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Aim: ST2 receptor is a member of toll-like/interleukin-1 receptor family. After the activation of IL-33/ST2 signaling pathway clinically detectable amount of soluble form of ST2 (sST2) is released into the circulation. Previous studies showed that sST2 levels were significantly higher in hypertension patients than in controls. In this prospective study, we aimed to analyze this relation and test the predictive accuracy of the sST2 level in diagnosis of nondipping hypertension in newly diagnosed hypertension patients., Methods: Three hundred thirty-seven patients (150 normal, 187 hypertension) who presented with symptoms of hypertension were included in the study. All patients underwent 24-h ambulatory blood pressure monitoring and sST2 measurement., Results: Of 187 hypertension patients, 92 of them had nondipping and 95 of them had dipping pattern. sST2 level was significantly higher in nondipping group compared to dipping group and control group (40.79 ± 7.77 vs. 32.47 ± 6.68; P  < 0.0001 and 40.79 ± 7.77 vs. 20.09 ± 7.09; P  < 0.0001 respectively). Binary logistic regression analysis revealed that; only sST2 level was an independent risk factor for hypertension [ P  < 0.0001, β : 1.258, odds ratio (OR) (95% confidence interval (CI)): 1.158-1.366]. and also nondipping hypertension [ P  < 0.0001, β : 1.208, OR (95% CI): 1.108-1.317]., Conclusion: Based on the present study it could be concluded that sST2 level is significantly associated with the newly diagnosed hypertension and nondipping hypertension. Hence it could reliably be used to diagnose hypertension and nondipping hypertension with high sensitivity and specificity., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Methods using for determining the subclinical atherosclerosis have gained growing interest in the recent years. However, the effects of pseudo-hypertension on the parameters of subclinical atherosclerosis are uncertain. We aimed to evaluate the relationship between pseudo-hypertension and subclinical atherosclerosis in individuals diagnosed with pseudo-hypertension., Methods: A total of 122 patients who underwent radial elective coronary angiography were included in the present study. These patients were divided into two groups based on the difference between invasive and noninvasive blood pressure (BP) measurements: pseudo-hypertension group who had a difference ≥15 mmHg in SBP or ≥10 mmHg in DBP levels between invasive and noninvasive measurements (n = 28), and the other group who did not have any difference as described on these levels (n = 94). In order to evaluate the subclinical atherosclerosis; flow-mediated dilatation (FMD), carotid intima-media thickness (IMT), pulse wave velocity (PWV), and augmentation index were recorded in all patients. Two groups were compared with respect to these parameters., Results: The median age of the pseudo-hypertension group was 76 years, while the median age of the other group was 63.5 years (P < 0.0001). The incidence of concomitant hypertension was higher in the pseudo-hypertension group as compared to the other group (P < 0.001). There was a significant difference in augmentation index, cardiac output, PWV, FMD, and IMT values between two groups (P = 0.016, P = 0.023, P <0.001, P < 0.001, P < 0.001, respectively)., Conclusions: The present results demonstrated that there was a strong correlation between pseudo-hypertension and the parameters of subclinical atherosclerosis; augmentation index, PWV, FMD, and carotids IMT., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Significant numbers of asymptomatic hypertensive patients are attacked by subclinical target organ damage (TOD) such as proteinuria, left ventricular hypertrophy and carotid atherosclerosis. Platelets become activated in uncontrolled hypertension and play a crucial role in increased thrombotic tendency. Mean platelet volume (MPV) is one of the markers that correlate closely with platelet activity. We aimed to investigate the relationship between MPV levels and subclinical TOD in newly diagnosed hypertensive patients., Methods: 80 newly diagnosed hypertensive patients were enrolled to this cross-sectional study. Ambulatory blood pressure monitoring was performed for all patients. Left ventricular mass index (LVMI), carotid intima-media thickness (IMT) and urine albumin/creatinine ratio (UACR) were measured as indices of cardiac, vascular and renal damage, respectively. MPV was measured from blood samples collected in EDTA tubes and high-sensitivity C reactive protein (hs-CRP) was measured by using nephlometer., Results: MPV was significantly correlated with 24-h systolic-diastolic blood pressure (r = 0.52 and r = 0.55, respectively). Correlation analysis indicated that MPV was moderately related with UACR, LVMI, carotid IMT and hs-CRP (r = 0.50, r = 0.55, r = 0.60 and r = 0.69, respectively, p = 0.0001). Multivariable analysis identified that MPV levels were independently associated with severity of proteinuria, carotid IMT and LVMI (p = 0.001)., Conclusion: Our findings suggested that MPV levels were associated with severity of subclinical TOD including; carotid atherosclerosis, left ventricular hypertrophy and renal damage, in hypertensive patients. In addition to this, MPV levels were significantly correlated with hs-CRP levels and 24-h ambulatory blood pressure measurements.

Objectives: Increased platelet activation plays an important role in the development of atherosclerosis. Mean platelet volume (MPV) is a determinant of platelet activation. In our study, we aimed to determine whether MPV levels are elevated in non-dipper patients compared with dippers and healthy controls. In addition, we tried to find out if MPV levels are correlated with blood pressure measurements in hypertensive patients., Methods: This cross-sectional study included 56 hypertensive patients; 27 age- and sex-matched healthy volunteers were enrolled to study as a control subjects. Ambulatory blood pressure monitoring was performed for all patients. Hypertensive patients were divided into two groups: 28 dipper patients (10 male, mean age 51 +/-8 years) and 28 non-dipper patients (11 male, mean age 53+/-10 years). MPV was measured in a blood sample collected in EDTA tubes and was also used for whole blood counts in all patients., Results: In non-dipper patients, 24-h systolic blood pressure (141.5+/-10.21 vs 132.3+/-7.7 mmHg, p<0.001), 24-h diastolic blood pressure (88.2+/-8.5 vs 81.0+/-8.2 mmHg, p<0.01) and 24-h average blood pressure (105.7+/-8.5 vs 97.7+/-7.4 mmHg, p<0.001) are significantly higher than dippers. Whereas daytime measurements were similar between dippers and non-dippers, there was a significant difference between each group during night-time measurements (night-time systolic 137.1 +/-11.0 vs 120.2+/-8.0 mmHg, p<0.001; night-time diastolic 85.3+/-8.0 vs 72.8+/-7.9 mmHg, p<0.001). Non-dipper patients (9.61 +/-0.42 fl) demonstrated higher levels of MPV compared with dippers (9.24+/-0.35 fl) and normotensives (8.87+/-0.33 fl) (p<0.001 and p<0.001, respectively). There was significant correlation between MPV and ambulatory diastolic and systolic blood pressure in non-dipper hypertensives., Conclusion: Our results suggest that MPV, a determinant of platelet activation, has a positively correlation with blood pressure and elevated in non-dipper compared with dippers and controls. Increased platelet activation could contribute to increase the atherosclerotic risk in non-dipper patients compared with dippers.

Objective: Non-dipper hypertensives had about three times the risk of atherosclerotic events than hypertensives whose blood pressure was >10% lower at night compared to daytime (dippers). Platelet activation and inflammatory response may derive from most atherosclerotic events. Mean platelet volume (MPV) is a determinant of platelet activation and high sensitive C-reactive protein (hs-CRP) is the best candidate assay to identify and monitor the inflammatory response. We aimed to determine whether MPV and hs-CRP levels are elevated in non-dipper patients compared to dippers and healthy controls. In addition, we tried to find out if MPV and CRP are related to each other or not in non-dipper hypertensives., Method: The total 126 patients study group included 86 patients with hypertension and 40 healthy subjects (16 male, mean age; 51+/-4) as control. Ambulatory blood pressure monitoring was performed for all patients. Hypertensive patients were divided into two groups; 46 dipper patients (18 male, mean age; 50+/-9) and 40 non-dipper patients (17 male, mean age; 53+/-11). Clinical baseline characteristics were similar between groups. We measured mean platelet volume in a blood sample collected in EDTA tubes and high-sensitive CRP was measured by using BN2 model nephlometer., Results: Non-dipper patients demonstrated higher levels of MPV compared to dippers and normotensives (9.72+/-0.52 fl vs 9.38+/-0.33 fl and 8.92+/-0.42 fl, p<0.05, respectively). High-sensitive CRP levels were also significantly higher in non-dippers compared to dippers and normotensives (4.9+/-1.7mg/l vs 3.8+/-1.5mg/l and 2.7+/-0.8mg/l, p<0.05, respectively). There was significant positive correlation between MPV and CRP levels (p=0.002, r=0.482) in non-dipper hypertensives., Conclusion: Our results suggest that patients with non-dipping tend to have increased platelet activation and inflammatory response. Increased platelet activation and inflammatory response could contribute to increase the atherosclerotic risk in non-dipper patients compared to dippers.

Aim: The serotonin levels in thrombocytes are decreased in hypertensive patients. The aim of our study was to investigate the relationship between serotonin levels and insufficient nocturnal blood pressure (BP) decrease (non-dipper) in hypertensive patients., Patients and Methods: Fifty-six hypertensive patients and 27 healthy control subjects were included in the study. Of the hypertensive patients, 28 were classified as dippers and 28 as non-dippers based on nocturnal BP drops of >10 mmHg and <10 mmHg, respectively. Thrombocyte serotonin levels, serum uric acid, and C-reactive protein (CRP), and urinary albumin/creatinine ratios were analysed. Thrombocyte serotonin levels were measured using an enzyme immunoassay., Results: The thrombocyte serotonin level was 378.9 +/- 69.5 ng/10(9) platelet in the non-dipper group, 424.7 +/- 58.6 ng/10(9) platelet in the dipper group, and 518.1 +/- 35.9 ng/10(9) platelet in the control group. Serotonin levels in the non-dipper group were significantly lower than in the dipper group. Serotonin levels negatively correlated with blood pressure (r = -0.6, p<0.001). CRP concentration in the non-dipper group was higher than in the dipper (4.8 +/- 1.4 vs 3.6 +/- 1.6, p<0.01) and control (2.4 +/- 0.9, p<0.001) groups, and microalbuminuria was significantly higher in the non-dipper group compared with dipper (24.9 +/- 8.6 vs 13.4 +/- 8.8, p<0.001) and control (9.6 +/- 4.8, p<0.001) groups. Serotonin level was negatively correlated with microalbuminuria (p<0.001, r = -0.3), uric acid (p<0.01, r = -0.3), and CRP (p<0.01, r = -0.35)., Conclusion: In non-dipper hypertensive patients, thrombocyte serotonin levels were significantly lower than in dipper and control groups. Serotonin levels may be related to insufficient nocturnal blood pressure decrease in hypertensive patients.

Aortic dissection (AD) is a disease characterized by tear of the aortic intimal layer and separation of the arterial wall. Some risk factor such as hypertension and Marfan syndrome is well known in AD. However, the role of genetic factors in AD is largely unknown. Insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with cardiovascular diseases; patients with D allele have higher serum and tissue ACE levels. We investigated the relationship between the I/D polymorphism of the ACE gene and non-syndromic acute AD. Sixteen patients diagnosed with AD were included in the study (mean age: 60.1 ± 6.2 years). The diagnosis was established by clinical evaluation and imaging technique. The control group consisted of 22 age-matched patients without AD (60.9 ± 7.3 years), who suffered from chest pain. Incidence of hypertension was similar in dissection and control groups (62% vs 59%). The I/D polymorphism was investigated in both groups by PCR analysis. Dissection types according to the DeBakey classification were identified as type 1 (proximal + distal) in 7 patients (43%), type 2 (proximal) in 5 patients (31%), and type 3 (distal) in 4 patients (25%). The D/D and D/I polymorphisms are present in 13 and 3 AD patients, respectively. None of patients with AD have the II polymorphism. The frequencies of the D allele (DD + ID) are significantly higher in dissection group than control (100% vs 68%, P < 0001). These results indicate that the D allele of ACE gene is a risk factor for AD. [ABSTRACT FROM AUTHOR]