Ugur Kucuk

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.

Evaluation of the mean platelet volume in patients with cardiac syndrome X

OBJECTIVE: Cardiac syndrome X is characterized by angina-like chest pain, a positive stress test, and normal coronary arteries. A patients mean platelet volume, which potentially reflects platelet function and activity, is associated with coronary atherosclerosis and endothelial dysfunction. The aim of the present study was to evaluate the mean platelet volumes of patients with cardiac syndrome X, those with coronary artery disease and normal subjects. METHODS: Two hundred thirty-six subjects (76 patients with cardiac syndrome X, 78 patients with coronary artery disease, and 82 controls) were enrolled in the study. All of the subjects were evaluated with a detailed medical history, physical examination, and biochemical analyses. The mean platelet volumes were compared between the three groups. RESULTS: The mean platelet volumes in the patients with cardiac syndrome X and with coronary artery disease were significantly higher than those that were observed in the control group. There were no significant differences in the mean platelet volumes between the cardiac syndrome X and the coronary artery disease groups. CONCLUSION: We have established that patients with cardiac syndrome X and coronary artery disease exhibit higher mean platelet volumes compared to controls. Patients with cardiac syndrome X exhibited higher mean platelet volumes compared to the controls, reflecting the presence of subclinical atherosclerosis. These findings suggest that, in addition to endothelial dysfunction, the presence of atherosclerosis may also contribute to the etiopathogenesis of cardiac syndrome X.

Neutrophils/Lymphocytes Ratio in Patients With Cardiac Syndrome X and Its Association With Carotid Intima–Media Thickness

Neutrophils and lymphocytes (N/L) ratio and carotid intima–media thickness (C-IMT) value have been studied as new predictors of cardiovascular risk. We aimed to investigate N/L ratio and C-IMT value in patients with cardiac syndrome X (CSX) and compare patients with coronary artery disease (CAD) and normal participants. A total of 288 participants were enrolled in the study. The N/L ratio and C-IMT value were compared among the 3 groups. There were no statistically significant differences in N/L levels between CSX and CAD groups. The N/L ratio was found significantly increased in patients with CSX and CAD, compared to the control group. Patients with CAD and CSX had significantly higher C-IMT value compared to control participants. Significant positive correlation was found between C-IMT value and plasma level of N/L ratio. The relationship among CSX and higher N/L ratio level and C-IMT suggests that endothelial dysfunction may contribute to the etiopathogenesis of the CSX.

Association between coronary artery ectasia and neutrophil-lymphocyte ratio.

Atherosclerosis plays an important role in the etiopathogenesis of coronary artery ectasia (CAE). Inflammation markers may play a part in the pathogenesis of CAE. We aimed to assess the association between the CAE and the neutrophil–lymphocyte (N/L) ratio. Consecutive eligible patients (n = 181) were divided into 3 groups: patients with CAE, those with newly diagnosed coronary artery disease (CAD), and those with a normal coronary angiogram. The N/L ratio and mean platelet volume (MPV) were measured as part of the automated complete blood count. There were no statistically significant differences in N/L ratio and MPV between the CAE and the CAD groups. The N/L ratio and MPV were significantly higher in patients in both CAE and CAD groups compared to those in the control group (P < .01). An increased N/L ratio may play a role not only in the pathogenesis of CAD but also in the pathophysiology of CAE.

The platelet lymphocyte ratio may be useful inflammatory indicator in clinical practice

was also measured for electrolytes with the following results: P = 1.48 mmol/L (4.6 mg/dL), Na = 146 mmol/L, K = 2.2 mmol/L, Cl = 108 mmol/L, total carbon dioxide (TCO2) = 38 mmol/L. In the second experiment, the dialysis machine was programmed to use concentrates similar to those employed in the first experiment to produce a final dialysate sodium concentration of 138 mmol/L and a final dialysate bicarbonate concentration of 37 mmol/L. The pH of the dialysate was found to be 7.2. The electrolyte concentrations were as follows: P = 1.39 mmol/L (4.3 mg/dL), Na = 141 mmol/L, K = 2.1 mmol/L, Cl = 103 mmol/L, TCO2 = 40 mmol/L. A final dialysate pH of 7.1–7.2 is low enough to prevent the precipitation of calcium and magnesium phosphate salts. When preparing this phosphate-enriched dialysate for clinical dialysis, an intravenous or a highly pure grade disodium monohydrogen phosphate should be used. If preferred, a mechanical agitator or mixer could aid the dissolution of the phosphate salt in the acid concentrate. Disodium monohydrogen phosphate is alkaline in nature. However, the amount used in the present method is small, causing only a minor increase in the level of the total buffer base in the final dialysate. Nevertheless, it would seem prudent to start with a lower final dialysate bicarbonate level at first and to closely monitor the postdialysis serum bicarbonate values. The optimal dialysate bicarbonate concentration can then be chosen by evaluating those post-dialysis levels. Although our previously described method of using a mixture of disodium monohydrogen phosphate (Na2HPO4.7H2O) and monosodium dihydrogen phosphate (NaH2PO4. H2O) is equally effective in enriching dialysate with phosphates, the present approach of using a single-phosphate salt is simpler and would appear to be the method of choice.

Carotid intima-media thickness in patients with slow coronary flow and its association with neutrophil-to-lymphocyte ratio: a preliminary report.

Background: The slow coronary flow (SCF) is characterized by angiographically normal or near-normal coronary arteries with delayed progression of the contrast agent into distal vasculature. We aimed to investigate neutrophil-to-lymphocyte (N/L) ratio and the carotid intima-media thickness (CIMT) value in patients with SCF compared to patients with newly diagnosed coronary artery disease (CAD) and normal patients. Materials and Methods: We enrolled 60 consecutive patients with SCF, 68 patients with CAD, and 72 normal patients. The association between thrombolysis in myocardial infarction frame count, CIMT, and N/L ratio and other clinical and laboratory parameters were evaluated. Results: The N/L ratio was significantly higher not only in patients with SCF but also in patients with CAD, compared to those of controls. The N/L ratio was positively and moderately correlated with CIMT in the whole study population. Conclusions: The NL ratio is significantly associated with reduced coronary blood flow, and elevated N/L ratio might be an independent predictor for the presence of SCF.

Assessment of the relationship between red cell distribution width and cardiac syndrome X

BACKGROUND Cardiac syndrome X (CSX) is characterised by angina-like chest pain, a positive stress test, and normal coronary arteries. Increased red cell distribution width (RDW) level may be indicative of an underlying inflammatory state. AIM To investigate RDW level in patients with CSX and compare patients having coronary artery disease (CAD) and normal subjects. METHODS 245 subjects (79 patients with CSX, 81 patients with CAD, and 85 controls) were enrolled in the study. The CSX group consisted of patients with anginal chest pain, ischaemia on noninvasive stress test and a normal coronary angiogram.CAD was defined as ≥ 50% stenosis in at least one coronary artery. The control group was selected from the patients with anginal symptoms but a normal stress test and a normal coronary angiogram. RDW measurements among the three groups were compared. RESULTS Baseline clinical and biochemical characteristics were not different among the three groups. There were no statistically significant differences in RDW levels between the CSX and CAD groups (p = 0.17). RDW measurements in both the CSX and CAD groups were found to be significantly higher than the control group (p < 0.01). CONCLUSIONS We discovered that patients with CSX and CAD have significantly higher RDW measurements compared to controls. The relationship between CSX and higher RDW level suggests that endothelial dysfunction may also contribute to the etiopathogenesis of the CSX phenomenon as it does with CAD.

Carotid Intima Media Thickness and its Association With Total Bilirubin Levels in Patients With Coronary Artery Ectasia.

Atherosclerosis plays an important role in the etiopathogenesis of coronary artery ectasia (CAE). The relationship between total bilirubin (TBil) and carotid intima media thickness (cIMT) in patients with CAE has not been fully investigated. Hence, we evaluated the relationship between TBil levels and cIMT in 142 consecutive eligible patients with CAE, newly diagnosed coronary artery disease (CAD), and normal coronary arteries. There were no significant differences in TBil (P = .772) and cIMT (P = .791) between the CAE and CAD groups. Bilirubin levels were significantly lower in both CAE and CAD groups compared to the controls (P < .01). The cIMT was significantly higher in both CAE and CAD groups compared to control participants (P < .01). A negative correlation between cIMT and TBil was found in all the groups (P < .01, r = .354). We show for the first time that patients with CAE and CAD have lower TBil and greater cIMT compared to controls with normal coronary angiograms.

Arterial Stiffness Itself Without Other Inflammatory Markers May Not Provide Information to Clinicians

To the Editor: We read the article “Association of Arterial Stiffness With Obesity in Australian Women: A Pilot Study” written by Pal and colleagues with interest. The authors investigated the arterial stiffness status in overweight/obese Australian women compared with their lean counterparts. They concluded that increased arterial stiffness existed in overweight patients compared with lean patients, as well as with a positive association of augmentation index with measurements of body composition and blood pressure (BP). These data suggest that greater cardiovascular risk in overweight/obese women may be related to increased arterial stiffness, as well as increased BP and cholesterol. We believe that these findings will act as a guide for further information regarding obesity and cardiovascular disease risk factors related to body composition. Arterial stiffness indicates the viscoelastic properties of the vessel wall. Arterial stiffness represents vascular damage and is a measure of the degree of atherosclerosis. Arterial stiffness has received increased attention because of its role as an independent prognostic factor for hypertension, chronic kidney disease, diabetes, and heart failure. Increased arterial stiffness is a common indicator of atherosclerotic involvement of the vascular structure indicating coronary artery disease (CAD), cerebrovascular disease, and peripheral arterial disease. It can also be affected by atherosclerotic risk factors such as smoking, alcohol consumption, hypercholesterolemia, hypothyroidism, and older age. In this point of view, in the present study, the authors did not mention some of the affecting factors of arterial stiffness, including smoking, alcohol consumption, hypercholesterolemia, hypothyroidism, heart failure, cerebrovascular disease, and peripheral arterial disease. It would have been useful had the authors provided information about these factors. Furthermore, some medications such as antihypertensive treatment including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and statins may influence arterial stiffness paremeters. Had the authors described these factors, it would have been beneficial to the readers and the results may have been different. In addition, the authors did not clearly define that obesity is independently associated with arterial stiffness paremeters. A multivariate regression analysis would have been valuable and adjusted for other related factors (such as hypertension, diabetes mellitus, smoking, hypercholesterolemia, and medications). Finally, arterial stiffness is a noninvasive method to assess endothelial dysfunction in clinical practice and can be affected by many factors. Arterial stiffness itself without other inflammatory markers may not provide information to clinicians about the endothelial inflammation. Therefore, we think that it should be evaluated together with other serum inflammatory markers.

Neutrophil–lymphocyte ratio as an important assessment tool

was measured by dividing neutrophil count to lymphocyte count. Left atrial thrombus was detected in 32 (10.3%) of 309 patients. Mean NLR (2.2 ± 1.0 vs 2.7 ± 1.1, p = 0.026) was significantly higher among patients with LA thrombus compared to patients without LA thrombus. On multivariate analysis, NLR (odds ratio 1.59; 95% CI: 0.87–4.18; p < 0.02) was an independent risk factor for the presence of LA thrombus in patients with non-valvular AF. We concluded that NLR, an emerging marker of inflammation, was independently associated with the presence of LA thrombus in patients with non-valvular AF [2] .I