Gulay Yetkin

Plasma soluble adhesion molecules; intercellular adhesion molecule-1, vascular cell adhesion molecule-1 and E-selectin levels in patients with isolated coronary artery ectasia.

Plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM)-1, vascular cell adhesion molecule-1 (VCAM-1) and E-selectin leves of patients with isolated coronary artery ectasia (CAE), patients with obstructive coronary artery disease without CAE and subjects with angiographically normal coronary arteries were evaluated. Patients with isolated CAE were detected to have significantly higher levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive coronary artery disease without CAE (ICAM, 673±153 versus 381±106, respectively, P<0.001; VCAM-1, 2366±925 versus 1136±208, respectively, P<0.001; E-selectin, 74±21 versus 61±18, respectively, P=0.01) and subjects with normal coronary arteries (ICAM-1, 673±153 versus 303±131, respectively, P<0.001; VCAM-1, 2366±925 versus 729±231, respectively, P<0.001; E-selectin, 74±21 versus 49±9, respectively, P<0.001), suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in patients with isolated CAE. BackgroundThe common coexistence of coronary artery ectasia (CAE) with coronary artery disease (CAD) suggests that it may be a variant of CAD. However, it is not clear why some patients with obstructive CAD develop CAE whereas most do not. İnflammation has been reported to be a major contributing factor to both obstructive and aneurysmatic vascular disorders and therefore, in the present study, the plasma soluble adhesion molecules, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin levels in isolated CAE were investigated. MethodsThe study population consisted of three groups: the first consisted of 32 patients with isolated CAE without stenotic lesion; the second of 32 patients with obstructive CAD without CAE; and the third group of 30 control subjects with normal coronary arteries. Coronary diameters were measured as the maximum diameter of the ectasic segment by use of a computerized quantitative coronary angiography analysis system. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is ≥1.5 times that of the adjacent normal segment in segmental ectasia. Plasma soluble ICAM-1, VCAM-1 and E-selectin levels were measured in all patients and control subjects using commercially available enzyme-linked immunosorbent assay kits. ResultsPatients with isolated CAE were found to have significantly higher levels of plasma soluble ICAM-1, VCAM-1, and E-selectin in comparison with patients with obstructive CAD without CAE (ICAM, 673±153 versus 381±106, respectively; P<0.001; VCAM-1, 2366±925 versus 1136±208, respectively; P<0.001; E-selectin, 74±21 versus 61±18, respectively; P=0.01) and control subjects with normal coronary arteries (ICAM-1, 673±153 versus 303±131, respectively;, P<0.001; VCAM-1, 2366±925 versus 729±231, respectively; P<0.001; E-selectin, 74±21 versus 49±9, respectively; P<0.001). In addition, we detected statistically significant positive correlation between the total length of ectasic segments and the levels of plasma soluble ICAM-1 (r=0.625; P<0.001), VCAM-1 (r=0.548; P=0.001) and E-selectin (r=0.390; P=0.027). Multivariate logistic regression analysis revealed a significant independent relation between isolated CAE and ICAM-1 [odds ratio (OR)=1.023; 95% confidence interval (CI)=1.0048–1.0414; P=0.0129] and VCAM-1 (OR=1.0057; 95% CI=1.0007–1.0106; P=0.0240). ConclusionsWe have shown that patients with isolated CAE have raised levels of plasma soluble ICAM-1, VCAM-1 and E-selectin in comparison with patients with obstructive CAD without CAE and control subjects with normal coronary arteries, suggesting the presence of a more severe and extensive chronic inflammation in the coronary circulation in these patients.

Are polycystic ovaries associated with cardiovascular disease risk as polycystic ovary syndrome

Aim. Our aim was to assess C-reactive protein (CRP) levels and insulin resistance in women with polycystic ovary syndrome (PCOS) or polycystic ovaries (PCO). Methods. The study population included 30 women with PCOS, 30 with PCO and 30 healthy controls. CRP and insulin resistance index (IRI) (fasting glucose/insulin) were measured. A receiver–operator characteristic (ROC) curve was constructed to determine the cut-off value of CRP to predict increased cardiovascular risk. Results. There were no statistically significant differences between the three groups with regard to age and body mass index. IRI was significantly lower in the PCOS group than in the PCO and control groups. No difference existed between the PCO and control groups. Median CRP levels in the control, PCO and PCOS groups were 0.75, 1.3 and 1.5 mg/l, respectively (p = 0.005). CRP could differentiate between women with and without increased cardiovascular risk at a cut-off value of 2.42 mg/l, with a sensitivity of 79% and a specificity of 81%. Conclusion. As in PCOS patients, women with PCO have higher serum CRP levels than healthy control women. This may contribute to increased cardiovascular disease risk in patients with PCO.

Predictors of left ventricular thrombus formation in patients with anterior myocardial infarction: role of activated protein C resistance.

BackgroundLeft ventricular mural thrombus formation is a well‐recognised consequence of acute anterior myocardial infarction. The vast majority of left ventricular thromboses occur in patients with anterior myocardial infarction and depressed left ventricular function. ObjectiveTo evaluate the factors predicting left ventricular thrombus formation in patients similiar for left ventricular function and left ventricular score indexes. MethodsWe evaluated 45 consecutive patients who met the inclusion criteria of anterior myocardial infarction resulting in apical, anterior or septal asynergy (akinesia, dyskinesia), without non‐Q‐wave myocardial infarction, dilated cardiomyopathy, or renal or hepatic dysfunction. Patients were divided into two groups: group I with, and group II without, left ventricular mural thrombus. The groups were compared for clinical, echocardiographic and hematologic parameters (activated protein C resistance (APC‐R), protein S and antithrombin III). ResultsSmoking and ACP‐R were significantly greater in group I than in group II (P  < 0.05 and P  < 0.005 respectively). Multivariate regression analysis showed that APC‐R was an independent risk factor for left ventricular thrombus formation in the patient group selected. Antithrombin III and protein C concentrations were not statistically different between two groups. All other clinical and echocardiographic characteristics of the patients were similiar in both groups. ConclusionAPC‐R is an independent risk factor for left ventricular thrombosis in patients with anterior myocardial infarction resulting in septal or anterior and apical akinesia or dyskinesia.

Detection of Chlamydia pneumoniae deoxyribonucleic acid in blood samples taken from coronary sinus after coronary angioplasty.

C pneumoniae (C. pneumoniae), a human respiratory pathogen, is the bacterium most often found to be associated with coronary heart disease. C. pneumoniae has been associated with atherosclerotic disease by seroepidemiologic analysis and by demonstration of the organism in atherosclerotic lesions by polymerase chain reaction. Recently, the presence of chlamydial deoxyribonucleic acid (DNA) was reported in peripheral blood mononuclear cells of patients with coronary artery disease. We aimed to investigate the effects of percutaneous transluminal coronary angioplasty on C. pneumoniae DNA detection in circulating white blood cells.

Changes in plasma levels of adhesion molecules after percutaneous mitral balloon valvuloplasty

BACKGROUND Adhesion molecules are expressed on vascular endothelium and on immune and inflammatory cells. Recently increased levels of adhesion molecules have been shown in patients with rheumatic mitral stenosis. This study examined the serum levels of the adhesion molecules intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin in patients with rheumatic mitral stenosis and the effects of percutaneous mitral balloon valvuloplasty (PMBV) on these adhesion molecules. MATERIALS AND METHODS Thirty five patients (3 men, 32 women, mean age 39+/-5 years) with severe rheumatic mitral stenosis who underwent percutaneous balloon mitral valvuloplasty, and 35 age and sex matched healthy control subjects were included in the study. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients who underwent PMBV and in all control subjects. Blood samples were taken for measurement of adhesion molecules immediately before and 24 h after the mitral balloon valvuloplasty. RESULTS The plasma levels of soluble adhesion molecules E-selectin, ICAM-1 and VCAM-1 were significantly elevated in patients with mitral stenosis compared to control subjects: E-selectin, 97+/-59 vs. 45+/-24 ng/ml (P=.001), sICAM-1, 874+/-301 ng/ml vs. 238+/-82 ng/ml (P<.0001); sVCAM-1, 3056+/-763 ng/ml vs. 985+/-298 ng/ml (P<.0001). Plasma levels of VCAM-1 significantly increased 24 h after the valvuloplasty procedure (3056+/-763 ng/ml vs. 3570+/-1225 ng/ml P=.013). Plasma levels of E-selectin showed a significant decrease after PMBV (97+/-59 vs. 70+/-58 ng/ml, P=.043) and plasma levels of ICAM-1 did not show any change after PMBV (874+/-301 vs. 944+/-377 ng/ml, P=.356). CONCLUSION Cellular adhesion molecules, sICAM-1, E-selectin, sVCAM-1 have shown changes in different directions in response to PMBV. These results necessitate further studies to clarify the mechanism underlying the association between adhesion molecules and PMBV as well as rheumatic mitral stenosis.

Comparison of the Antibacterial Activity of Lidocaine 1% Versus Alkalinized Lidocaine In Vitro

BACKGROUND Infections after epidural and spinal blocks are rare. The topical anesthetic liclocaine used in these procedures has been found to have antibacterial effects on various microorganisms. OBJECTIVE The aim of this study was to assess the antibacterial effects of alkalinized liclocaine on Staphylococcus aureus, Escherichia coli, and Pseudomonas aeruginosa. METHODS Lidocaine 2%, alkalinized lidocaine, and physiologic saline (as a control solution) were added to standard bacterial preparations. The final concentration of the lidocaine was 10 mg/mL (1%). At baseline and 3 and 6 hours after incubation at 37°C, 3-mL aliquots were vortexed and pipetted into sterile polystyrene spectrophotometer cuvettes. Baseline referred to the end of the period of preparation of the solution (≤20 minutes). Growth was measured as the optical density at a wavelength of 540 nm. RESULTS Compared with the control, lidocaine significantly inhibited the growth of S aureus, E coli, and P aeruginosa at baseline and 3 and 6 hours after incubation (all, P < 0.05). Alkalinized lidocaine significantly inhibited the growth of S aureus at baseline and 3 and 6 hours (all, P < 0.05), while it significantly inhibited the growth of E coli and P aeruginosa only at 6 hours (both, P < 0.05). The growth of E coli was significantly less in lidocaine than in alkalinized lidocaine at 0 and 3 hours (both, P < 0.05). CONCLUSION The antibacterial effect of lidocaine 1% on S aureus was not changed after alkalinization. The effect of alkalinized lidocaine on E coli and P aeruginosa was significant only at 6 hours. Lidocaine significantly inhibited the growth of these 3 microorganisms at all study periods.

Inflammation in Coronary Artery Ectasia Compared to Atherosclerosis

We have read with great enthusiasm the article recently published by Boles et al. [...].