Saliva/serum ghrelin, obestatin and homocysteine levels in patients with ischaemic heart disease.

BACKGROUND: We aimed to compare ghrelin, obestatin, homocysteine (Hcy), vitamin B12 and folate levels in the serum and saliva of ischaemic heart disease patients. METHODS: Serum and saliva were collected from 33 ischaemic heart disease (IHD) patients and 28 age- and body mass index-matched healthy individuals. Levels of acylated and desacylated ghrelin, obestatin and Hcy were determined using the ELISA method. RESULTS: Acylated ghrelin, desacylated ghrelin and obestatin levels in the saliva were found to be higher than those in the serum of the control group, while acylated and desacylated ghrelin levels in the saliva were significantly lower than those in the serum. Obestatin levels were higher in IHD patients (p = 0.001). Saliva and serum vitamin B12 and folate levels in IHD patients were significantly lower than in the control group (p = 0.001). CONCLUSIONS: It was determined that serum ghrelin levels increased in ischaemic heart disease patients, while serum levels of obestatin decreased.

The Incidence and Related Risk Factors of Chronic Thromboembolic Pulmonary Hypertension after Acute Pulmonary Embolism.

OBJECTIVES: More than half of (> 50%) the patients with choronic thromboembolic pulmonary hypertension (CTEPH) have no acute pulmonary embolism history with clinical signs, so determining the actual incidence and prevalence of CTEPH is difficult. This study aimed to investigate the incidence of CTEPH and the risk factors that may be associated with CTEPH in patients with acute pulmonary thromboembolism (PTE). MATERIAL AND METHODS: Three hundred and eighteen patients with acute pulmonary embolism diagnosed by thorax CT or ventilation/perfussion scintigraphy in our clinic were included into this study. Patients with risk factors for pulmonary hypertension other than thromboembolic disease were excluded from the study. Patients with pulmonary hypertension (PHT) (systolic PAB > 35 mmHg) determined by echocardiography performed in the 6th month were enrolled into the study. RESULTS: Fifty-seven of the 112 patients were female, and the mean age was 57.09 ± 17.30 (16-86) years. Presence of PHT was determined in the 6th month in 45 of the 112 patients (8 of them were symptomatic) and CTEPH incidence (symptomatic + asymptomatic) was identified as 40.16%. Symptomatic CTEPH incidence was calculated as 7.14%. When we searched about the risk factors that may have a role in the development of CTEPH; we determined that CTEPH risk was increased 4.59 times by only being male (95% CI 1.071-19.683, p= 0.040), 218 times by previous history of DVT (95% CI 1.235-38543.073, p= 0.041), and 56.903 times by PaO2 < 80 mmHg (95% CI 2.656-1219.228, p= 0.010). CONCLUSION: CTEPH development after PTE is a situation that can occur in many patients. If probable risk factors are known, patients can be closely monitorized for CTEPH development.

QT interval dispersion in the patients with central serous chorioretinopathy.

AIM: To evaluate QT dispersion (QTD) in patients with central serous chorioretinopathy (CSC). METHODS: This clinical, comperative, case-control study included 30 patients with CSC at acute phase (Group 1) and 30 age- and sex-matched healthy subjects (Group 2, the control group). From all subjects, a 12-lead surface electrocardiography was obtained. The heart rate (HR), QT maximum (QTmax), QT minimum (QTmin), QT corrected (QTc), QTD and Tmean were manually measured and analyzed. Student's t-test and Pearson's method of correlation were used for statistical analysis. RESULTS: The patient and control groups were matched for age, smoking status (rate and duration) and gender. There were no significant differences with regard to these among the groups (P>0.05). The participants included 19 men (63.3%) and 11 women (36.7%) in Group 1, 20 men (66.7%) and 10 women (33.3%) in Group 2. QTmax, QTD and QTc were significantly higher than those of healthy controls (P<0.001 for QTmax, P=0.01 for QTD and P=0.001 for QTc). QTmin, Tmean and HR did not differ significantly between the study groups (P=0.28 for QTmin, P=0.56 for Tmean and P>0.05 for HR). No significant correlation was found between duration of the disorder and QTD values (r=0.13, P>0.05). CONCLUSION: These findings suggest that CSC may be associated with an increase in QTD and that the patients might be at risk for ventricular arrhythmia.

The effect of acute allergic reactions on diastolic heart function.

PURPOSE: Diastolic heart failure is characterized by the presence of heart failure symptoms despite preserved systolic function. Cytokines released during allergic reactions may impair diastolic heart function, either through their direct toxic effects or by inducing coronary artery spasm. The purpose of this study was to examine the effects of acute allergic reactions on diastolic heart function. METHODS: Fifty patients, randomly selected from those who were admitted to the emergency room between May 2010 and December 2010 with the complaints of rash and itching, and who were subsequently diagnosed with allergic reactions based on the clinical and laboratory findings, were included in the study as the allergy group. Thirty healthy volunteers, in whom the diagnosis of allergy was ruled out based on the clinical and laboratory data, were use as the control group. Diastolic heart functions were evaluated in patients presenting with allergic reaction as well as in control subjects. RESULTS: There was no significant difference between the two groups in terms of basal systolic functions, diameters of the cavities and wall thicknesses, and biochemical parameters. Color M mode flow progression velocities, E ratios, E/A ratios and mitral lateral annulus tissue Doppler velocities measured by echocardiography at Day 0 and Day 5 were significantly altered in the allergy group (p < 0.05). CONCLUSION: Impairment in diastolic functions was observed following acute allergic reactions. Acute allergic reactions could be a cause of mortality and morbidity if they lead to the development of diastolic heart failure.

Relationship between mean platelet volume elevation and left ventricular mass index in hypertensive patients.

OBJECTIVES: To compare the mean platelet volume (MPV; a general marker of platelet activation) in groups of patients with and without hypertension and to analyse its relationship with left ventricular mass index (LVMI). METHODS: This cross-sectional, observational study enrolled newly diagnosed patients with untreated stage I-II hypertension and healthy control subjects without hypertension. MPV was measured using a haematology analyser. Echocardiography was performed on all of the study participants. RESULTS: A total of 50 newly diagnosed patients with hypertension and 50 healthy control subjects were enrolled in the study. The majority of the demographic characteristics and laboratory findings were not significantly different between the two groups. The mean ± SD MPV was significantly higher in the hypertensive group compared with the control group (10.3 ± 1.4 fl versus 9.2 ± 1.8 fl, respectively). The mean ± SD LVMI was significantly higher in the hypertensive group compared with the control group (115.9 ± 23.0 g/m(2) versus 95.7 ± 23.4 g/m(2), respectively). There was no significant correlation between MPV and LVMI. CONCLUSION: In patients with untreated hypertension, despite elevated MPV levels there was no correlation between LVMI and MPV.

Twenty four hour imaging delay improves viability detection by Tl-201 myocardial perfusion scintigraphy.

OBJECTIVE: Since twenty-four-hour imaging by Tl-201 myocardial perfusion scintigraphy has been introduced as an effective additional procedure, the aim of this study was to compare this method's result with only rest redistribution procedure in the diagnosis of myocardial viability. METHODS: Thirty patients (Seven female, 23 male; mean: 59.8 ± 10.7, 55.8-63.8 years old) with diagnosis of coronary artery disease were involved in this study. All patients had anamnesis of previous myocardial infarction and/or total occlusion of any main artery in the coronary angiography. Myocardial perfusion scintigraphy with Tl-201 with rest four hour (early) redistribution and 24 hour delayed redistribution protocol were performed to all of the patients. The images were evaluated according to 17 segment basis by an experienced nuclear medicine physician and improvement of a segment by visual interpretation was considered as viable myocardial tissue. RESULTS: Viability was found at 52 segments in the early redistribution images and additional 18 segments in the 24 hour delayed redistribution images on segment basis in the evaluation of 510 segments of 30 patients. On per patient basis, among the 26 patients who had viable tissue, 14 (54%) had additional improvement in 24 hour delayed images. Three (12%) patients had viable tissue in only 24 hour delayed images. CONCLUSION: Delayed imaging in Tl-201 MPS is a necessary application for the evaluation of viable tissue according to considerable number of patients with additional improvement in 24 hour images in our study, which is restricted to the patients with myocardial infarct.

The investigation of serum vaspin level in atherosclerotic coronary artery disease.

BACKGROUND: It was speculated that fatty tissue originated adipocytokines may play role in pathogenesis of atherosclerosis. These adipocytokines may alter vascular homeostasis by effecting endothelial cells, arterial smooth muscle cells and macrophages. Vaspin is a newly described member of adipocytokines family. We aimed to investigate whether plasma vaspin level has any predictive value in coronary artery disease (CAD). METHODS: Forty patients who have at least single vessel ≥ 70 % stenosis demostrated angiographically and 40 subjects with normal coronary anatomy were included to the study. The vaspin levels were measured from serum that is obtained by centrifigation of blood and stored at -20 (o)C by ELISA method. The length, weight and body mass index of patients were measured. Biochemical parameters including total cholesterol, low density lipoprotein, high density lipoprotein, creatinine, sodium, potassium, hemoglobine, uric acid and fasting glucose were also measured. RESULTS: Biochemical markers levels were similar in both groups. Serum vaspin levels were significantly lower in CAD patients than control group (respectively; 256 ± 219 pg/ml vs. 472 ( 564 pg/ml, P < 0.02). Beside this serum vaspin level was lower in control group with high systolic blood pressure. CONCLUSION: Serum vaspin levels were found significantly lower in patients with CAD than age-matched subjects with normal coronary anatomy. Vaspin may be used as a predictor of CAD. KEYWORDS: Coronary artery disease; Vaspin; Adipokine.

Serum salusin-alpha level in rheumatoid arthritis.

Rheumatoid arthritis (RA), a chronic inflammatory disease, leads to early and accelerated atherosclerosis; however, its pathogenesis is not yet fully documented. Salusin-α and ß are novel bioactive peptides. Salusin-α suppresses macrophage foam cell formation, while salusin-ß stimulates. Moreover, decreased serum salusin-α level has been reported previously in patients with coronary artery disease. The aims of the study were to assess serum salusin-α level and its association with predictors of atherosclerosis in a cohort of patients with RA. The study included 56 RA patients, 37 Behcet's disease (BD) patients, and 29 healthy controls (HC). TNF-α, IL-6 and salusin-α levels, homeostasis model assessment (HOMA-IR) index and common carotid intima-media thickness (IMT) were determined. In the RA and BD groups, salusin-α levels (p<0.001 and p<0.01, respectively) and IMTs (p<0.001 for both) were higher compared to the HC group. However, the level of salusin-α was not directly associated with the IMT in all the groups. Serum salusin-α levels are increased in RA and BD, although they have increased IMT. Salusin-α has been reported to have anti-atherogenic effects in previous studies. However, it seems that salusin-α does not directly affect the atherogenesis in RA and BD. Further studies are needed to understand the regulation of salusin-α and determination of its relations with the predictors of atherosclerosis in RA and BD.

Visfatin levels and intima-media thicknesses in rheumatic diseases.

Chronic inflammatory rheumatic diseases lead to increased prevalence of atherosclerosis. However, this early and accelerated atherosclerosis cannot be explained by traditional cardiovascular risk factors alone. The permanent overexpression of cellular adhesion molecules and pro-inflammatory cytokines in chronic inflammatory conditions may participate in accelerated atherosclerosis. Visfatin, a novel adipocytokine, has a potential insulin-like action and pro-inflammatory effects. Therefore, the aim of the study was to determine serum visfatin level and its association with common carotid intima-media thickness (IMT), which is a predictor of atherosclerosis, in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), and Behçet's disease (BD). The study involved 29 RA, 26 SLE, 25 SSc, 30 BD patients, and 29 healthy controls (HC). Serum levels of TNF-α, IL-6, and visfatin were analyzed using enzyme-linked immunosorbent assay method and homeostasis model assessment for insulin resistance (HOMA-IR) indexes, and IMTs were determined. Serum visfatin level was higher in the RA group than all the other groups. In addition, visfatin level was higher in the active BD subgroup than the inactive BD subgroup. In the study groups, visfatin levels were not correlated with HOMA-IR indexes and IMTs. Whereas visfatin serum concentration was not associated with insulin resistance and carotid atherosclerosis in selected rheumatic diseases, it was higher in the RA and active BD groups, but not in the SLE and SSc groups. Visfatin levels may be associated with Th1/Th2 balance. Further studies are needed for more precise elucidation of the pro-inflammatory activities of visfatin.

Serum adiponectin and vaspin levels in rheumatoid arthritis.

BACKGROUND AND AIMS: The risks of insulin resistance and accelerated atherosclerosis are increased in chronic inflammatory diseases including rheumatoid arthritis (RA). Adipo-(cyto)kines are associated with insulin resistance, atherosclerosis and inflammation. This study aimed to determine serum adiponectin and vaspin levels and their associations with the predictors of atherosclerosis in RA and Behcet's disease (BD). METHODS: The study involved 56 patients with RA, 37 patients with BD, and 29 healthy controls (HC). Serum adiponectin and vaspin levels, homeostasis model assessment for insulin resistance (HOMA-IR) index, and common carotid intima-media thickness (IMT) were determined. RESULTS: Serum adiponectin levels in both patient groups and serum vaspin level in only the RA group were higher, whereas serum vaspin level was lower in the active BD subgroup, compared to the HC group. However, adiponectin and vaspin levels were correlated with neither HOMA-IR index nor IMT in the RA group. Adiponectin level was correlated with DAS-28 and IL-6 level in the RA group, and it was higher in the active BD subgroup than in the inactive BD subgroup and the HC group. CONCLUSIONS: Adiponectin and vaspin levels are higher in RA but associated with neither HOMA-IR index nor IMT. Adiponectin is related with disease activity remarks in RA and BD. Therefore, it may be suggested that adiponectin may be involved in the regulation of inflammatory responses in inflammatory diseases. Moreover, in contrast to in RA, vaspin level declines in active BD, and these results suggest that different chronic inflammatory diseases exert different influences on either adipokines.

[Percutaneous closure of two atrial septal defects with individual septal occluder devices]. / Iki adet atriyal septal defekti olan bir olguda ayri cihazlarla perkütan kapama.

A 20-year-old male patient presented with dyspnea and palpitation. An atrial shunt was detected on transthoracic echocardiography. Transesophageal echocardiography (TEE) showed two secundum atrial septal defects (ASD), 13 mm and 15 mm in size, respectively. There was no other congenital heart disease. During right heart catheterization, pulmonary artery pressure was 40 mmHg and the Qp/Qs ratio was 1.9. His coronary arteries were normal. The patient underwent elective percutaneous ASD closure under general anesthesia and continuous TEE monitoring. The distance between the two defects was 16 mm. Two 25-mm PTS sizing balloon catheters were simultaneously inflated, yielding maximum defect diameters of 13 mm and 15 mm. First the smaller defect, then the larger defect were closed with 15 mm and 18 mm Occlutech Figulla ASD occluders, respectively. Total fluoroscopy time was 25 min, and total procedural time was 95 min. No residual shunt was observed. The patient was discharged the next day without any complication.

Is inflammatory bowel disease a risk factor for early atherosclerosis?

OBJECTIVES: Chronic inflammatory diseases are associated with an accelerated atherosclerotic process. Recent studies have discussed whether inflammatory bowel diseases (IBDs) can predict early atherosclerosis. We investigated this possibility. METHODS: The study consisted of IBD cases (group 1, n = 40) and healthy persons (group 2, n = 40). The IBD group was selected so as not to have vascular disease or the presence of established major cardiovascular risk factors. RESULTS: Group 1 cases showed a significant increase in carotid intima media thickness (cIMT; P = .01). Carotid artery stiffness was impaired in group 1 (P = .03) and high-sensitivity C-reactive protein (hsCRP), homeostasis model assessment of insulin resistance (HOMA-IR), and homocysteine (Hyc) were higher in group 1 patients (P = .02, P = .03, P = .05). CONCLUSIONS: Inflammatory bowel disease patients have an increased risk of early atherosclerosis as shown by greater values of cIMT, carotid artery stiffness, Hyc, hsCRP, and insulin resistance.

Adiponectin levels in coronary artery ectasia.

Etiopathogenesis of coronary artery ectasia (CAE), which is defined as abnormal dilatation of a segment of the coronary artery to 1.5 times of an adjacent normal coronary artery segment, is unclear. However, it is speculated that CAE develops in the atherosclerosis process through degeneration of coronary artery media layer. Our objective in this study is to compare levels of adiponectin between cases with CAE and normal coronary anatomy, and to examine whether adiponectin plays a role in CAE etiopathogenesis. The study registered a total of 66 cases, consisting of CAE cases (group 1, n = 36) and cases with normal coronary anatomy (group 2, n = 30). Taking coronary artery diameters of the control group cases as the reference, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. Serum adiponectin levels were 4.31 +/- 2.02 microg/ml in group 1 and 6.73 +/- 4.0 microg/ml in group 2 (P = 0.02). High-sensitivity C-reactive protein was 4.8 +/- 3.8 mg/l in group 1 and 3.6 +/- 3.4 mg/l in group 2 (P > 0.05). There was a negative correlation between ectatic coronary artery diameter and plasma adiponectin level (P = 0.03; r = -0.339). It was known that adiponectin levels dropped in atherosclerotic heart disease. In this study we found low plasma adiponectin levels in acquired CAE, attributed to atherosclerosis. Therefore, we think that adiponectin might be playing a role in etiopathogenesis and progression of CAE. This in turn may indicate that hypo-adiponectinemia may be useful in revealing a realized risk in CAE. However, larger, randomized, multicenter studies are required to examine the role of adiponectin in the development of CAE.

Insulin resistance is related with oxidative stress in systemic lupus erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) patients have increased risk of coronary heart disease (CHD) that cannot be fully explained by the traditional risk factors. Metabolic alterations like oxidative stress and insulin resistance may be additional risk factors to contribute early and accelerated atherosclerosis in SLE. Our aim was to evaluate malondialdehyde (MDA) level, oxidative stress indicator, and homeostasis model assessment of insulin resistance (HOMA-IR), and possible relationship between oxidative stress and insulin resistance, in SLE. METHODS: This cross-sectional controlled study included 30 SLE patients (SLE group) and 15 age- and sex-matched healthy controls (HC group). The SLE patients were classified into subgroups based on the disease activity index as active or inactive. Serum MDA, insulin, C-peptide, fasting blood glucose, lipid profile, acute phase reactants, tumor necrosis factor (TNF)-a, interleukin (IL)-6 and HOMA-IR were determined. Statistical analyses were performed using Kruskal-Wallis, Mann-Whitney U and Pearson tests. RESULTS: In the SLE group, TNF-a (7.9 [0.5-57.8] vs. 3.9 [0.3-6.3] pg/ml, p<0.01), IL-6 (9.2 [0.1-33.9] vs. 2.2 [0.1-4.8] pg/ml, p<0.01), MDA (2.3 [0.1-6.7] vs. 0.95 [0.5-2.96] nmol/ml, p<0.01) and C-peptide (1.9 [0.9-3.5] vs. 1.5 [1.1-2.4] ng/ml, p<0.01) levels were higher than in the HC group, while HOMA-IR index (1.7 [0.5-6.5] vs. 1.2 [0.8-2.9], p>0.05) was nonsignificantly higher. In the SLE group, MDA levels were correlated with insulin (r=0.614, p<0.05) and HOMA-IR (r=0.601, p<0.05). CONCLUSION: In inflammatory diseases, relations between oxidative stress and insulin resistance, each of them triggers or enhances the other one, come to an impasse. In conclusion, this modifiable impasse might be important to prevent the development of atherosclerosis in SLE.

The effect of rapid blood pressure control on P-wave dispersion in hypertensive urgency.

INTRODUCTION: A sharp increase in blood pressure, increase in atrial pressure and atrial strain, left ventricular diastolic dysfunction, and left ventricular hypertrophy (LVH) lead to heterogeneity and instability in atrial conduction. The resulting physiopathological situation may elevate maximum Pwave duration (P(max)) and P-wave dispersion (PWD) in electrocardiography. The objective of our study was to explore the effect of the sudden change in atrial hemodynamics on P(max) and PWD, which may indicate the risk of atrial fibrillation (AF) development in hypertensive urgency. METHODS: The study included patients diagnosed as hypertensive urgency (systolic blood pressure > or =180 mmHg, diastolic blood pressure > or =110 mmHg). Nitroprusside was started at a dose of 0.2 microg/kg/min, and the ensuing dose was arranged according to blood pressure. Echocardiography and electrocardiography were used to noninvasively measure changes in diastolic function and PWD and P(max), respectively. RESULTS: The study enrolled 102 patients (mean age 57.9+/-11.6 years; 32 [31.4%] males, and 70 [68.6%] females). P(max) decreased from 99.9+/-11.1 msec (95% confidence intervals [CI] 97.7, 102) to 88.5+/-9.3 msec (95% CI 86.6, 90.3) (P<0.001), while PWD decreased from 60.1+/-7.4 msec (95% CI 58.7, 61.6) to 43.9+/-6.7 msec (95% CI 42.5, 45.2) (P<0.001). In addition, most patients had LVH and diastolic dysfunction. After nitroprusside treatment improvements in indicators of diastolic functions such as E/A ratio, deceleration time, and isovolumetric relaxation time were observed. CONCLUSION: The change observed in P(max) and PWD in hypertensive urgency may be associated with the rapid change in blood pressure and atrial strain, sympathetic nervous system activation, relative myocardial ischemia, and left ventricular diastolic dysfunction. Rapid regulation of blood pressure with nitroprusside brought about a marked decrease in P(max) and PWD in our patients. This improvement was interpreted as atrial conduction acquiring a stable and homogeneous character, which may reduce the risk of AF development in hypertensive urgency.

Obestatin is present in saliva: alterations in obestatin and ghrelin levels of saliva and serum in ischemic heart disease.

Ghrelin and obestatin are a single gene products and are a multiple functional peptides that regulates energy homeostasis, and food intake. In the present work, we studied the secretion of ghrelin and its co-secreted peptide obestatin in 44 patients with ischemic heart disease with that of 27 healthy matched controls. Here we first conducted using an immunohistochemistry assay to screen whether human salivary glands have any obestatin immunoreactivity. Then, serum and saliva obestatin and acylated ghrelin levels were determined by using Radioimmunoassay. Our immunohistochemical analysis demonstrated that obestatin was localized in the striated and excretory duct of human salivary gland. We also report for the first time that obestatin, like ghrelin, is present in human salivary gland and saliva. No evidence of the role of obestatin or ghrelin saliva levels in the context of ischemic heart disease was found. Salivary ghrelin and obestatin levels are correlated in controls with the blood levels. Determination of salivary values could represent a non-invasive alternative to serum ones that can be useful in clinical practice.

Are maximum P wave duration and P wave dispersion a marker of target organ damage in the hypertensive population?

BACKGROUND: High blood pressure, left ventricular hypertrophy and diastolic dysfunction may cause hemodynamic and morphological changes in the left atrium, consequently instability and heterogeneity in atrial conduction. This is seen as an increase in maximum P wave duration (P(max)) and P wave dispersion (PD) on the electrocardiogram (ECG). P wave dispersion on ECG has been encountered as a risk factor for atrial fibrillation (AF). The aim of this study is to examine whether PD and P(max) can be used as a non-invasive marker of target organ damage (LVH and diastolic dysfunction) in a hypertensive population. MATERIAL AND METHODS: The study registered a total of 120 cases (mean age 46.9 +/- 10.6 years; 58 [48.3%] males and 62 [51.7%] females), of whom 60 were patients diagnosed as essential hypertension (group 1), and 60 were healthy individuals, who constituted the control group (group 2). Systolic and diastolic functions of all cases were evaluated by echocardiography, and maximum P wave duration (P(max)), and PD was calculated. RESULTS: Maximum P wave duration was 91.6 +/- 10.2 ms in group 1, and 64 +/- 10.2 ms in group 2 (p < 0.01), while PD was 56.1 +/- 5.8 ms in group 1, and 30.3 +/- 6.6 ms in group 2 (p < 0.01). Blood pressure, left atrium diameter, DT, IVRT, and E/A ratio, as well as left ventricular mass index increased markedly in group 1. CONCLUSION: High blood pressure, LVH, diastolic dysfunction and increased left atrium diameter and volume shows parallelism in hypertensive cases. These physiopathological changes may cause different and heterogeneous atrial electrical conduction. This led to a marked increase in P(max) and PD in our cases. Thus, the results support the hypothesis that PD can be used as a non-invasive marker of target organ damage (LVH and LV diastolic dysfunction) in the hypertension population.

B-type natriuretic peptide level in the diagnosis of asymptomatic diastolic dysfunction.

OBJECTIVE: Brain natriuretic peptide (BNP) reflects the left ventricular pressure and volume overload. It is known that it increases in systolic dysfunction proportionally with left ventricular pressure increase. The BNP levels are well correlated with NYHA classification and prognosis. Our aim was to evaluate the predictive value of BNP in patients with diastolic dysfunction but normal systolic dysfunction demonstrated by echocardiography. METHODS: Fifty patients (mean age: 48.5+/-6.75 years; 29 males, 21 females) were included in this cross-sectional, case-controlled study. Systolic dysfunction was the exclusion criterion. The following parameters were used to evaluate diastolic function: isovolumetric relaxation time, transmitral early to late filling flow velocities (E/A) ratio, deceleration time E, pulmonary vein Doppler findings and color mitral flow propagation velocity. Diastolic dysfunction was determined in 30 hypertensive patients (Group 1), whereas 20 patients who had normal diastolic flow patterns on echocardiography (Group 2). Blood samples were taken for serum BNP level measurements. RESULTS: The BNP levels were 12.0+/-4.97 pg/ml in individuals with normal filling pattern and 66.17+/-17.56 pg/ml in individuals with abnormal filling patterns (p<0.001). The accuracy of BNP in detection of diastolic dysfunction was assessed with receiver-operating characteristic (ROC) analysis. The area under the ROC curve for BNP test accuracy in detection any abnormal diastolic dysfunction was 0.969 (95% CI, 0.909 to 1.029; p<0.001). A BNP value of 37.0 pg/ml had sensitivity of 80%, specificity of 100%, a positive predictive value of 100%, a negative predictive value of 23% and accuracy of 88% in identifying asymptomatic prolonged relaxation pattern. We found a strong correlation between left ventricular mass index and plasma BNP levels (r=0.62, p<0.05). CONCLUSION: Estimation of BNP values could be accepted as a fast and reliable blood test in the diagnosis of asymptomatic diastolic dysfunction.

The effects of high dose pravastatin and low dose pravastatin and ezetimibe combination therapy on lipid, glucose metabolism and inflammation.

OBJECTIVE: Coronary artery disease (CAD) is presently the major cause of mortality and morbidity. Anti-hyperlipidemic treatment is one of the main treatment steps in the management of CAD. Statins are the cornerstones in this treatment. Ezetimibe can be reliably used, when statins prove ineffective in treatment, or to reduce their side effects. In the present study we examined the effects of high-dose pravastatin (40 mg) and low-dose pravastatin (10 mg) + ezetimibe (10 mg) combination therapy on lipid and glucose mechanism, as well as inflammation. METHODS: This study registered 100 cases. Of the cases, 50 [57.1 +/- 11.1 years (24 (48%) females and 26 (52%) males)] were administered 40 mg/day pravastatin (group 1) and 50 [53.2 +/- 12.2 years (27 (54%) females and 23 (46%) males)] were administered 10 mg pravastatin + 10 mg ezetimibe (group 2). RESULTS: In group 1, total cholesterol fell from 231.1 +/- 83.5 mg/dl to 211.3 +/- 37.2 mg/dl (p = 0.03), triglyceride from 243.5 +/- 96.8 mg/dl to 190.9 +/- 55.2 mg/dl (p = 0.003), and LDL cholesterol from 165.7 +/- 29.7 mg/dl to 133.4 +/- 26.6 mg/dl (p = 0.02). In group 2, total cholesterol dropped from 250.9 +/- 51.8 mg/dl to 187.9 +/- 34.9 mg/dl (p = 0.001), triglyceride from 270.3 +/- 158.9 mg/dl to 154.6 +/- 60.7 mg/dl (p = 0.001), and LDL cholesterol from 158.1 +/- 47.5 mg/dl to 116.9 +/- 26.4 mg/dl (p = 0.001). Insulin resistance decreased from 4.05 +/- 2.31 to 3.16 +/- 1.90 (p = 0.07) in group 1 and from 2.96 +/- 1.50 to 2.05 +/- 0.55 (p = 0.009) in group 2. High sensitive C-reactive protein fell from 6.69 +/- 6.11 mg/l to 3.02 +/- 1.70 mg/l (p = 0.01) in group 1 and from 6.36 +/- 2.06 mg/l to 2.68 +/- 1.69 mg/l (p = 0.001) in group 2. CONCLUSION: Both therapy regimes are effective. However, we found that low-dose pravastatin and ezetimibe combination therapy is more effective than high-dose pravastatin therapy on lipid metabolism, glucose metabolism and inflammation.

P-wave dispersion in panic disorder.

BACKGROUND: P-wave dispersion (PWD) is defined as the difference between the maximum and the minimum P-wave (Pmax and Pmin, respectively) duration. Significant variation in cardiac atrial PWD has been correlated with changes in systemic autonomic tone such as during periods of anxiety. It is also known that the degree of PWD seen on 12-lead electrocardiogram (ECG) may be a predictor of susceptibility of the atrial myocardium to future atrial fibrillation (AF). Therefore, we firstly aimed to show an association between PWD and panic disorder, a state of high sympathetic tone. METHODS: PWD was measured in 40 outpatients with panic disorder and in 40 physically and mentally healthy age- and gender-matched controls. In addition, the Panic Agoraphobia Scale (PAS) and the Hamilton Depression Rating Scale (HDRS) were scored concomitantly. RESULTS: Both Pmax and Pmin were significantly higher than those of healthy controls. PWD was significantly greater in the panic disorder group than in the controls. As expected, the mean score on PAS was significantly higher for the panic disorder group than for the controls and correlated significantly with PWD. Heart rate (measured as RR intervals in milliseconds on electrocardiogram) did not differ significantly between the groups. CONCLUSIONS: The findings of the present study suggest that the disorder may be associated with an increase in PWD. This association may result from prolonged anxiety and increase in sympathetic modulation, which are main characteristics of panic disorder.