Aldosterone levels and inflammatory stimulation in essential hypertensive patients.

Recent studies indicate that the pro-inflammatory action of aldosterone (ALDO) or the activation of mineralocorticoid receptors contribute to the increased risk of cardiovascular disease (CVD). The aim of the present study was to investigate the grade of the inflammatory activation, in relation to ALDO levels, in a large cohort of essential hypertensive patients. The study included 3770 consecutive essential hypertensive patients who attended our outpatient clinics. Patients were evaluated with medical history, repeated office blood pressure and 24-h ambulatory blood pressure monitoring (ABPM), physical examination and full laboratory assessment including ALDO in 24-h urine collection, plasma renin activity (PRA), high-sensitivity C-reactive protein (hsCRP), total fibrinogen, serum homocysteine (Hcy), serum amyloid A (SAA) and white blood cells (WBC) measurements in morning blood samples. Patients were divided according to PRA (high PRA >1 ng ml(-1) h(-1), low PRA <1 ng ml(-1) h(-1)) and ALDO levels (high ALDO >12 but <24 µg per 24 h, low ALDO <12 µg per 24 h) in four groups. The hsCRP (P<0.022) and SAA (P<0.001) levels increased in parallel with the ALDO metabolism. Similar differences were observed for Hcy (P<0.001), fibrinogen (P=0.001) and WBC (P<0.02). High ALDO levels within normal range are related to the presence of subclinical inflammation in essential hypertension. These data indicate that ALDO and PRA influence the process of subclinical inflammation involved in the increased risk of CVD.

Atorvastatin therapy is associated with improvement of oxidized low-density lipoprotein cholesterol levels, which correlates with the degree of stenosis in patients with carotid atheromatosis with and without prior angioplasty.

AIM: Oxidized low-density lipoprotein (oxLDL) is a pivotal factor of the atheromatous process. Statins reduce atheromatosis and cardiovascular risk. The aim of the present study was to investigate the effect of statin therapy on circulating oxLDL and the possible impact of such effect on stenosis due to carotid artery atheromatosis. METHODS: A total of 100 patients (76 males, median age 68 years) with carotid atheromatosis were enrolled. Those with stenosis >70% (n=50) were pre-treated with carotid angioplasty, whereas those with <70% were treated conservatively. Both groups were given low-dose atrorvastatin, tittered to maintain LDL cholesterol <100 mg/dL. Anthropometrics, complete lipid profile, and oxLDL were obtained in 1, 3, 6 and 12 months. Stenosis was evaluated by ultrasonography at baseline and 12 months. RESULTS: Lipid profile significantly improved at 12 months and oxLDL fell from 62.26+/-22.03 mg/dL at baseline to 44.49+/-21.75 mg/dL at 12 months (P<0.001). In the invasively pretreated group no restenosis was noticed; in the conservatively treated group a significant reduction of stenosis was demonstrated (47.6+/-13.2% vs 37.7+/-15.7%, P<0.001). The decrease of oxLDL correlated with the reduction of stenosis (r=0.17, P=0.018). In multivariate analysis, oxLDL was an independent risk factor for re-stenosis (hazard ratio=4.319, P<0.001). CONCLUSION: A marked reduction of oxLDL was shown in patients with carotid atheromatosis treated with low-dose atorvastatin. Moreover, oxLDL could be a measure of the degree of stenosis in such patients.

Associations between plasma homocysteine levels, aortic stiffness and wave reflection in patients with arterial hypertension, isolated office hypertension and normotensive controls.

The aim of this study was to evaluate any possible association of homocysteine with arterial stiffness indices in patients with essential arterial hypertension (AH), isolated office hypertension (IOH) and normotensive controls. The final cohort comprised 231 normotensives (NTs, 119 males), 480 patients with IOH (196 males) and 1188 patients with essential AH (713 males). All patients were screened for plasma homocysteine levels and lipidaemic profile and underwent aortic compliance and wave reflection assessment by using carotid-femoral pulse wave velocity (PWVc-f) and aortic augmentation index corrected for heart rate (AIx) accordingly. In the total population, stepwise multiple linear regression analysis showed that homocysteine levels remained a significant determinant of PWV (beta (SE): 0.056 (0.007), P<0.001) and AIx (beta (SE): 0.236 (0.052), P<0.001) independently of the traditional factors affecting arterial stiffness and wave reflection. When the three groups were examined separately, homocysteine levels remained an independent determinant of PWFc-f in all groups (NT: beta (SE): 0.070 (0.022), P=0.002; IOH: beta (SE): 0.109 (0.015), P<0.001; AH: beta (SE): 0.040 (0.009), P<0.001). However, homocysteine levels remained an independent determinant of AIx only in the IOH and AH, but not in the NT group (IOH: beta (SE): 0.302 (0.124), P=0.015; AH: beta (SE): 0.183 (0.057), P=0.001; NT: beta (SE): 0.308 (0.240), P=0.200). This study points to an independent relationship between circulating homocysteine levels, aortic compliance and wave reflection.