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Serum uric acid (SUA) levels discriminating across the different strata of cardiovascular risk is still unknown. By utilizing a large population-based database, we assessed the threshold of SUA that increases the risk of total mortality and cardiovascular mortality (CVM). The URRAH study (Uric Acid Right for Heart Health) is a multicentre retrospective, observational study, which collected data from several large population-based longitudinal studies in Italy and subjects recruited in the hypertension clinics of the Italian Society of Hypertension. Total mortality was defined as mortality for any cause, CVM as death due to fatal myocardial infarction, stroke, sudden cardiac death, or heart failure. A total of 22 714 subjects were included in the analysis. Multivariate Cox regression analyses identified an independent association between SUA and total mortality (hazard ratio, 1.53 [95% CI, 1.21-1.93]) or CVM (hazard ratio, 2.08 [95% CI, 1.146-2.97]; P<0.001). Cutoff values of SUA able to discriminate total mortality (4.7 mg/dL [95% CI, 4.3-5.1 mg/dL]) and CVM status (5.6 mg/dL [95% CI, 4.99-6.21 mg/dL]) were identified. The information on SUA levels provided a significant net reclassification improvement of 0.26 and of 0.27 over the Heart Score risk chart for total mortality and CVM, respectively (P<0.001). Sex-specific cutoff values for total mortality and CVM were also identified and validated. In conclusion, SUA levels increasing the risk of total mortality and CVM are significantly lower than those used for the definition of hyperuricemia in clinical practice. Our data provide evidence of a cardiovascular SUA threshold that might contribute in clinical practice to improve identification of patients at higher risk of CVM. [ABSTRACT FROM AUTHOR]

A meta-analysis was performed of the effect of 3hydroxy3methylglutaryl-coenzyme A reductase inhibitors (statins) on blood pressure in humans including the randomized, controlled trials of statin therapy (20 trials and 828 patients) in which concomitant antihypertensive treatment (if any) remained unchanged throughout the study. A total of 291 and 272 patients were given a statin or placebo, respectively, in parallel group trials, whereas 265 took part in crossover trials receiving a statin and placebo (or probucol, in 1 trial). Systolic blood pressure was significantly lower in patients on statin than in those on placebo or control hypolipidemic drug (mean difference: -1.9 mm Hg; 95% CI: -3.8 to -0.1). The effect was greater when the analysis was restricted to studies with a baseline systolic blood pressure >130 mm Hg (Delta systolic blood pressure: -4.0; 95% CI: -5.8 to -2.2 mm Hg). There was a trend for lower diastolic blood pressure in patients receiving statin therapy compared with control: -0.9 mm Hg (95% CI: -2.0 to 0.2) overall and -1.2 mm Hg (95% CI: -2.6 to 0.1) in studies with a baseline diastolic blood pressure >80 mm Hg. In general, the higher the baseline blood pressure, the greater the effect of statins on blood pressure (P=0.066 for systolic blood pressure and P=0.023 for diastolic blood pressure). The blood pressure response to statins was unrelated to age, changes in serum cholesterol, or length of the trial. In conclusion, statin therapy has a relatively small but statistically significant and clinically meaningful effect on blood pressure. [ABSTRACT FROM AUTHOR]

Background: Prospective cohort studies estimated the predictive role of exposure to coffee consumption and risk of hypertension (HP) or cerebrovascular disease, with contrasting results. Therefore, we carried out a meta-analysis to assess the relation between habitual coffee intake and risk of HP and stroke in the general population. Methods: We performed a systematic search for prospective studies published without language restrictions between 1966 and July 2013. Inclusion criteria were: original article, prospective design, adult general population study, assessment of coffee intake as baseline exposure, assessment of HP or stroke as outcome, and follow-up of at least 2 years. To evaluate risks of HP and stroke, relative risks and 95% confidence intervals for "low-moderate" (2-3 cups/d), "high"(4-6) and "very high"(>6) compared with "reference" (0-1) coffee intake categories were extracted and pooled using a random effect model. Heterogeneity, publication bias, subgroup and meta-regression analyses were performed. Results: Four studies for HP (171,460 participants and 39,851 HP diagnoses) and 10 for stroke (969,656 participants with 12,990 events) met the inclusion criteria. Coffee intake was assessed by dietary questionnaire. In pooled analyses, "lowmoderate" and "high" coffee intake were both inversely associated with the risk of stroke (RR=0.84, 95% C.I. 0.78 to 0.91 and 0.83, 0.72 to 0.96, respectively) but not with risk of HP. "Very high" coffee intake was not significantly associated with either risk of stroke or of HP. There was significant heterogeneity between studies, while some evidence of publication bias was detected only in the analysis of HP risk. Subgroup analysis suggested an influence of gender and of geographic location, and meta-regression analysis detected age at baseline and length of follow-up as further sources of heterogeneity. Decaffeinated coffee consumption was not related to risk of stroke or HP. Conclusions: This meta-analysis of the available prospective studies showed that habitual coffee intake is not associated with higher risk of HP in the general population and that moderate-high coffee consumption is inversely associated with risk of stroke. A protective effect of coffee consumption towards cerebrovascular disease might be exerted through mechanisms independent of changes in blood pressure. [ABSTRACT FROM AUTHOR]

Background: Urinary albumin excretion (UAE) is a predictor of chronic kidney disease and of higher cardiovascular morbidity and mortality. A number of studies investigated the effect of reduced dietary sodium intake on UAE but their results were not consistent. Therefore, our study assessed the effect of sodium restriction on UAE and/or on albumin/creatinine ratio (ACR) through an updated metaanalysis of the available randomised controlled trials (RCT). Methods: A systematic search of the on-line databases was conducted including RCTs that assessed UAE/ACR at the start and the end of the trial and outcomes expressed as difference between the effect of two different sodium intake regimens. For each study, the mean difference (MD) and 95% confidence intervals (95%CI) were extracted and pooled using a random effect model. Heterogeneity, publication bias, subgroup, and meta-regression analyses were performed. Results: Nine studies were identified, providing 21 cohorts with overall 454 participants and 1-6 weeks follow-up time. In the pooled analysis, lower sodium intake was associated with a 26.7% (95% CI: -40.7 to -12.6) reduction of UAE, with no evidence of publication bias. The effect of lower sodium intake was highest in the cohorts including patients on concomitant RAAS-blocking therapy (-37.7%; -56.5 to -19.9), in those with intervention lasting at least 2 weeks (-32.4%; -47.2 to -17.7), and among participants with evidence of kidney damage (-32.6%; -47.5 to -17.6). The changes in BP occurring during intervention were a significant source of heterogeneity. >The analysis of changes in ACR, where available, provided similar results. Conclusions: This meta-analysis indicated that sodium intake reduction markedly reduces albumin excretion, more so among patients with hypertension and/or kidney damage and during concomitant RAAS-blocking therapy. [ABSTRACT FROM AUTHOR]