Evidence for no global effect of metabolic syndrome per se on early hypertensive sequelae.

OBJECTIVE: In the present study we assessed the impact of metabolic syndrome (MS) and its components on markers of cardiovascular and renal damage in a population of essential hypertensives. METHODS: A total of 651 consecutive, untreated and non-diabetic hypertensives (age 54 +/- 12 years, 340 males) who were included in the 3H Study, an ongoing registry of hypertension-related target organ damage, were considered for analysis. Left ventricular mass was indexed both for body surface area (LVMBSA) and for height2.7 (LVMheight2.7). Diastolic function was estimated by means of both conventional and tissue Doppler imaging (TDI) methods. Arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (c-f PWV) and microalbuminuria (MA) as albumin to creatinine ratio (ACR) 22-300 mg/g in men and 31-300 mg/g in women in two non-consecutive morning spot urine samples. RESULTS: MS (Adult Treatment Panel III criteria) was present in 201 hypertensives (30.9%). Hypertensives with MS had increased logACR (by 10%, P = 0.01) and higher prevalence of MA (17 versus 8%, P < 0.001). Both groups exhibited similar values of LVMBSA, transmitral and TDI-derived indexes and c-f PWV (NS for all) while LVMheight2.7 was significantly higher in hypertensives with MS (by 2.6 g/m2.7, P = 0.023). Multiple regression analysis revealed that MS was an independent predictor only of logACR (beta = 0.110, P = 0.007) and MA (odds ratio = 2.577, P < 0.001), while components of blood pressure affected all studied indices of organ damage. CONCLUSIONS: MS per se does not deteriorate cardiac adaptations and aortic stiffness beyond haemodynamic load in hypertension. The MS-related unfavourable effect is limited to the level of the glomerulus.

Diverse associations of microalbuminuria with C-reactive protein, interleukin-18 and soluble CD 40 ligand in male essential hypertensive subjects.

BACKGROUND: Microalbuminuria (MA) and low-grade inflammation constitute emerging markers of subclinical atherosclerosis. We investigated whether urinary albumin excretion, expressed as the albumin-to-creatinine ratio (ACR), is associated with high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-18, and soluble CD40 ligand (sCD40L), in hypertensive subjects. METHODS: The study population consisted of 108 nondiabetic male patients with newly diagnosed untreated stage I to II essential hypertension (aged 44.6 years, office blood pressure [BP] 148/95 mm Hg). According to ACR values determined as the average of two nonconsecutive overnight spot urine samples, subjects were divided into microalbuminurics (n = 28) (mean ACR = 30 to 300 mg/g) and normoalbuminurics (n = 80) (mean ACR <30 mg/g). RESULTS: Although microalbuminurics as compared to normoalbuminuric hypertensives had greater hs-CRP levels (2.55 +/- 1.18 v 1.45 +/- 0.52 mg/L, P < .0001), independently of confounding factors, these two groups did not differ regarding IL-18 and sCD40L values (P = not significant [NS] for both cases). In the entire population, ACR exhibited a positive correlation with hs-CRP (r = 0.623, P < .0001), whereas there was no association with both IL-18 and sCD40L (P = NS for both cases). When multiple linear regression analysis was performed, it was revealed that age, body mass index, office systolic BP, total cholesterol, and hs-CRP levels were significant independent predictors of the ACR (P < .05). CONCLUSIONS: In essential hypertensive subjects, MA is accompanied by elevated hs-CRP levels, but not by augmented IL-18 and sCD40L concentrations, suggesting activation of different inflammatory pathways in the progression of renal and cardiovascular atherosclerotic disease. The pathophysiologic mechanisms of these associations remain to be further elucidated in future studies.