inflammation, questions remain regarding the factors that are pivotal for improvement of endothelial function by RAS inhibition. We therefore performed a prospective, randomized crossover trial in which an angiotensin II type 1 receptor antagonist, olmesartan and calcium channel blocker, amlodipine, were compared in 31 essential hypertensive patients. Results showed that, although both treatments achieved comparable lowering of blood pressure (BP), olmesartan, but not amlodipine, significantly improved endothelial function as evaluated by flow-mediated vasodilation (FMD) in the brachial artery. Although no significant changes in diabetic and lipid parameters were observed with either drug, olmesartan slightly decreased estimated glomerular filtration rate, which, surprisingly, translated into decreased microalbuminuria. In a similar vein, olmesartan reduced serum C-reactive protein and increased urine antioxidant levels compared with baseline, and reduced urine 8-epi-prostaglandin F2α levels compared with both baseline and amlodipine. Finally, although overall changes in plasma extracellular superoxide dismutase (EC-SOD) levels were not modulated by either treatment, for olmesartan there was a positive correlation between changes in FMD and those in EC-SOD levels. In conclusion, olmesartan improved endothelial function in hypertensive patients independent of its BP-lowering effect, which was due, at least in part, to its antioxidative property. Therefore, olmesartan might provide a greater long-term benefit for hypertensive patients with impaired endothelial function than amlodipine.

Ultrasonic evaluation of the relationship between left ventricular hypertrophy or left ventricular geometry and endothelial function in patients with essential hypertension

Objective To assess the relationship between left ventricular hypertrophy (LVH) or left ventricular geometry (LVG) and endothelial function in patients with essential hypertension (EH). Methods Seventy-six patients and 30 normal subjects were first examined by echocardiography. Brachial artery dilatation induced by reactive hyperemia (DIRH) or nitroglycerin (DING) was detected using high-resolution ultrasonography. Results DIRH was lower in patients with hypertension than in the controls, and the decrease in DIRH was greater in the patients with LVH than that in patients without LVH (4.36±2.54% vs 8.56±1.87 %; P < 0.0001). There were no significant differences in age, serum concentrations of total cholesterol, triglycerides or sugar, blood pressure and the brachial artery dilatation induced by nitroglycerin between the two groups ( P > 0.05). While there was no significant difference in DIRH between the patients with normal left ventricular geometry or cardiac remodeling, the patients showing either eccentric or concentric left ventricular hypertrophy had lower DIRH than the patients with normal left ventricular geometry or cardiac remodeling. The DIRH was the lowest in patients with concentric hypertrophy. Although bivariate analysis showed that the left ventricular mass index (LVMI) correlated well with the brachial artery dilatation induced by reactive hyperemia, diastolic blood pressure and mean blood pressure ( r=-0.61, P < 0.0001; r = 0.27, P < 0.05; r = 0.31, P < 0.05, respectively), a multivariate stepwise regression demonstrated that LVMI correlated only with the brachial artery dilatation induced by reactive hyperemia. Conclusion Left ventricular hypertrophy was related to endothelial dysfunction in essential hypertension. The endothelial dysfunction might be basic and important in the progression of left ventricular hypertrophy.

Endothelial Function Assessment in Complicated Hypertension

A large body of evidence indicates that patients with essential hypertension, and even more those with complicated hypertension, are characterized by endothelial dysfunction characterized by impaired NO availability secondary to oxidative stress production. A dysfunctioning endothelium is an early marker of the development of atherosclerotic changes and can also contribute to cardiovascular events. Vascular reactivity tests represent the most widely used methods in the clinical assessment of endothelial function. In the last two decades, many studies have evaluated the endothelium in hypertensive patients, using different techniques. Several methodologies were developed to study microcirculation (resistance arteries and arterioles) and macrocirculation (conduit arteries), both in coronary and peripheral vascular districts. This review will centre on the most relevant available techniques in the research on endothelial dysfunction in essential hypertension, their advantages and limitations, focusing on available data on endothelial dysfunction which characterizes patients with complicated hypertension. No available test to assess endothelial function has sufficient sensitivity and specificity to be used in clinical practice. Therefore, the optimal methodology for investigating the multifaceted aspects of endothelial dysfunction is still under debate. Only the growing concordant results from different reproducible and reliable methods exploring endothelial function with different stimuli will support and strengthen experimental findings, thus providing conclusive answers in this area of research.

Inflammation as a Mediator of the Link Between Mild to Moderate Renal Insufficiency and Endothelial Dysfunction in Essential Hypertension.

Inflammation as a Mediator of the Link Between Mild to Moderate Renal Insufficiency and Endothelial Dysfunction in Essential Hypertension.

Uric Acid and Endothelial Dysfunction in Essential Hypertension

Recent epidemiologic and experimental evidence suggests that serum uric acid (UA) is an independent risk factor for cardiovascular and renal diseases. However, endothelial dysfunction is an early predictor of cardiovascular events, particularly in hypertensive patients. For assessment of the association between UA and endothelial function, 217 (108 men, 109 women; aged 48.0 +/- 10.6 yr) white never-treated hypertensive patients were studied. All patients underwent the following procedures: BP measurements, laboratory tests (C-reactive protein [CRP], insulin resistance by homeostasis model assessment, serum creatinine, and UA), and endothelial function evaluated by intra-arterial infusion of acetylcholine (ACh). Serum creatinine, CRP, and maximal vasodilatory response to ACh were related to the UA (all P < 0.0001). In the multiple regression analysis, serum UA ranked as the third correlate of peak of forearm blood flow predictor, after homeostasis model assessment and CRP. The data show an independent link between UA and endothelial function, also in a statistical model that included CRP. In conclusion, the data demonstrate an inverse and significant relationship between UA and ACh-stimulated vasodilation in patients with uncomplicated, untreated essential hypertension, independent of traditional cardiovascular risk factors. Probably, the chronic inflammation that was documented in these patients may be considered the mechanistic link between serum UA and vascular damage.