Endocan and Non-Dipping Circadian Pattern in Newly Diagnosed Essential Hypertension

BACKGROUND AND OBJECTIVES: Non-dipper hypertension is frequently accompanied by endothelial dysfunction and activation. Previous studies suggested that endocan may be a novel endothelial dysfunction marker. This study aims to investigate the association between circadian blood pressure (BP) pattern and plasma endocan levels together with high-sensitivity C-reactive protein (hsCRP) in patients with newly diagnosed untreated hypertension. SUBJECTS AND METHODS: Twenty-four hour ambulatory blood pressure monitoring was recorded in 35 dipper, 35 non-dipper hypertensives and 35 healthy controls. Endocan levels were measured by enzyme-linked immunosorbent assay. Serum levels of hsCRP were also recorded. RESULTS: Despite similar daytime and 24-hour average BP values between dippers and non-dippers, statistically significant high nocturnal BP was accompanied by a non-dipping pattern (Systolic BP: 132±9 vs. 147±11 mmHg; Distolic BP: 80±7 vs. 91±9 mmHg, respectively, p<0.001 for both). Non-dipper patients demonstrated higher endocan levels compared to dippers and normotensives (367 (193-844) pg/mL, 254 (182-512) pg/mL and 237 (141-314) pg/ml, respectively, p<0.001). HsCRP levels were significantly higher in non-dippers than the other groups (p=0.013). In a multivariate logistic regression analysis, endocan (p=0.021) and hsCRP (p=0.044) were independently associated with a non-dipping pattern. CONCLUSION: Elevated endocan levels were found in non-dipper groups. Endocan and hsCRP were found to be independently associated with a non-dipping pattern. We suggest that elevated levels of endocan in non-dipper hypertensive patients might be associated with a longer duration of exposure to high BP. These results point to the possible future role of endocan in selection of hypertensive patients at higher risk or target organ damage.

Plasma homocysteine concentrations and serum lipid profile as atherosclerotic risk factors in subclinical hypothyroidism

Because subclinical thyroid dysfunction may be a risk factor for cardiovascular disease, we evaluated the atherosclerosis tendency in subclinical hypothyroid [SCH] patients. Fifty-three subclinical hypothyroid patients [serum thyrotropin [TSH] concentrations >4.12 mU/L] were compared with a control group of 50 euthyroid subjects whose age, sex and body mass indices were similar to the patient group. We tested whether serum TSH concentrations were correlated with plasma total homocysteine concentration [tHcy], low-density lipoprotein cholesterol [LDL-C], very low-density lipoprotein cholesterol [VLDL-C], high-density lipoprotein cholesterol [HDL-C], total cholesterol [TC] and triglycerides [TG]. There was a significant statistical difference between the patient and control groups for normal freeT4 [1.02 +/- 0.1 7 vs. 0.86 +/- 0.13, P<.001], TSH [1.64 +/- 1.02 vs. 6.62 +/- 2.61, P<.001], TC [1 85 +/- 39 vs. 206 +/- 42, P=.01], TG [103 +/- 54 vs. 132 +/- 85, P=.04], LDL-C [114 +/- 33 vs. 127 +/- 36, P=.04], and TC/HDL-C [3.81 +/- 106 vs. 4.19 +/- 1.02, P=.04], respectively. No statistically significant difference was found between the two groups for HDL-C, VLDL-C, LDL-C/HDL-C, and tHcy. Serum TSH was significantly correlated with plasma tHcy [r=0.55; P=.001], TC [r=0.52; P=.001], LDL-C [r=0.49; P=.001], TC/HDL-C [r=0.38; P=.002] and LDL-C/HDL-C [r=0.36; P=.004] across all participants. Our study suggests that the atherogenicity of SCH is not mediated by hyperhomocysteinemia. Associated hyperlipidemia may explain the observed increased risk of coronary artery disease in patients with SCH