Mehmet Balin

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

BackgroundHigh 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 (Pmax) 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 Pmax can be used as a non-invasive marker of target organ damage (LVH and diastolic dysfunction) in a hypertensive population.Material and methodsThe 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 (Pmax), and PD was calculated.ResultsMaximum 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.ConclusionHigh 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 Pmax 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.

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 Behcets 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.

Deficiency of a new protein associated with cardiac syndrome X; called adropin.

The pathophysiology of cardiac syndrome X (CSX) is still unclear, but most patients with CSX have endothelial dysfunction. It has been shown that adropin uniquely effects the regulation of endothelial function. The purpose of the study was to evaluate the role of adropin in CSX. Eighty-six consecutive cardiac syndrome X-diagnosed patients and 86 age-sex matched healthy subjects were enrolled into the study. Serum adropin levels, nitrite/nitrate levels were measured in each subject. The adropin levels were significantly lower in patients with CSX than healthy subjects (1.7 ± 0.8 ng/mL and 3.4 ± 1.8 ng/mL, respectively; P < 0.001). The BMI values of patients with CSX were significantly higher than control subjects (28.1 ± 2.4 kg/m(2) and 26.0 ± 3.7 kg/m(2) , respectively; P < 0.001). Plasma nitrite/nitrate levels were lower in patients with CSX than control subjects (15.9 ± 1.6 μmol/L vs. 25.4 ± 2.8 μmol/L, respectively; P < 0.001), and they have a significantly positive correlation with plasma adropin levels (r = 0.463, P < 0.001). In the multiple linear regression analysis, nitrite/nitrate levels, BMI, and adropin were found to be independent risk factors for CSX. A ROC curve is used to identify the ability of adropin levels to predict the cardiac syndrome X. The area under the ROC curve was 0.854 for adropin levels (P = 0.0001). The sensitivity and specificity values of adropin levels were 90.7 and 70.9%, respectively (cut-off value 2.73). In conclusion, lower serum adropin levels were associated with CSX. Adropin is an independent risk factor for CSX.

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. PWD = P-wave dispersion; Pmax = maximum P-wave duration; Pmin = minimum P-wave duration; HRV = heart rate variability; AF = atrial fibrillation; ECG = electrocardiogram; PAS = The Panic Agoraphobia Scale; HDRS = Hamilton Depression Rating Scale; ANS = autonomic nervous system; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders IV.

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 oC 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

The level of hs-CRP in coronary artery ectasia and its response to statin and angiotensin-converting enzyme inhibitor treatment.

Background/Aim. Coronary artery ectasia (CAE) was thought of as a variant of atherosclerosis. C-reactive protein (CRP) which is among the most sensitive markers of systemic inflammation, and elevation of systemic and local levels of this inflammatory marker which has been associated with an increased risk for cardiovascular disease in the obstructive coronary artery disease (O-CAD) are well known, but little was known in CAE. The anti-inflammatory effects of statins and the effect of angiotensin-converting enzyme (ACE) inhibitors on endothelial dysfunction are well established in atherosclerosis. The aim of the present study was to investigate CRP level and its response to statin and ACE inhibitor treatment in CAE. Materials and method. We measured serum hs-CRP level in 40 CAE (26 males, mean age: 56.32 ± 9 years) and 41 O-CAD (34 males, mean age: 57.19 ± 10 years) patients referred for elective coronary angiography at baseline and after 3-month statin and ACE inhibitor treatment. Results. Plasma hs-CRP levels were significantly higher in CAE group than O-CAD group at baseline (2.68 ± 66 mg/L versus 1, 64 ± 64, resp., P < .0001). Plasma hs-CRP levels significantly decreased from baseline 3 months later in the CE (from 2.68±0.66 mg/L to 1.2±0.53 mg/L, P < .0001) as well as in the O-CAD group (from 1.64±0.64 mg/L to 1.01±0.56 mg/L, P < .001). Conclusion. We think that hs-CRP measurement may be a good prognostic value in CAE patients as in stenotic ones. Further placebo-controlled studies are needed to evaluate the clinical significance of this decrease in hs-CRP.

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 β are novel bioactive peptides. Salusin-α suppresses macrophage foam cell formation, while salusin-β 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 Behcets 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.

Adiponectin levels in coronary artery ectasia

Etiopathogenesis of coronary artery ectasia (CAE), which is defi ned 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 µg/ml in group 1 and 6.73 ± 4.0 µg/ml in group 2 (P = 0.02). High-sensitivity Creactive 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.

Circulating Soluble Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Levels Are Associated With Erectile Dysfunction in Patients Without Known Coronary Artery Disease

AIM Endothelial dysfunction and microvascular damage are involved in the pathogenesis of erectile dysfunction (ED). Soluble lectin-like oxidized low-density lipoprotein receptor-1 (sLOX-1) is identified endothelial receptor for oxidized low-density lipoprotein (ox-LDL) that plays a pivotal role in ox-LDL-induced endothelial dysfunction. The purpose of the current study was to determine the association between sLOX-1 and ED in patients without known coronary artery disease (CAD). MAIN OUTCOME MEASURES Diagnosis of ED was based on the International Index of Erectile Function Score-5. Levels of sLOX-1 were measured in serum by enzyme-linked immunosorbent assay. METHODS One hundred thirty-eight subjects with ED patients without known CAD (ED group) and 75 age-matched subjects without ED and known CAD (Non-ED Group) were included in this study. RESULTS Plasma levels of sLOX-1 were significantly higher in ED than in Non-ED group (95±87 and 49±30 pg/mL, respectively, P<0.001). The levels of sLOX-1 highly negative correlated with score of ED (r=-0.618, P<0.001). The sLOX-1 levels>75 pg/mL predicts ED with 26.8% sensitivity and 96.0% specificity on receiver operator characteristic analysis. CONCLUSIONS Our study demonstrated that serum sLOX-1 levels were associated with endothelial dysfunction that predicts ED. Moreover, the current study revealed that there was strong negative correlation between the levels of circulating sLOX-1 and score of ED. This study suggested sLOX-1 may be involved in the pathogenesis of ED in patients without known CAD.

The effect of nesfatin-1 levels on paroxysmal supraventricular tachycardia.

Background Nesfatin-1 was originally identified as a neuropeptide of the hypothalamus, which is a key integration area of the brain, where numerous neuropeptides and transmitters are released to participate in the control of essential body functions. In the literature, there are no studies showing the relationship between the nesfatin-1 level and paroxysmal supraventricular tachycardia. We hypothesize that the circulating levels of nesfatin-1 may increase during supraventricular tachycardia, to engage the vagal stimulation to terminate by the inhibition of neuropeptide-Y, and may activate oxytocin and the corticotropin-releasing hormone. Materials and Methods This study includes 120 cases (80 patients and 40 controls). Patients with paroxysmal supraventricular tachycardia were compared with the control group with regard to sex, nesfatin-1 level, comorbid diseases, serum renal function values, and patients’ vital findings. Results The nesfatin-1 levels were significantly higher in the paroxysmal supraventricular tachycardia group than in the control group and positively correlated highly with heart rate (r = 0.634; P < 0.001). The area under the receiver operating characteristic curve was 0.644 for the nesfatin-1 levels (P = 0.0051). The sensitivity and specificity values of the nesfatin-1 levels were 41.2% and 95%, respectively (cutoff value >1743.7 pg/mL). Conclusion At the end of this study, a statistically significant correlation was found between the serum nesfatin-1 level and supraventricular tachycardia. Although multifactorial causes may explain the relationship, we based our hypothesis on the relationship of the antagonistic effects of nesfatin-1 on the neuropeptide-Y and activated oxytocin.