Serum uric acid and resistance to antihypertensive treatment: data from the European Lacidipine Study on Atherosclerosis.

AIM: Whether increased serum uric acid (SUA) favours resistance to antihypertensive drugs is not clear. METHODS: The European Lacidipine Study on Atherosclerosis (ELSA) was a randomized, double-blind, multicenter trial comparing the effects of a 4-year treatment with either lacidipine or atenolol on progression of carotid atherosclerosis in patients with moderate hypertension. SUA was assessed at randomization and at the study end, office blood pressure (BP) was measured at each titration visit and every 6 months thereafter, ambulatory BP was measured at randomization and every year thereafter. RESULTS: No difference was found in office and ambulatory BP reduction achieved after 1 and 4 years of treatment in baseline SUA tertiles. This was the case for both treatments. The percentage of patients with controlled office BP (<140/90 mmHg) after 1 year (36.5, 34.2 and 33.8%, P = 0.56) and 4 years (39.9, 39.4 and 38%, P = 0.82) was not different in SUA tertiles. Similar results were obtained basing the analysis on the control of ambulatory BP (<130/80 mmHg) or when data were analyzed taking into account SUA extreme values (≥7 and <3.5 mg/dl). The average and percentage changes of SUA (baseline-study end) were not different between patients who achieved or did not achieve office BP control (5.31 ±â€Š1.26 vs. 5.4 ±â€Š1.29 mg/dl, P = 0.22 e 0.13 ±â€Š0.33 vs. 0.13 ±â€Š0.68, P = 0.87, respectively). This was the case also for control of ambulatory BP. CONCLUSION: In the ELSA study, SUA levels do not affect the responsiveness to antihypertensive treatment.

Reliability of heart rate as neuroadrenergic marker in the metabolic syndrome.

BACKGROUND: Metabolic syndrome is characterized by a pronounced sympathetic overactivity as documented by the marked increase in muscle sympathetic nerve traffic (MSNA) as well as in plasma norepinephrine values reported in this condition. Whether and to what extent heart rate (HR) reflects the abovementioned adrenergic alterations in metabolic syndrome remains largely undefined. It is also undefined the validity of the abovementioned adrenergic markers in reflecting the main features of the metabolic syndrome. METHODS: In 65 metabolic syndrome patients, aged 56.5 ±â€Š1.3 years (mean ±â€ŠSEM), we measured over a 30-min resting period blood pressure, HR (ECG), venous plasma norepinephrine (HPLC) and MSNA (microneurography). We also evaluated anthropometric and metabolic variables including HOMA index, correlating them with the adrenergic markers. The same measurements were also made in 48 age-matched healthy controls. RESULTS: HR was significantly greater in the metabolic syndrome patients than in controls (74.6 ±â€Š1.5 versus 67.5 ±â€Š1.5 bpm, P < 0.001) and significantly and directly correlated with the elevated norepinephrine and MSNA values (r = 0.25 and 0.33, P < 0.05 and 0.01, respectively). MSNA was significantly and directly related to blood pressure (r = 0.27 and 0.31 SBP and DBP, respectively, P < 0.05 for both), BMI (r = 0.36, P < 0.01), waist circumference (r = 0.34, P < 0.01), waist-to-hip ratio (r = 0.49, P < 0.01) and plasma insulin (r = 0.57, P < 0.01). In contrast, no significant correlation was detectable between HR or norepinephrine and the abovementioned anthropometric and metabolic variables. CONCLUSION: Our data show that in the metabolic syndrome not only peripheral but also cardiac sympathetic drive is markedly potentiated and HR can be regarded as a marker of adrenergic overdrive characterizing this clinical condition. The reliability of HR (and of plasma norepinephrine) as sympathetic marker appears to be limited, however, this variable being unable to reflect, at variance from MSNA, the main metabolic and anthropometric abnormalities characterizing the metabolic syndrome.

Relationship among morning blood pressure surge, 24-hour blood pressure variability, and cardiovascular outcomes in a white population.

Cardiovascular events have their greatest prevalence in the early morning period. Whether this is attributable to an arousal-dependent blood pressure (BP) increase is far from being clear. It is also not clear to what extent this phenomenon reflects overall 24-hour BP variability. In 2051 subjects (aged 25-74 years) representative of the population of Monza (Italy), we measured 24-hour ambulatory systolic BP (SBP) and calculated the difference between the 2-hour average values after morning arousal and the lowest 3 or average 2-hour values before arousal (morning BP surge 1 and 2, respectively). For either measure, we sought the relationship with a variety of indices of 24-hour SBP variability and collected information on (1) the occurrence of cardiovascular and all cause deaths during a follow-up of ≈16 years and (2) the appearance of echocardiographic left ventricular hypertrophy after 10 years from the baseline visit. Morning SBP surge 1 was directly related to indices of 24-hour SBP variability, including those made independent on the magnitude of the day-night SBP difference. There was a weak positive relationship between morning SBP surge 1 and the risk of cardiovascular and all-cause death, which disappeared after adjustment for confounders. This was the case also for development of left ventricular hypertrophy. Morning SBP surge 2 was smaller, inconsistently related to 24-hour SBP variability and not at all related to fatal events or new-onset left ventricular hypertrophy. In a white population, morning BP surge was not found to be an independent predictor of cardiovascular death, all-cause death, or development of high cardiovascular risk (as documented by new-onset cardiac damage) even when appropriately assessed by measures that reflect its association with 24-hour BP variability.