Endocan, a novel marker of endothelial dysfunction in patients with essential hypertension: comparative effects of amlodipine and valsartan.

Vascular inflammation plays an important role in the pathophysiology of hypertension and high levels of endocan may reflect ongoing vascular inflammation in hypertensive patients. In the present hypothesis-generating study, we aimed at investigating the comparative effects of amlodipine and valsartan on endocan levels in newly diagnosed hypertensive patients. The study population consisted of 37 untreated hypertensive patients who were randomized to the two treatment arms. After baseline assessment, each patient was randomly allocated to either 10 mg daily of amlodipine (n = 18, 7 males) or 160 mg daily of valsartan (n = 19, 3 males) and treated for a 3-month period. Sphygmomanometric blood pressure (BP) and serum endocan were measured before and every 2 weeks during drug treatment. There was no statistically significant difference between the two treatment arms as far as baseline socio-demographic and clinical characteristics are concerned. After a 3-month treatment period, systolic and diastolic BP values significantly reduced by antihypertensive treatment (p < 0.001). Furthermore, endocan levels were significantly decreased in both treatment arms (p < 0.05). However, amlodipine caused a greater percent decrease in circulating endocan levels compared with valsartan at the end of the treatment period. Both drugs reduced high sensitivity C-reactive protein values. However, the statistical significant difference vs baseline was achieved only in the group treated with amlodipine. No correlation was found between endocan plasma levels and BP reduction. The results of this hypothesis-generating study suggest that amlodipine and valsartan decrease endocan levels in newly diagnosed hypertensive patients. The effects, which are more evident with amlodipine, may contribute to the anti-inflammatory effects exerted by the two drugs on the vascular target.

Serum endocan levels as a marker of disease activity in patients with Behçet disease.

BACKGROUND: Endocan is a novel human endothelial cell-specific molecule. The central role of leukocytes and endothelial dysfunction in the development of Behçet disease (BD) led us to hypothesize that endocan might be a marker of this disease. OBJECTIVE: We investigated the relationship between serum levels of endocan and disease activity in patients with BD. METHODS: In all, 33 patients (16 active, 17 inactive) with BD and 35 healthy persons were included in the study. Endocan and C-reactive protein were measured in all subjects. RESULTS: Patients with BD had significantly higher serum endocan levels. Mean serum levels of endocan were 1.29 ± 0.60 ng/mL (range: 0.58-2.99) in patients with BD and 0.75 ± 0.16 ng/mL (range: 0.48-1.21) in control subjects (P < .001). In patients with BD, serum endocan levels correlated moderately but significantly with C-reactive protein, erythrocyte sedimentation rate, and disease activity. Receiver operating characteristic curve analysis suggested that the optimum endocan level cut-off point for patients with BD was 0.87 ng/mL, with a sensitivity and specificity of 75.8% and 80%, respectively (area under curve 0.835, 95% confidence interval 0.738-0.932). LIMITATIONS: The main limitation of our study is the relatively small sample size. CONCLUSIONS: Circulating endocan may be a marker of BD activity.

Why aortic elasticity differs among classical and non-classical mitral valve prolapsed?

BACKGROUND: Mitral valve prolapse (MVP) is the most common valvular heart disease and characterized by the displacement of an abnormally thickened mitral valve leaflet into the left atrium during systole. There are two types of MVP, broadly classified as classic (thickness ≥5 mm) and non-classic (thickness <5 mm) according to the morphology of the leaflets. We aimed to investigate elastic properties of the aorta in young male patients with classical and non-classical MVP. MATERIAL/METHODS: In the present study, 63 young adult males (mean age: 22.7 ± 4.2) were included. Patients were divided into classic MVP (n = 27) and non-classic MVP (n = 36) groups. Aortic strain, aortic distensibility and aortic stiffness index were calculated by using aortic diameters obtained by echocardiography and blood pressures measured by sphygmomanometer. RESULTS: There was no significant difference between the groups in terms of age, body mass index, left ventricular mass and ejection fraction. When comparing the MVP group it was found that aortic strain and aortic distensibility were increased (p = 0.0027, p = 0.016, respectively) whereas the aortic stiffness index was decreased (p = 0.06) in the classical MVP group. CONCLUSION: We concluded that the elastic properties of the aorta is increased in patients with classic MVP. Further large scale studies should be performed to understand of morphological and physiological properties of the aorta in patients with MVP.

The relationship between microalbuminuria, left ventricular hypertrophy, retinopathy, and sex hormone status in newly diagnosed hypertensive women.

An increased incidence of hypertension (HT) in postmenopausal female population has been shown in previous studies and this has been ascribed to an association with altered status of estrogen (E2) and other female sex hormones. Hypertension is associated with certain target organ damage (TOD) and related clinical conditions. The aim of this study was to determine the relationship between microalbuminuria, left ventricular hypertrophy (LVH), retinopathy, and sex hormone status in newly diagnosed hypertensive women. A total of 66 hypertensive women (39 postmenopausal and 27 premenopausal) were included in the study. Along with the tests recommended in the HT guidelines, LVH, hypertensive retinopathy, and microalbuminuria were investigated in all the patients. Sex hormones (follicle stimulating hormone, luteinizing hormone, progesterone, and E2) of the patients were also measured. The results show that there was no statistically significant difference between the two groups in regard to TOD except microalbuminuria. The frequency of microalbuminuria in premenopausal group patients was higher than that of the postmenopausal group patients (P = .038). This study suggests that TOD caused by HT is a very important health problem, seeming to be related with female sex hormones.

The relationship between some of the cardiovascular risk factors and arterial stiffness parameters in essentially hypertensive patients.

Hypertensive patients have strong evidence of endothelial dysfunction. We aimed to explore the relationships between cardiovascular risk factors and arterial stiffness parameters in hypertensive patients. The study population included 109 hypertensive patients (63 females, 46 males). Arterial stiffness measures including pulse wave velocity, augmentation index, and central aortic pressure were applied. Augmentation index and central aortic pressure were found to be significantly higher (P < .001 and P = .03, respectively) in women. The higher augmentation index and central aortic pressure values were observed in women than in men. These data offer new evidences for the role of sex hormones in the pathogenesis of atherosclerosis in women.

Skinfold thickness as a predictor of arterial stiffness: obesity and fatness linked to higher stiffness measurements in hypertensive patients.

Hypertensive patients have strong evidence of endothelial dysfunction. Some novel endothelial dysfunction parameters such as pulse wave velocity (PWV), augmentation index (AIx), and central aortic pressure (CAP) have been investigated as predictive markers of atherosclerosis. It is well known that obesity has relationships with endothelial dysfunction and atherosclerosis. We aimed to investigate relationships between anthropometric measurements and arterial stiffness parameters in essentially hypertensive patients. The study population included 100 patients (56 females, 44 males) newly or formerly diagnosed as essentially hypertensive in an outpatient clinic. Arterial stiffness measurements, including PWV, AIx, CAP, and body mass index (BMI); waist circumference, hip circumference; waist/hip ratio; and triceps, biceps, subscapular, and suprailiac skinfold thicknesses were also applied to all the study patients. Then, the relationships between BMI, anthropometric measurements, and arterial stiffness parameters were investigated. The mean systolic arterial blood pressure of the study population was 135.85 ± 15.27 mm Hg and the mean diastolic arterial blood pressure of the study population was 84.17 ± 9.58 mm Hg. The parameters such as PWV, AIx, and CAP measured for arterial stiffness had correlations between BMI and different anthropometric measurements. The statistically significant correlations were present between PWV and triceps skinfold thickness (TST) (r = 0.377, P < .001) and it was also seen when regression analysis was performed (PWV = 6.41 + [0.072 × TST]; R(2) = 0.142, F[1-98] = 16.23, P < .001). Triceps skinfold thickness among these correlations may be used to estimate the carotid-femoral PWV, which is an indicator of subclinical organ damage due to hypertension.

The comparative effects of valsartan and amlodipine on vWf levels and N/L ratio in patients with newly diagnosed hypertension.

High levels of circulating Von Willebrand factor (vWf) and increased neutrophil to lymphocyte (N/L) ratio may reflect vascular inflammation in hypertensive patients. In present study, we aimed to investigate the effects of valsartan as an angiotensin II receptor antagonist and amlodipine as a calcium channel blocker on the vWf levels and N/L ratio in patients with essential hypertension. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 20 mean age = 51.85 ± 11.32 y) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 26 mean age = 49.12 ± 14.12 y). Endothelial dysfunction and vascular inflammation were evaluated with vWf levels and N/L ratio in hypertensive patients before treatment and after treatment in the 12th week. No statistically significant differences were found among the groups in terms of age, sex, and body mass index (BMI). There was a significant decrease in vWf levels (P < .001) and N/L ratio after treatment (P = .04, P < .001, respectively) in both the groups. Von Willebrand factor levels and N/L ratio are very important markers having a role in vascular inflammation and antihypertensive treatment with amlodipine and valsartan may improve cardiovascular outcomes by decreasing these biomarkers.

The comparative effects of valsartan and amlodipine on vascular microinflammation in newly diagnosed hypertensive patients.

Pentraxin 3 (PTX3) is a new candidate immunoinflammatory marker that has been reported to be associated with cardiometabolic risk factors. We aimed to investigate the effects of valsartan and amlodipine on the PTX3 and C-reactive protein (CRP) levels in patients with essential hypertension. Patients with a newly diagnosed essential hypertension were admitted to our internal medicine outpatient clinic. Patients were randomized to one of the following intervention protocols: calcium channel blocker (amlodipine, 5-10 mg/day) as group A (n = 22; mean age ± standard deviation [SD]: 52 ± 11 year) and angiotensine II receptor blocker (valsartan, 80-320 mg/day) as group B (n = 28; mean age ± SD: 50 ± 14 year). Endothelial dysfunction and systemic inflammation were evaluated with PTX3 and CRP. There was a significant decrease in the level of PTX3 after treatment in two groups (P < .05). Although there was a significant decrease in the level of CRP after treatment in amlodipine group, there was no significant decrease in the levels of PTX3 and CRP after treatment in two groups. There were no significant differences in the systolic and diastolic blood pressure reduction between the two treatment groups. In the treatment of hypertension, prior knowledge of the level of plasma PTX3 could be important in antihypertensive drug choice. C-reactive protein and PTX3 are the markers that have role in vascular inflammation and are found associated with the prognosis of cardiovascular outcomes in many trials. In our study, PTX and CRP levels were decreased when compared to baseline levels.

An additional LDL-lowering effect of amlodipine; not only an antihypertensive?

Hypertension is a modifiable risk factor for cardiovascular diseases and is associated with several metabolic disorders like dyslipidemia. Higher levels of triglyceride and low-density lipoprotein (LDL) are quite strong factors for the development of cardiovascular diseases. In this study, we investigated the effects of valsartan and amlodipine on the lipid profile in patients with newly diagnosed essential hypertension. We observed a beneficial effect of amlodipine on the lipid profile with a significant reduction of LDL compared to valsartan. In the treatment of hypertension, prior knowledge of the plasma cholesterol levels can be important in antihypertensive drug choice.

Amlodipine seems to be superior to valsartan in decreasing microalbuminuria in newly diagnosed hypertensive patients: a novel effect to be explained with hyperfiltration?

BACKGROUND: Microalbuminuria (MA) is common in hypertensive population and is a marker for endothelial dysfunction and a predictor of increased cardiovascular risk. A great body of data shows the importance of MA as a strong predictor of renal and cardiovascular disease (CVD) risk in hypertensive population. AIM: In this study, we aimed to compare the anti-albuminuric effects of an angiotensin II receptor antagonist, valsartan, with a calcium channel blocker, amlodipine, in newly diagnosed hypertensive patients. MATERIAL AND METHODS: Totally, 20 patients were recruited into the study. Patients were randomized to one of the following intervention protocols: An (a) angiotensin II receptor blocker (valsartan, 80-320 mg/day) or (b) calcium channel blocker (amlodipine, 5-10 mg/day), for 12 weeks immediately after baseline measurements. Ten patients were randomized into valsartan group and 10 patients into the amlodipine group. Twenty-four-hour urinary albumin excretion (UAE) levels of the patient groups were measured before treatment and on the 12th week. RESULTS: Patients of the two groups were matched for age and body mass index. In the amlodipine group, baseline urine microalbumin levels were higher compared to valsartan group, although the difference was not statistically significant (p = 0.082). At the 12th week, there was a significant decrease in urine microalbumin levels in the amlodipine group, but no significant change was observed in the valsartan group. CONCLUSION: Amlodipine seems to be superior to valsartan in decreasing UAE. To reduce cardiovascular risks, endothelial dysfunction, and microinflammation, these factors are taken into consideration while prescribing antihypertensive drugs in hypertensive patients.

Amlodipine increases vitamin D levels more than valsartan in newly diagnosed hypertensive patients: pointing to an additional effect on bone metabolism or a novel marker of inflammation?

Hypertension is a major challenge for public health. Appropriate antihypertensive treatment seem to provide a better life with lower morbidity and mortality rates. Another pathologic condition, osteoporosis, mainly affects postmenouposal women, and constitutes a growing body of risks after a particular age. As bone is a dynamic organ system that is directly related to calcium and phosphor metabolism, imbalance in these two parameters upon aging or menopause finally may lead to osteoporosis. Today, both osteoporosis and high blood pressure are major morbidities, especially in the elderly population. There are some intriguing results on the effects of antihypertensive agents on bone metabolism in the literature. In this study, we aimed to investigate the effects of widely used antihypertensive agents, valsartan and amlodipine on vitamin D levels in newly diagnosed hypertensive population. We found that amlodipine increased vitamin D levels significantly in patients with a newly diagnosed hypertension on a 12-week treatment duration compared to valsartan.

Nutritional anemia in reproductive age women with postadolescent acne.

CONTEXT: Postadolescent acne has been defined as the presence of acne beyond the age of 25 years. Postadolescent acne affects approximately 14% of women between the ages of 25 and 50 years. Namely, postadolescent acne usually occurs in women of reproductive age. Nutritional anemia occurs from an insufficient intake of nutrients such as iron, folate and vitamin B12. It is very common in women of reproductive age. Nutritional anemia causes irritability, apathy, fatigue, depressive symptoms and difficulty in concentration. The major etiological factor in adult acne can be increased levels of emotional stress, leading to increase in adrenal androgens. Thus, nutritional anemia may aggravate the lesions of acne by affecting the emotional status in women of reproductive age. OBJECTIVE: We aimed to investigate the relationship between postadolescent acne and nutritional anemia in this study. MATERIALS AND METHODS: The study population comprised of 52 patients with postadolescent acne and 52 healthy control subjects. Hemogram, vitamin B12, folate, serum iron, ferritin and total iron-binding capacity (TIBC) were measured. RESULTS: No significant differences were observed between both groups in hemoglobin, vitamin B12, serum iron, ferritin and TIBC levels. Serum folate levels were significantly decreased in postadolescent acne patients (p < 0.001). There were no significant correlations between hemoglobin, vitamin B12, folate, serum iron, ferritin and TIBC levels and acne severity. DISCUSSION AND CONCLUSION: We could not find any relationship between postadolescent acne and nutritional anemia in our study. However, serum folate levels were decreased in postadolescent acne patients. Prospective research studies are needed to clarify the role of nutrition in the pathophysiology of postadolescent acne. We think that nutritional interventions can be inexpensive, safe, easy to administer and generally acceptable to patients with postadolescent acne.

Three-dimensional echocardiographic imaging of biventricular false tendons mimicking hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is characterized by hypertrophy of the left ventricle, with variable clinical manifestations and morphologic and hemodynamic abnormalities. False tendons (FTs) are discrete, fibromuscular structures of varying length and thickness that tranverse either left and right ventricular cavities. Left and right ventricular FTs were giving a false impression of HCM. Misdiagnosis of HCM can lead to undue anxiety, unnecessary medication, and further evaluation. Three-dimensional (3D) transthoracic echocardiography is additive to conventional two-dimensional imaging in these patients in terms of 3D perspective and anatomically correct examination. We present a 32-year-old male who was misdiagnosed as asymetrical septal hypertrophy.

Parachute tricuspid valve in a patient with atrial septal defect detected by two- and three-dimensional echocardiography.

Atrioventricular valve parachute deformity was generally seen in the mitral position, which is called parachute mitral valve. Parachute deformity is also seen in the tricuspid position, but this has rarely been reported as sporadic cases. All of these cases were associated with other congenital defects, such as double outlet right ventricle, left to right shunt. We herein present two- and three-dimensional echocardiographic features of a parachute tricuspid valve in a patient with atrial septal defect and prominent eustachian valve.

The impact of mitral stenosis on left atrial function assessed by two-dimensional speckle tracking echocardiography.

AIMS: The aim of this study is to investigate the effect of mitral stenosis (MS) on left atrial (LA) function using two-dimensional speckle tracking echocardiography (2DSTE). METHODS AND RESULTS: The study subjects consisted of 52 patients with asymptomatic MS and 52 control subjects. LA function was assessed using prototype speckle tracking software and manual tracking method. Maximal LA volume (LAVmax) and minimal LA volume (LAVmin) and LA volume before atrial contraction (LAVpre-a) were measured. Using these volumes, LA reservoir, conduit and booster pump fuction parameters were calculated. Indexed LAVmax, LAVmin, and LAVpre-a measurements via speckle tracking were highly correlated with manual tracing methods in both groups. Expansion index (67.8 ± 36.4 vs. 148.3 ± 44.2), diastolic emptying index (37.7 ± 12.9 vs. 58.0 ± 8.5), passive emptying (37.3 ± 14.1 vs. 70.4 ± 10.4) and passive emptying index (13.3 ± 6.3 vs. 41.3 ± 10.6) were decreased significantly in MS patients (P < 0.001). In contrast active emptying index (62.6 ± 4.1 vs. 29.5 ± 10.1) increased in MS group (P < 0.001) while active emptying (28.1 ± 13.0 vs. 28.3 ± 6.9) remained same among both groups. CONCLUSIONS: This is the first study relating LA volumes and function assessed by 2DSTE to MS. 2D speckle tracking analysis of LA volume is relatively easy and provides more detailed information regarding the changes in LA volumes during the cardiac cycle.

Circadian variation of acute st segment elevation myocardial infarction by anatomic location in a Turkish cohort.

BACKGROUND: To evaluate the relationship between site of infarction (anterior vs. inferior) and circadian variation in patients with ST segment elevation myocardial infarction (STEMI) in a Turkish cohort. MATERIAL/METHODS: This restrospective study enrolled 465 patients (407 male, mean age 65±7 years) with STEMI. Patients were then categorised into 4 6-hour increments according to the time of day during which the symptoms began (12:00 AM-06:00 AM, 06:00 AM-12:00 PM; 12:00 PM-06:00 PM and 06:00 PM-12:00 AM hours). Characteristics of patients by site of infarction (anterior vs. inferior) were compared. RESULTS: The frequency of onset of acute anterior MI as determined by onset of pain demonstrated significant circadian variation among the 4 time periods, demonstrating bimodal peaks (afternoon and morning) and a trough between 06:00 PM to 06:00 AM. The incidence of occurrence of MI between 06:00 AM to 06:00 PM was 4.50 times that of the average frequency of the remaining 12 hours of the day. The frequency of onset of acute inferior MI as determined by onset of pain exhibited significant circadian variation among the 4 time periods, demonstrating bimodal peaks (midnight to 06:00 AM and 06:00 AM to noon) and a trough between noon to midnight. The incidence of occurrence of MI between midnight to noon was 4.25 times that of the average frequency of the remaining 12 hours of the day. CONCLUSIONS: Different circadian periodicity in the time of onset of STEMI was found regarding infarction site in a Turkish cohort. This may be related to genetic and/or demographic characteristics of the Turkish population.

Increased platelet activation in young patients with prehypertension.

Mean platelet volume (MPV) and sP-selectin levels are considered as indicators of platelet activation. In this study, we assessed platelet activation in prehypertensive patients by comparing MPV and sP-selectin levels of these patients with healthy conrols. The study population consisted of 25 newly diagnosed prehypertensive individuals (18 men, mean age = 34 ± 6 y) and 25 healthy control subjects (16 men, mean age = 33 ± 6 y) eligible for the current study. Blood pressure (BP) , lipid profile, plasma glucose, HOMA-IR values, sP-selectin levels, platelet counts, and MPV were measured in both groups. Other than systolic blood pressure (SBP) and diastolic blood pressure (DBP), baseline demographic characteristics of both groups were similar. No significant difference was found between the platelet counts of the two groups. Despite comparable platelet counts, platelet activation parameters were found significantly higher in the prehypertensives. Prehypertensives had larger a MPV value compared to that of the control group (8.24 ± 0.46 fl vs. 7.70 ± 0.64 fl; P = 0.001) and plasma sP-selectin levels were also significantly higher in the prehypertensive patients (163.60 ± 41.21 ng/ml vs. 132.80 ± 36.46; P = 0.007). Spearman correlation analysis revealed moderate positive correlation between SBP and platelet activation parameters (for SBP and MPV, r = 0.60, p = 0.001; for SBP and sP-selectin r = 0.51, p = 0.009). Prehypertension causes platelet activation as evidenced by increased MPV and plasma sP-selectin levels. Increased platelet activation might be related to increased vascular thrombotic risk in those patients.