D. De Palma

High-Circulating Leptin Levels Are Associated with Greater Risk of Hypertension in Men Independently of Body Mass and Insulin Resistance: Results of an Eight-Year Follow-Up Study

BACKGROUND We previously reported a significant association between plasma leptin (LPT) concentration and blood pressure (BP), which was partly independent of serum insulin levels and insulin resistance. The aims of this study were to detect whether serum LPT levels predict the development of hypertension (HPT) in the 8-yr follow-up investigation of a sample of an adult male population (the Olivetti Heart Study), and to evaluate the role of body mass index (BMI) and insulin resistance in this putative association. PATIENTS AND METHODS The study population was made up of 489 untreated normotensive subjects examined in 1994-1995 (age: 50.1 +/- 6.7 yr; BMI: 26.3 +/- 2.8 kg/m(2); BP: 120 +/- 10/78 +/- 6 mm Hg; and homeostatic model assessment index: 2.1 +/- 1.6). RESULTS The HPT incidence over 8 yr was 35%. The participants with incident HPT had similar age but higher BMI (P < 0.001), serum LPT (P < 0.001), and BP (P < 0.01) at baseline. One sd positive difference in baseline serum LPT log was associated at univariate analysis with a 49% higher rate of HPT [95% confidence interval (CI) 22-83; P < 0.001]). In three different models of multivariable logistical regression analysis, LPT was respectively associated with a 41% greater risk to develop HPT (95% CI 15-74; P < 0.001) upon adjustment for age and baseline BP, with a 48% (95% CI 20-81) greater risk when adding the homeostatic assessment model index to the model, and with 33% greater risk (95% CI 6-67; P < 0.02) upon adjustment for BMI. CONCLUSIONS In this sample of originally normotensive men, circulating LPT level was a significant predictor of the risk to develop HPT over 8 yr, independently of BMI and insulin resistance.

ROLE OF DIFFERENT METABOLIC SYNDROME COMPONENTS ON THE RISK TO DEVELOP SLEEP APNOEA: PP.32.275

Objective: In various clinical studies, apnoea sleep disorders have been associated with different cardiovascular and metabolic abnormalities. The aim of this analysis was to assess the relation between a multivariable apnoea prediction index, metabolic syndrome (MS) and its single components in an unselected sample of adult male population. Design and Method: The relationship between MS (AHA 2005 criteria) and a high apnoea risk (HAR) evaluated by a multivariable apnoea prediction index higher than 0.5, was investigated in 612 (mean age ± SD = 59.7 ± 6.4 years) participants at the 2002–04 Olivetti Heart Study follow-up. Results: The prevalence of MS and of HAR were respectively 36.6% (n = 224) and 60.8% (n = 372). MS and HAR were strongly associated (χ2 = 26.3; p < 0.0001). The prevalence of HAR increased gradually with increasing number of MS components. (χ2 = 36.4; p < 0.0001), the higher the MS score, the higher the prevalence of HAR. Using a logistic regression analysis with apnoea risk as dependent variable and MS components and age as independent factors, hypertension (blood pressure > 130/85 mmHg or treatment) and central adiposity (waist circumference > 102 cm) remained the only determinants of HAR with odds ratio (95%CI) of respectively 2.57 (1.53 to 4.33) and 3.84 (2.47 to 5.98). Conclusion: In this sample of adult male population the prevalence of high apnoea risk was related to both presence and severity of metabolic syndrome. Among different components of MS, blood pressure and central adiposity were the factors more strongly associated to the risk to be affected by sleep apnoea disturbances.

PROXIMAL SODIUM REABSORPTION IS AN INDEPENDENT PREDICTOR OF HYPERTENSION: 2D.05

Objective: Given the association between salt-sensitivity of blood pressure (BP) and risk of future hypertension (HPT), we investigated the predictive role of alterations in segmental renal tubular sodium handling in the development of HPT during the 8 year follow-up of the Olivetti Heart Study participants. Methods: A selected sample (n = 314) of OHS population was examined at baseline and after 8 years. The participants were included if they were normotensive (SBP/DBP <140/90 mm Hg without anti-hypertensive treatment) and had normal renal function (creatinine clearance - CrCl> 60 ml/min) at baseline. Proximal and distal fractional tubular sodium reabsorption were calculated using the clearance of exogenous lithium. Results: The baseline sample characteristics were: age 49.3 ± 6.8 yrs, BMI 26.4 ± 2.8 kg/m2, SBP/DBP 119.8 ± 9.6/78.9 ± 6.4 mm Hg, CrCl 90.9 ± 18.2 mL/min (M ± SD). The HPT incidence in 8 years was 52%. The participants who developed HPT (group A) compared with those who did not (group B) had higher baseline SBP (122.4 ± 8.4 mm Hg vs 117.0 ± 10.0, p < 0.0001), DBP (80.6 ± 5.6 VS 77.1 ± 6.7 mm Hg, p < 0.0001), BMI (27.0 ± 2.9 vs 25.9 ± 2.6 kg/m2, p < 0.0001) and fractional proximal reabsorption of sodium (75.8 ± 6.3 vs 73.8 ± 7.3 %, p = 0.01). At logistic regression analysis using standardised variables, a 1SD-higher proximal sodium reabsorption at baseline predicted a 44% greater risk of HPT in 8 years (95% C.I. 13–84, p = 0.003), independently of baseline SBP (OR: 1.88, 95% C.I. 1.43–2.47, p < 0.001), BMI (OR: 1.51, 95% C.I. 1.16–1.95, p = 0.002), age and creatinine clearance used as an index of glomerular filtration rate. Conclusions: In this sample of healthy adult male population, proximal sodium reabsorption indexed to glomerular filtration rate was an independent predictor of future HPT.

SERUM URIC ACID PREDICTS THE DEVELOPMENT OF HYPERTENSION IN A SAMPLE OF MALE NORMOTENSIVE ADULTS: 1B.07

Objective: Cross-sectional and prospective studies showed that serum uric acid levels (SUA) and hypertension (HPT) are related. Our aim was to evaluate this relationship in a sample of healthy male adults, during an 8 year follow-up, in the Olivetti Heart Study. Methods: The population sample was made of 253 participants (mean age 49.5 years, range 26–71) examined both at the beginning (1994–95) and at the end of follow-up (2002–04). The participants were included in the analysis if at baseline they were non-diabetic, normotensive, not on pharmacological treatment for HPT, they had blood pressure (BP) less than 130/85 mmHg and normal renal function (creatinine clearance – CrCl > 60 ml/min). Results: Baseline SUA was directly related to BMI (r = 0.27; p < 0.0001), diastolic BP (r = 0.22; p < 0.0001) and HOMA index (r = 0.28; p < 0.0001) and inversely related to CrCl (r = −0.14; p = 0.02). The incidence of HPT (BP> = 140 and/or 90 mmHg or anti-hypertensive treatment) over 8 years was 45%. The participants who developed HPT had higher basal SUA compared with participants who did not (M ± SE: 5.76 ± 0.11 vs 5.36 ± 0.09 mg/dL; p = 0.006). Logistic regression analysis showed that standardised basal SUA significantly predicted the risk to develop HPT during 8 years (for 1SD higher SUA: OR = 1.40, 95% C.I. 1.06 to 1.86, p = 0.018), after adjustement for age, BMI, SBP, CrCl and HOMA index at baseline. Conclusions: This study revealed the predictive role of SUA on the development of hypertension in previously non diabetic normotensive subjects with normal renal function.