Hyperhomocysteinemia: an additional risk factor in white coat hypertension.

The association between homocysteine and sustained hypertension (HT) has been studied. The aim of this study was to assess homocysteine levels in white coat hypertension (WCH) as an indicator of increased risk in the development of cardiovascular diseases. WCH was defined as clinical hypertension and a daytime ambulatory blood pressure of < 135/85 mmHg. Plasma levels of homocysteine were determined in patients with WCH, hypertension, and normotension (NT). The study group included 100 subjects, 33 with WCH (16 males, 17 females) aged 49.1 +/- 1.9; 35 sustained hypertensives (17 males,18 females) aged 48.5 +/- 1.7 and 32 normotensive control subjects (15 males, 17 females) aged 48.8 +/- 2.2. The subjects were matched for age, gender, and body mass index. Patients with a smoking habit, dyslipidemia, or diabetes mellitus were not included in the study. Homocysteine levels were analyzed by ELISA. Plasma homocysteine levels were significantly higher in the WCH group compared to the controls (12.32 +/- 1.07 versus 5.35 +/- 1.38 micromol/L; P < 0.001) and the WCH group had significantly lower homocysteine values than the hypertensives (19.03 +/- 0.76 micromol/L P < 0.001). Total cholesterol and tri-glycerides were not different among the groups. There were no statistically significant differences in urinary albumin excretion (UAE) or creatinine clearance between the three groups. Hypertensive retinopathy was observed in the WCH group, but was less severe and less frequent compared to HTs. LVMI was greater in the WCH group compared to the NTs, but significantly less than HTs. The data demonstrate that WCH is associated with high levels of homocysteine. The increase in homocysteine level in WCH is not as high as in SHT. Since an elevated plasma homocysteine level is a strong risk factor for coronary artery disease and there was target organ damage in our WCH group, we conclude that WCH should not be considered to be an innocent trait.

Effects of low and high doses of atorvastatin on arterial compliance.

At the beginning of atherosclerosis before evidence of morphological lesions or plaques, vascular distensibility or arterial compliance decreased gradually. This endothelial dysfunction is regarded as an early feature of atherosclerosis. In a randomized, double-blind study design, group 1 (12 patients; 7 males, 5 females) with serum LDL-C levels higher than 170 mg/dL and without any other risk factor for atherosclerosis received three months of 20 mg/day atorvastatin treatment while group 11 (8 males, 4 females) with the same characteristics received 80 mg/day. Baseline and posttreatment serum lipid fractions and arterial compliance were measured. Arterial compliance was measured noninvasively in the left common carotid artery with color Doppler ultrasound. Atorvastatin reduced total cholesterol (TC), LDL-C, and triglyceride levels by 32% (P < 0.001), 40.8% (P < 0.001), and 19% (P < 0.001), respectively, and increased HDL-C by 6.9%, (P = 0.002) in the first group. In the second group these reductions were 38.5% (P < 0.001), 46.2% (P < 0.001), and 26.78% (P < 0.001), respectively, and the increase in HDL was 7.8% (P = 0.03). It was observed that the decrease in serum TC, LDL-C and triglyceride levels were significantly higher in the second group than the first group. With atorvastatin, the distensibility coefficient (DC) and compliance coefficient (CC) increased from 18.7 +/- 3.4 to 21.3 +/- 2.9 10(-3) x kPa(-1) (P < 0.001) and from 0.69 +/- 0.05 to 0.77 +/- 0.03 mm2 x kPa(-1) (P < 0.001) in the first group while they changed from 18.3 +/- 3.6 to 21.9 +/- 3.0 10(-3) x kPa(-1) (P < 0.001) and from 0.70 +/- 0.04 to 0.81 +/- 0.01 mm2 x kPa(-1) (P < 0.001) respectively, in the second group. DC and CC increased in both groups, but the differences between the groups were not significant. High doses of atorvastatin reduce blood lipid levels more than conventional doses, however, the change in compliance is not dose-dependent. As endothelial dysfunction is regarded as an early feature of atherosclerosis, there would be no need to administer aggressive doses in a patient without any risk factors other than hyperlipidemia.