Closer look at white-coat hypertension

This review aims to clarify novel concepts regarding the clinical and laboratory aspects of white-coat hypertension(WCHT). Recent studies on the clinical and biological implications of WCHT were compared with existing knowledge. Studies were included if the WCHT patients were defined according to the 2013 European Society of Hypertension guidelines, i.e., an office blood pressure(BP) of ≥ 140/90 mm Hg, a home BP of ≤ 135/85 mm Hg, and a mean 24-h ambulatory BP of ≤ 130/80 mm Hg. WCHT studies published since 2000 were selected, although a few studies performed before 2000 were used for comparative purposes. True WCHT was defined as normal ABPM and home BP readings, and partial WCHT was defined as an abnormality in one of these two readings. The reported prevalence of WCHT was 15%-45%. The incidence of WCHT tended to be higher in females and in non-smokers. Compared with normotensive(NT) patients, WCHT was associated with a higher left ventricular mass index, higher lipid levels, impaired fasting glucose, and decreased arterial compliance. The circadian rhythm in WCHT patients was more variable than in NT patient's, with a higher pulse pressure and non-dipping characteristics. Compared with sustained hypertension patients, WCHT patients have a better 10-year prognosis; compared with NT patients, WCHT patients have a similar stroke risk, but receivemore frequent drug treatment. There are conflicting results regarding WCHT and markers of endothelial damage, oxidative stress and inflammation, and the data imply that WCHT patients may have a worse prognosis. Nitric oxide levels are lower, and oxidative stress parameters are higher in WCHT patients than in NT patients, whereas the antioxidant capacity is lower in WCHT patients than in NT patients. Clinicians should be aware of the risk factors associated with WCHT and patients should be closely monitored especially to identify target organ damage and metabolic syndrome.

Relation of Biochemical Parameters with Flow-mediated Dilatation in Patients with Metabolic Syndrome

Background： Metabolic syndrome （MetS） is one of the high cardiovascular （CV） situations. Endothelial dysfunction, which is a common finding in patients with MetS, is related with increased CV risk. In patients with MetS, the effect of the major CV risk factors, not included in the MetS definition, on endothelial dysfunction is not well known. The aim of this study was to determine the effect of major CV risk factors such as gender, smoking, family history, and biochemical parameters on endothelial dysfunction in patients with MetS. Methods： The study was performed between December 2010 and August 2014. A total of 55 patients （ 15 females and 40 males） with MetS and 81 healthy controls （37 females and 44 males） with a body mass index 〈25 kg/m2 were enrolled in the study. Endothelial dysfunction was measured by flow-mediated dilatation （FMD）, oxidative stress parameters; high-sensitivity C-reactive protein （hs-CRP）, oxidized low-density lipoprotein （ox-LDL）, endothelial nitric oxide synthase （e-NOS）, nitric oxide, and cell adhesion markers; yon Willebrand factor, and e-selectin. Platelet aggregation （endothelial adenosine diphosphate）, total platelet count, and mean platelet volume were additionally analyzed and demographic parameters were explored. Student＇s t-test, Mann-Whitney U-test, and Chi-square test were used to analyze the results. Results： The fasting blood glucose （z = 3.52, P = 0.001 ）, hs-CRP （z - 3.23, P = 0.004）, ox-LDL （z = 2.62, P= 0,013）, and e-NOS （z = 2.22, P = 0.026） levels and cardiac risk score （z - 5.23, P 〈 0.001） were significantly higher in patients with MetS compared with the control group. Smoking was correlated with decreased FMD （χ2 = 9.26, P = 0.002） in MetS patients but not in the control group. Conclusions： Increased ox-LDL, hs-CRP, and e-NOS are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive nitrogen and oxygen species. In addition, in patients with MetS, smoking is independently related to endothelial dysfunction.