Nesligul Yildirim

The Levels of Tumor Necrosis Factor-Alpha and Interleukin-6 in Patients with Isolated Coronary Artery Ectasia

Background/Aim. Coronary artery ectasia (CAE) is considered as a variant of atherosclerosis. Tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) are among the sensitive markers of systemic inflammation. The aim of this study was to evaluate the plasma levels of the cytokines; TNF-α and IL-6 in CAE patients. Methods. Plasma concentrations of TNF-α and IL-6 were measured in 36 patients with CAE (28 males, mean age: 58.2 ± 12 years), and results were compared with age and sex-matched controls (n = 32) without coronary artery ectasia. TNF-α and IL-6 concentrations in blood were assesed by enzyme-linked immunosorbent assay (ELISA). Results. Baseline characteristics of the two groups were similar. TNF-α and IL-6 levels were significantly higher in CAE group than controls (15.6 ± 11.2 pg/mL versus 7.8 ± 3.7 pg/mL, P < .001, and 17.2 ± 12.6 versus 7.6 ± 2.1 P < .0001, resp.). Conclusion. CAE patients showed increases in TNF-α and IL-6 levels compared to the controls. This study provides evidence for alterations in the proinflamatory cytokines which suggest the involvement of the immune system in the pathophysiology of CAE. Further placebo-controlled studies are needed to evaluate the clinical significance of this increase in TNF-α and IL-6 levels.

Effects of acute carbon monoxide poisoning on the P-wave and QT interval dispersions

OBJECTIVE The aim of our study was to investigate atrial conduction and ventricular repolarization inhomogeneities using P-wave dispersion (Pwd) and QT dispersion (QTd) analyses in acute carbon monoxide (CO) poisoning. METHODS Sixty patients were retrospectively included in this case-controlled study. Thirty acute CO poisoning patients were assigned to the Group with acute CO poisoning (ACOP). Patients who did not have acute CO poisoning were assigned to the control group (Group C, n=30). Anthropometric measurement, body mass index, electrocardiogram (ECG) and serum electrolyte levels were recorded in all patients. Also, carboxyhemoglobin (COHb) levels were recorded in Group ACOP. Pwd, QT interval and QTd durations were measured. Corrected QT (QTc) and QTc dispersion (QTcd) intervals were determined with the Bazett formula. Independent samples t and Chi-square tests were used for statistical analysis. RESULTS No statistically significant difference was found between the age, gender distribution, anthropometric measurement, serum electrolytes, PR and QT durations between the groups. The Pwd (56.33 ± 17.11 msec vs 28.33 ± 11.16 msec, p=0.001) and QTd (63.33 ± 26.69 msec vs 42.16 ± 7.84 msec, p=0.001) were significantly longer in Group ACOP than in Group C. In addition, QTc and QTcd durations of Group ACOP were also found to be significantly longer than in Group C (p=0.001). CONCLUSION In our study, we found in ECG analyses of patients with acute CO poisoning that the Pwd, QTc and QTcd durations were significantly prolonged when compared with control group. For this reason, patients with acute CO poisoning need close attention because of arrhythmias, which can be related to increased QTcd and Pwd durations.

Further increase in the expression of activation markers on monocyte-derived dendritic cells in coronary artery disease patients with ectasia compared to patients with coronary artery disease alone.

Background. Coronary artery ectasia (CAE) is defined as localized or diffuse dilation of the coronary arteries. There are scarce data about the role of dendritic cells in CAE development. In this study we investigated the activation markers on the surface of monocyte-derived dendritic cells (mDCs) in coronary artery disease (CAD) patients with or without CAE. Method. The study consisted of 6 patients who had obstructive CAD with CAE, 6 CAD patients without CAE and 6 subjects with angiographically normal coronary arteries. mDCs were cultivated from peripheral blood monocytes. Surface activation markers were detected by flow cytometry. Results. CAD patients with CAE were detected to have significantly higher mean fluorescence intensities of CD11b, CD11c, CD54 , CD83, CD86 and MHC Class II molecules on mDCs in comparison to CAD patients without CAE and normal controls (P < .001 for all). A significant positive correlation was found between the number of vessels with CAE and the levels of CD11c, CD86, and MHC Class II molecules. Conclusion. mDCs display an increased cell surface concentration of activation molecules in CAD patients with CAE compared to patients with CAD alone. DC activation may play an important role for CAE development in patients with CAD.

Right bundle branch block : A new parameter revealing the progression rate of mitral stenosis

Background: Mitral stenosis has a generally slow but often variable clinical course. However, the factors that influence the rate of stenosis progression have not been completely identified. The aim of this study was to evaluate whether right bundle branch block (RBBB) may be related to the rapid progression of pure mitral stenosis besides echocardiographic parameters. Methods: Four hundred and thirty-six patients (300 females) were reviewed retrospectively. The patients were classified according to RBBB existence in electrocardiography: group A included 83 patients with RBBB existence, and group B contained 353 patients without RBBB. The patients were further classified as subjects who had an echocardiographic valve score ≤8 (325 patients, group 1) and those with a valve score >8 (111 patients, group 2). Results: The mean age of the patients was similar in groups A and B. In group A, the mean mitral valve gradient was higher (12.63 ± 4.43 vs. 10.58 ± 3.37 mm Hg; p < 0.0001), the mitral valve area smaller (1.05 ± 0.2 vs. 1.14 ± 0.52 cm2; p = 0.011), and the systolic pulmonary artery pressure higher (53.5 ± 16.2 vs. 46.9 ± 13.2 mm Hg; p = 0.001) than in group B. The mean age and mitral valve area were similar in groups 1 and 2. The mean mitral valve gradient (10.5 ± 3.7 vs. 12.3 ± 3.0 mm Hg; p < 0.0001) and systolic pulmonary artery pressure were higher in group 2 (46.7 ± 13.3 vs. 52.5 ± 15 mm Hg; p < 0.0001). Conclusion: These findings indicate that RBBB existence correlates with the severity of the disease and the grade of valve calcification in moderate and severe pure mitral stenosis.

[The association of eccentricity indexes with cardiac biomarkers in normotensive acute pulmonary embolism patients: an observational study].

OBJECTIVE The present study aims at investigating the association of systolic and diastolic eccentricity indexes with cardiac biomarkers in hemodynamically stable patients with acute pulmonary embolism (APE). METHODS Thirty hemodynamically stable (systolic blood pressure >90 mmHg) patients with APE (17M, mean age 61.67±17.6 years) were included in this cross-sectional observational study. The associations of serum troponin I, D-dimer, brain natriuretic peptide (BNP) and heart type fatty acid binding protein (hFABP) levels with systolic and diastolic eccentricity indices, tricuspid annular plane systolic excursion (TAPSE), myocardial performance index (MPI), systolic pulmonary artery pressure and the index of the inferior vena cava were investigated. The relationships between parameters were evaluated by Pearson and Spearman correlation analysis according to the distribution of data. RESULTS Correlation analysis revealed that the most significant relationship between cardiac biomarkers and echocardiographic measurements was in the BNP value. Meanwhile, systolic and diastolic eccentricity indexes were found to have significant correlation with serum troponin I (respectively r=0.470, p=0.009/r=0.310, p=0.095) and BNP (respectively r=0.402, p=0.028/r=0.384, p=0.036) values. On the other hand, elevated D-dimer levels led to statistical significance in none of the echocardiographic parameters. CONCLUSION According to our results, hFABP was rarely positive in normotensive patients with APE. An elevated D-dimer alone was not significant in predicting RVD. Eccentricity indexes revealed significant relationship with BNP and troponin I values. The results obtained indicate that early echocardiographic evaluation is important in patients with abnormal cardiac biomarkers.

Iron deficiency and anemia in heart failure

Heart failure is an important community health problem. Prevalence and incidence of heart failure have continued to rise over the years. Despite recent advances in heart failure therapy, prognosis is still poor, rehospitalization rate is very high, and quality of life is worse. Co-morbidities in heart failure have negative impact on clinical course of the disease, further impair prognosis, and add difficulties to treatment of clinical picture. Therefore, successful management of co-morbidities is strongly recommended in addition to conventional therapy for heart failure. One of the most common co-morbidities in heart failure is presence of iron deficiency and anemia. Current evidence suggests that iron deficiency and anemia are more prevalent in patients with heart failure and reduced ejection fraction, as well as those with heart failure and preserved ejection fraction. Moreover, iron deficiency and anemia are referred to as independent predictors for poor prognosis in heart failure. There is strong relationship between iron deficiency or anemia and severity of clinical status of heart failure. Over the last two decades, many clinical investigations have been conducted on clinical effectiveness of treatment of iron deficiency or anemia with oral iron, intravenous iron, and erythropoietin therapies. Studies with oral iron and erythropoietin therapies did not provide any clinical benefit and, in fact, these therapies have been shown to be associated with increase in adverse clinical outcomes. However, clinical trials in patients with iron deficiency in the presence or absence of anemia have demonstrated considerable clinical benefits of intravenous iron therapy, and based on these positive outcomes, iron deficiency has become target of therapy in management of heart failure. The present report assesses current approaches to iron deficiency and anemia in heart failure in light of recent evidence.