Association of thyroid function with white coat hypertension and sustained hypertension.

This study aimed to explore the relationship of thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), and free thyroxine (FT4) levels with hypertension subtypes. 1056 euthyroid adults were included as research samples. They underwent measurement of clinic blood pressure and 24-hours ambulatory blood pressure monitoring. Then, they were divided into normotension (NT), white coat hypertension (WCH), masked hypertension (MHT), and sustained hypertension (SHT) groups. The 24-hours dynamic electrocardiogram was performed to analyze the heart rate variability (HRV), so as to reflect the cardiac autonomic function. The relationship between hypertension subtypes, thyroid function, and HRV was analyzed. The TSH concentration was significantly higher in the SHT group than in the NT group (P = 0.001). The FT3 concentration was higher in the SHT group than in the NT and MHT groups (P = 0.013, P = 0.008), while the FT4 concentration was significantly higher in the WCH group than in the NT group (P = 0.002). The changes in HRV were observed between the SHT, WCH, and MHT groups and the NT groups, as well as between the SHT and the MHT groups. The multiple linear regression analysis also showed that FT3, HRV (RMSSD and PNN50), and blood pressure levels linearly correlated with one another (P < 0.05). Meanwhile, the linear regression analysis showed a linear negative correlation between FT4 and HRV (SDANN) in the WCH + NT group (P = 0.001). Thyroid function was closely related to hypertension subtypes such as WCH probably due to the changes in the cardiac autonomic function.

Association of office and ambulatory blood pressure with blood lead in workers before occupational exposure.

In view of decreasing lead exposure and guidelines endorsing ambulatory above office blood pressure (BP) measurement, we reassessed association of BP with blood lead (BL) in 236 newly employed men (mean age, 28.6 years) without previous lead exposure not treated for hypertension. Office BP was the mean of five auscultatory readings at one visit. Twenty-four-hour BP was recorded at 15- and 30-minute intervals during wakefulness and sleep. BL was determined by inductively coupled plasma mass spectrometry. Systolic/diastolic office BP averaged 120.0/80.7 mm Hg, and the 24-hour, awake, and asleep BP 125.5/73.6, 129.3/77.9, and 117.6/65.0 mm Hg, respectively. The geometric mean of blood lead was 4.5 µg/dL (interquartile range, 2.60-9.15 µg/dL). In multivariable-adjusted analyses, effect sizes associated with BL doubling were 0.79/0.87 mm Hg (P = .11/.043) for office BP and 0.29/-0.25, 0.60/-0.10, and -0.40/-0.43 mm Hg for 24-hour, awake, and asleep BP (P ≥ .33). Neither office nor 24-hour ambulatory hypertension was related to BL (P ≥ .14). A clinically relevant white coat effect (WCE; office minus awake BP, ≥20/≥10 mm Hg) was attributable to exceeding the systolic or diastolic threshold in 1 and 45 workers, respectively. With BL doubling, the systolic/diastolic WCE increased by 0.20/0.97 mm Hg (P = .57/.046). Accounting for the presence of a diastolic WCE, reduced the association size of office diastolic BP with BL to 0.39 mm Hg (95% confidence interval, -0.20 to 1.33; P = .15). In conclusion, a cross-sectional analysis of newly hired workers before lead exposure identified the WCE as confounder of the association between office BP and BL and did not reveal any association between ambulatory BP and BL.

Association of parathyroid hormone and vitamin D with untreated hypertension: Is it different in white-coat or sustained hypertension?

BACKGROUND: Previous reports about the relationship between a high parathyroid hormone (PTH) and low vitamin D levels with blood pressure in different hypertension groups are conflicting. OBJECTIVE: We studied serum PTH and vitamin D levels in white-coat (WCHT) and sustained hypertension (SHT) patients who had not been on antihypertensive treatment. We also investigated the association between serum PTH and vitamin D levels with respect to blood pressure in SHT and WCHT patients. METHODS: We included 52 SHT patients (54.06 ± 9.2 years, 32 newly diagnosed and 20 previously diagnosed with SHT who had not been treated with antihypertensive medication for 3 months or more), 48 WCHT patients (53.64 ± 9.5 years), and 50 normotensive (NT) healthy controls (53.44 ± 8.4 years) in our study. In addition to routine tests, PTH and vitamin D levels were measured. RESULTS: Serum PTH levels were significantly higher in SHT patients not taking antihypertensive medications than in WCHT patients and NT controls (p = 0.004). Although PTH levels were higher in WCHT than in NT groups, the difference was not statistically significant. In SHT patients, PTH levels showed a positive correlation with office systolic (r = 0.363, p = 0.008), office diastolic (r = 0.282, p = 0.038), home systolic (r = 0.390, p = 0.004), and home diastolic blood pressures (r = 0.397, p = 0.003). Serum vitamin D levels were similar in SHT, WCHT and NT groups. Vitamin D levels were not associated with blood pressures in the entire study group. Furthermore, no significant relation was found between vitamin D and PTH levels in SHT and WCHT groups. CONCLUSION: PTH levels are significantly higher in untreated SHT patients than WCHT patients and NT subjects. However, vitamin D levels are similar in SHT, WCHT and NT groups. There is a significant association between PTH levels and blood pressures suggesting PTH has a role in increase of blood pressure in SHT.

The relationship between soluble CD40 ligand level and atherosclerosis in white-coat hypertension.

This study was designed to examine the distribution of plasma soluble CD40 ligand (sCD40L), and its relationship with carotid intima-media thickness (CIMT) in healthy controls and subjects with white-coat hypertension (WCH) or hypertension (HT). Thirty-five patients with HT, 35 patients with WCH, and 35 healthy controls were enrolled. The normal group (CIMT < 0.9 mm), subclinical atherosclerosis group (0.9 mm ≤ CIMT < 1.2 mm) and atherosclerosis group (CIMT ≥ 1.2 mm) were grouped based on the value of CIMT. The highest level of sCD40L was observed in HT group, followed by WCH group and healthy controls. The level of sCD40L was significantly increased in atherosclerosis group compared with subclinical atherosclerosis group and healthy controls. In the WCH group, sCD40L level was significantly and positively correlated with CIMT and systolic blood pressure. Multiple logistic regression indicated that sCD40L was a risk factor for increased CIMT (odds ratio, 1.504; 95% confidence interval, 1.054-1.956, P < 0.001). The data provided evidence that sCD40L levels in subjects with WCH and HT were significantly and consistently higher than those in healthy controls. SCD40L may represent a potential non-invasive atherosclerosis marker in WCH patients.

The impact of protein oxidation on sustained and white coat hypertension.

OBJECTIVE: The present study compared the unfavorable effects of protein oxidation and deoxyribonucleic acid damage on patients with white coat hypertension (WCH), sustained hypertension (HT), and normotensives. METHODS: Participants were allocated into 3 groups: 40 healthy controls, 36 patients with WCH, and 40 patients with sustained HT. Patients with risk factors for atherosclerosis, endocrine diseases, alcoholism, or masked hypertension were excluded. Plasma level of protein carbonyl (PCO), ischemia modified albumin (IMA), total thiol (T-SH), prooxidant-antioxidant balance (PAB), advanced protein oxidation products (AOPPs), and urinary level of 8-hydroxy-2'-deoxyguanosine (8-OHdG) were measured and relationship between these oxidative stress parameters and WCH and sustained HT was analyzed. RESULTS: Ambulatory 24-hour, daytime and night-time systolic and diastolic blood pressure readings of sustained HT group were significantly higher than those of WCH and control groups (p<0.001, all). AOPPs, PCO, IMA, 8-OHdG, and PAB levels were significantly higher in HT group than WCH and control groups (p<0.001, all). Additionally, T-SH level was significantly lower in HT group than WCH and control groups (p<0.001). A similar statistically significant relationship was detected between WCH and control groups. CONCLUSION: Results indicate that increased level of AOPPs, PCO, IMA, 8-OHdG, PAB, and decreased level of T-SH are likely to be indicators of oxidative stress, which may play a key role both in WCH and sustained HT.

Vitamin D levels in white coat and sustained hypertension.

OBJECTIVE: The plasma levels of vitamin D in patients with white coat hypertension (WCHT) have not been studied previously. The aim of this study was to evaluate vitamin D levels in WCHT and compare with sustained hypertension (SHT) and with normotension (NT). PATIENTS AND METHODS: Fifty-three normotensive, 42 WCHT, and 59 SHT patients were recruited in this study. The participants were matched for age, sex, and BMI. The vitamin D levels were determined using the electrochemiluminescence immunoassay method. RESULTS: Plasma vitamin D levels were significantly lower in SHT than in the WCHT and NT groups (26.4±4.9, 34.3±3.6, and 36±5 ng/ml, respectively), and were similar in the WCHT and NT groups. There was a negative correlation between vitamin D levels and blood pressure parameters such as clinic systolic blood pressure (SBP), clinic diastolic blood pressure (DBP), 24-h SBP, 24-h DBP, daytime SBP, daytime DBP, night-time SBP, and night-time DBP (r=-0.554, -0.419, -0.629, -0.427, -0.559, -0.534, -0.607, -0.462, respectively, and all P<0.001) in the entire study group. Clinic SBP (B±SE=-0.97±0.037, P=0.009) and 24-h SBP (B±SE=-0.138±0.055, P=0.013) were identified as predictors for vitamin D levels in the entire study group. CONCLUSION: Our data show that sustained hypertensive patients have lower vitamin D levels than white coat hypertensive and normotensive individuals. White coat hypertensive patients without other cardiovascular risk factors have higher vitamin D levels than sustained hypertensive patients, suggesting that they have a lower cardiovascular risk.

Procalcitonin and Pentraxin-3: Current biomarkers in inflammation in white coat hypertension.

An association has been described between inflammation and the progression of hypertension (HT) and is shown with several biochemical parameters. Our aim was to examine the distribution of the serum procalcitonin (PCT), pentraxin (PTX)-3 and interleukin (IL)-33 levels and their relationship with carotid intima-media thickness (CIMT) in subjects with white coat HT (WCH), HT and normotension (NT) groups. Thirty-three patients with HT, 33 patients with WCH and 33 healthy subjects were enrolled in this study. PCT, PTX-3 and C-reactive protein (CRP) levels significantly increased in the HT group compared with the NT group. In addition, PCT and CRP levels were significantly higher in the WCH group than in the NT group. CIMT measurements were significantly higher in the WCH and HT groups than in the NT group. In the HT and WCH groups, there were significant positive correlations between PTX-3, PCT and CRP. In the WCH group, PTX-3 and PCT levels were significantly positively correlated with CIMT. PCT had area under the curve value of 0.817 which demonstrates its sufficiency to distinguish WCH from NT individuals. Our results suggest that in subjects with WCH and HT, which are characterized by increased cardiovascular risk, PTX-3 and PCT levels in the HT group and PCT levels in the WCH group are significantly and consistently higher than normotensives. Systemic inflammation moderately occurs in the WCH and HT groups. PCT monitoring may be a useful biomarker in inflammation related to atherosclerosis and early stage HT.

Endothelial damage in white coat hypertension: role of lectin-like oxidized low-density lipoprotein-1.

The aims of this study included an examination of soluble lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (sLOX-1) levels in hypertensive (HT) patients. Another aim examined sLOX-1 associations with oxidized LDL (oxLDL), nitric oxide synthase (eNOS) and nitric oxide (NOx). A final aim was to compare these parameters between HT patients, white-coat hypertensive (WCH) patients and healthy controls. The three groups, HT, WCH and controls, were comprised of 35 patients each. sLOX-1 and oxLDL levels were significantly increased in WCH and HT patients compared with controls. The eNOS activation was significantly lower in HT than in the control group. sLOX-1 and oxLDL levels were significantly negatively correlated with eNOS levels in the WCH and HT groups. Carotid intima-media thickness (CIMT) measurements were significantly higher in the WCH and HT groups compared with controls. There was a significant positive correlation between CIMT and sLOX-1 and oxLDL; however, there was a negative correlation with eNOS in WCH. Regression analysis revealed that sLOX-1 was the variable that had a significant effect on blood pressure (P<0.001, odds ratio (95% confidence interval=23.273 (5.843-92.688)). A possible endothelial impairment may act as a cardiovascular risk factor in WCH. Necessary measures should be considered in terms of atherosclerosis risk with HT, especially in early identification of endothelial damage by looking at sLOX-1 levels. We believe sLOX-1 levels are strong biomarkers for determining early endothelial damage in HT, and especially in WCH patients.

Serum copeptin levels in adolescents with primary hypertension.

BACKGROUND: The prevalence of hypertension continues to rise in the pediatric population. In recent years, there has been an increasing amount of reports on serum arginine vasopressin and its derivative, copeptin, in blood pressure control, but its role is still unclear. The objective of this study was to assess serum copeptin in adolescents with essential hypertension. METHODS: The study cohort consisted of 84 subjects (30 girls and 54 boys) aged 11-18 years, divided into two groups: hypertension (HT) - 53 subjects with confirmed primary hypertension and R - reference group - 31 subjects in whom hypertension was excluded on the basis of ambulatory blood pressure monitoring (ABPM) (white-coat hypertension). Serum copeptin concentration was measured using a commercially available enzyme-linked immunosorbent assay kit (USCN). RESULTS: Hypertensive patients had higher serum copeptin levels (median, 267 [Q1-Q3: 151.1-499.7 pg/ml]) than controls (median, 107.3 [Q1-Q3: 36.7-203.4 pg/ml]), (p < 0.01). Statistically significant difference was found both in males and females. In both groups, positive correlations between serum copeptin and uric acid levels (r = 0.31, p < 0.01), albuminuria (r = 0.45, p < 0.01), serum triglycerides (r = 0.3, p < 0.05), body mass index (BMI) standard deviation score (SDS) (r = 0.24, p < 0.05) and 24-h systolic blood pressure (SBP) (r = 0.37, p < 0.01) and diastolic blood pressure (DBP) (r = 0.23, p < 0.05) were found. CONCLUSIONS: In summary, higher serum copeptin levels, a surrogate for arginine vasopressin (AVP) release, are associated not only with systolic and diastolic blood pressure but also with several components of metabolic syndrome including obesity, elevated concentration of triglycerides, albuminuria, and serum uric acid level. However, for the time being, more research is needed in order to confirm the role of serum copeptin as a novel marker of elevated blood pressure and predictor of metabolic syndrome.

Relationships of different blood pressure categories to indices of inflammation and platelet activity in sustained hypertensive patients with uncontrolled office blood pressure.

Failure to decrease blood pressure (BP) normally during nighttime (non-dipping) in hypertension is associated with higher cardiovascular morbidity and mortality. In addition, non-dipping BP is associated with increased platelet activity and inflammatory response; however, there has been no study to evaluate the relationship of non-dipping BP to indices of platelet activity and inflammation in uncontrolled hypertensive patients. In the present study, hypertensive subjects with uncontrolled office BP were firstly divided into three groups: 84 subjects with white coat effect and 365 subjects with true uncontrolled hypertension. Then, true uncontrolled hypertensive patients were divided into two groups: 158 patients with dipping and 207 patients with non-dipping. Mean platelet volume (MPV), uric acid (UA), γ-glutamyltransferase (GGT), C-reactive protein (CRP), and high-sensitivity CRP (hs-CRP) levels were studied. The general characteristics and risk factors for coronary artery disease (CAD) of the study population were similar among the groups. MPV, UA, GGT, CRP, and hs-CRP levels were significantly higher in non-dipper group than both dipper and white coat effect groups, and were significantly higher in dipper group than in white coat effect group (MPV: 9.1 ± 1.3, 8.7 ± 1.1, and 8. ± 0.9 fL; UA: 6.9 ± 1.2, 5.9 ± 1.4, and 4.1 ± 0.8 mg/dL; GGT: 38.9 ± 11.1, 33.6 ± 14.9, and 25.2 ± 9.2 U/L; CRP: 7.1 ± 2.4, 6.2 ± 1.9, and 3.9 ± 0.8 mg/dL; hs-CRP: 3.8 ± 1.5, 3.3 ± 1.2, and 2.0 ± 0.6, non-dipper, dipper, and white coat effect groups, respectively, all p values <0.01). All study parameters strongly correlated with each other. In conclusion, in hypertensive patients with uncontrolled office BP, presence of non-dipping BP is associated with increased platelet activity and inflammation, which can be one of the underlying plausible mechanisms of non-dipping BP status.

Comparison of demographic, clinical, and laboratory parameters between patients with sustained normotension, white coat hypertension, masked hypertension, and sustained hypertension.

BACKGROUND: After measurement of office blood pressure (BP) and ambulatory BP monitoring (ABPM), 4 groups of patients were identified namely: (i) sustained normotensive patients (BPs are normal both clinically and by ABPM); (ii) white coat hypertensive patients (clinical BP were above limits, but ABPM were normal); (iii) masked hypertensive patients (clinical BP were normal, but ABPM were high); (iv) sustained hypertensive patients (both office and ABPM were high). The exact pathophysiologic mechanisms of these conditions are not exactly known. Besides in the literature there are only few studies that compare the 4 groups of patients together. Thus the study was carried out to compare patients with sustained normotension (SNT), white coat hypertension (WCHT), masked hypertension (MHT), and sustained hypertension (SHT). METHODS: All patients underwent history taking, physical examination, laboratory analysis, and ABPM. They were referred to the cardiology department for echocardiographic evaluation. RESULTS: In total 85 patients with SNT, 112 patients with WCHT, 31 patients with MHT, and 81 patients with SHT were included. Going from SNT to SHT, body mass index (p<0.0001), waist circumference (p<0.0001), fasting blood glucose (p=0.002), and uric acid (p=0.029) rose progressively. Presence of metabolic syndrome was also highest in SHT and lowest in SNT (p<0.0001). CONCLUSION: Most of the metabolic risk factors were higher in patients with MHT and SHT when compared to SNT and WCHT. Studies are needed to determine whether metabolic risk factors play a causative role for the development of MHT and SHT.

Nocturnal hypertension: poor correlation with office blood pressure but strong prognostic factor for target organ damage.

INTRODUCTION: We investigated the correlation between systolic and diastolic nocturnal blood pressure (BP) values and office BP values, as well as parameters of 24-hour ambulatory BP monitoring, in patients with hypertension. In addition, we compared nocturnal hypertensives with nocturnal normotensives regarding their demographic, clinical, and laboratory characteristics, as well as other data from 24-hour BP monitoring. METHODS: The study included 182 consecutive patients who had newly diagnosed, never treated, uncomplicated arterial hypertension. Blood samples were obtained from all patients for the determination of glycaemic and lipidaemic profiles. All underwent a complete echocardiographic examination, including tissue Doppler imaging, measurement of carotid intima-media thickness, measurement of carotid-femoral pulse wave velocity, and determination of the augmentation index of reflected waves (Aix@75), as well as 24-hour ambulatory BP monitoring. The population was divided into nocturnal normotensives (NN, n=77) and nocturnal hypertensives (NH, n=105, nocturnal BP >120/70 mmHg). RESULTS: Although the NH did not differ from the NN as regards the classical cardiovascular risk factors, they showed an excessive inotropic response to exercise (61.9% vs. 22.7%, p=0.028), higher levels of serum uric acid (5.5 ± 1.56 mg/dl vs. 4.7 ± 1.36 mg/dl, p=0.003), as well as greater arterial stiffness, as expressed by a higher carotid-femoral pulse wave velocity (8.6 ± 1.6 m/s vs. 7.9 ± 1.4 m/s, p=0.009), and a greater carotid intima-media thickness (0.74 ± 0.17 mm vs. 0.68 ± 0.15 mm, p=0.007). In addition, although the two groups did not differ significantly as regards office BP values and did not show strong correlations between nocturnal and office BP, both nocturnal diastolic and, especially, systolic BP showed strong correlations with levels of serum uric acid and with subclinical lesions in the heart, central aorta, peripheral vessels, and renal vasculature. CONCLUSIONS: Nocturnal BP is poorly correlated with office BP values. However, the presence of nocturnal hypertension is associated with morphological and functional disturbances of the cardiovascular net. 24-hour ambulatory BP monitoring is an essential tool for revealing this subgroup of hypertensive patients who are at increased cardiovascular risk.

C-reactive protein and nitric oxide level in patients with white coat hypertension.

BACKGROUND: There are controversial results regarding the endothelial function in patients with white coat hypertension (WCH). The aim of this study was to assess endothelial function measuring nitric oxide (NO) and C-reactive protein (CRP) level in WCH and to compare those with essential hypertension (EH) and healthy subjects. METHODS: The 40 newly diagnosed patients with EH, 40 patients with WCH and 40 healthy volunteers were included to study. Plasma CRP levels were measured by immunonephelometery method. Plasma NO level was also detected by using the Griess method. RESULTS: Plasma CRP level was significantly higher in patients with EH when compared with those with WCH and healthy subjects (6.3 ± 2.1 mg/l, 2.1 ± 0.9 mg/l and 1.6 ± 1.3 mg/l, p < 0.05, respectively). However, there was no significant difference with respect to CRP level between those with WCH and healthy subjects. NO level was significantly lower in patients with EH when compared with those with WCH and healthy subjects (4.6 ± 1.1 µmol/l, 6.9 ± 1.2 µmol/l and 8.1 ± 1.5 µmol/l, p < 0.05, respectively). There was no significant difference with respect to NO level between those with WCH and healthy subjects. Plasma CRP level was positively correlated with office, daytime, night-time and 24-h blood pressure values, whereas NO level was inversely correlated with these parameters. Plasma CRP level was also inversely correlated with NO level. CONCLUSIONS: Our data suggest that CRP concentration is significantly higher and NO level is meaningfully lower in patients with essential hypertension when compared with those with WCH and controls. This may suggest that endothelial functions are preserved in patients with WCH in contrast to essential hypertension.