Uric Acid, Hypertensive Phenotypes, and Organ Damage: Data from the Pamela Study

Abstract

Purpose of Review To examine published and unpublished data collected in the context of the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) study on the relationships between serum uric acid (SUA), office and out-of-office blood pressure (BP), and organ damage. Recent Findings SUA values were directly and significantly related to a large number of covariates that participate at cardiovascular risk determination, such as blood glucose, total serum cholesterol, serum triglycerides, body mass index, and serum creatinine. Additional variables included echocardiographically-determined left ventricular mass index and BP values, the latter not just when measured in the office but also when evaluated at home or over the 24-h period. White-coat hypertension and masked hypertension were characterized, as sustained hypertension, by a significant increase in SUA levels, which were also directly related to different indices of 24-h BP variability. No substantial difference in SUA levels was found when data were analyzed according to the dipping or non-dipping nocturnal BP profile. Summary Data collected in the frame of the PAMELA study document the presence of a close relationship between SUA levels and BP values independently on the hypertensive phenotype patterns of BP increase (office, 24 h, or both) and nighttime BP profile. They also document the increase in SUA as a potential factor favoring the occurrence of new hypertension and new left ventricular hypertrophy.

Allopurinol and blood pressure variability following ischemic stroke and transient ischemic attack: a secondary analysis of XILO-FIST

“…Despite previously reported associations between hyperuricaemia and BPV [ 19 , 20 ], we conclude that allopurinol does not affect clinic visit-to-visit BPV in people with recent stroke or TIA. Where an association has been seen between hyperuricaemia and BPV, the population studied has typically been younger and healthier than those in our study [ 19 , 20 ].…”

“…The underlying mechanisms by which hyperuricaemia may cause hypertension include upregulation of the renin-angiotensin-aldosterone system [ 15 ], endothelial dysfunction [ 16 ], oxidative stress [ 17 ], and increased arterial stiffness [ 18 ]. High serum uric acid levels have also been independently associated with increased BPV [ 19 , 20 ].…”

Uric Acid and Hypertension: a Review of Evidence and Future Perspectives for the Management of Cardiovascular Risk

“…60 The prevalence of hyperuricemia is higher in patients with more severe hypertension 31 and is associated with an increased risk of uncontrolled BP values 61 and resistance to antihypertensive treatment. 62 Higher SUA level is associated with HTN-related target organ damage, as renal function impairment, 63 left ventricular hypertrophy, 64,65 and subclinical myocardial damage. 66 Increased SUA levels have also been described as a risk factor for coronary artery disease, [67][68][69] atrial fibrillation, 70 stroke, 71 and heart failure 72 particularly in patients with hypertension.…”

Uric acid and left ventricular hypertrophy: a gender-based meta-analysis of echocardiographic studies

“…A growing body of evidence based on both experimental and clinical observations, supports the view that hyperuricemia is linked to increased risk of subclinical organ damage, cardiovascular morbidity and mortality [27,28]. Whether hyperuricemia plays a causative role in determining cardiovascular complications or is a marker for other conventional risk factors such hypertension, dyslipidaemia, As for subclinical cardiac organ damage recent studies have shown that hyperuricemia may activate smooth muscle cell proliferation and inflammatory mediators, such as tumor necrosis factor and stimulate mitogen-activated protein kinases which are known to promote adverse LV remodelling [29,30].…”

“…A growing body of evidence based on both experimental and clinical observations, supports the view that hyperuricemia is linked to increased risk of subclinical organ damage, cardiovascular morbidity and mortality [27,28]. Whether hyperuricemia plays a causative role in determining cardiovascular complications or is a marker for other conventional risk factors such hypertension, dyslipidaemia, metabolic syndrome and renal dysfunction is not yet definitively established.…”