A b s t r a c tBackground: Atherosclerosis is a chronic systemic inflammatory disease. Neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are systemic inflammatory markers that are correlated with poor cardiovascular outcomes. Aim:To explore the relation of NLR and PLR with severity of coronary artery disease (CAD). Methods:The study population consisted of 180 consecutive patients who underwent elective coronary angiography (CAG). While 100 patients (22 female, mean age: 60.6 ± 12.6 years) had abnormal CAG, 80 patients (44 female, mean age: 57.2 ± 10.9 years) had normal CAG. NLR and PLR were calculated as the ratio of neutrophil count to lymphocyte count and as the ratio of platelet count to lymphocyte count, respectively. Results:Although age distribution was similar between the two groups (p = 0.073), female gender was significantly higher in the normal CAG group (p < 0.001). Patients with abnormal CAG had significantly higher NLR and PLR when compared to patients with normal CAG (3.7 ± 2.6 vs. 2.2 ± 1.7, p < 0.001 and 125.9 ± 72.3 vs. 102.6 ± 33.8, p = 0.027, respectively). NLR and PLR were significantly correlated with SYNTAX score and GENSINI score. In logistic regression analyses, only NLR (odds ratio: 1.576, confidence interval: 1.198-2.072, p = 0.001) was an independent predictor of CAD. An NLR of 2.3 or higher predicted the CAD with a sensitivity of 66% and specificity of 70%.Conclusions: NLR and PLR seem to be a simple method to predict severity of CAD in patients undergoing elective CAG, and it may be part of cardiovascular examination before CAG.

Vitamin D deficiency is associated with impaired myocardial deformation parameters and cardiovascular disease (CVD). Increased epicardial fat thickness (EFT) is also associated with increased risk of CVD. The aim of the study is to evaluate the effect of vitamin D deficiency and supplementation on myocardial deformation parameters and EFT. The study population consisted of 50 patients with vitamin D deficiency who were free of cardiovascular risk (mean age: 42.6 ± 8.9 years, 37 female). Patients were treated with oral administration of vitamin D3. Myocardial deformation parameters and EFT were evaluated before and after treatment of those patients. Vitamin D levels significantly increased after treatment (30.5 ± 10.5 vs. 9.9 ± 5.3 nmol/l, p < 0.001). There was no significant difference between conventional echocardiographic parameters before and after treatment. Baseline EFT was significantly higher than post-treatment measurements (35.2 ± 8.0 vs. 27.5 ± 5.6 mm, p < 0.001). Post-treatment myocardial deformation parameters were also significantly higher than baseline measurements. Baseline vitamin D levels correlated with baseline EFT and left ventricular global longitudinal strain (LV-GLS). Post-treatment vitamin D levels also correlated with post-treatment EFT, body mass index, and LV-GLS. Baseline vitamin D level was an independent predictor of baseline LV-GLS (p = 0.002). Patients with impaired LV-GLS had significantly lower vitamin D levels than patients with normal LV-GLS (6.6 ± 3.8 vs. 11.0 ± 5.3 nmol/l, p = 0.005). Baseline vitamin D level was also an independent predictor of baseline impaired LV-GLS (p = 0.010). Vitamin D supplementation has beneficial effects on myocardial deformation parameters and EFT. Moreover, baseline vitamin D levels are a predictor of impaired LV-GLS.

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Vitamin D supplementation has beneficial effects on arterial stiffness. Arterial stiffness parameters may aid in the assessment of cardiovascular risk in patients with vitamin D deficiency.

Our results show that the mandibular angle is weaker than the mandibular body under bending loads.

Introduction: There is limited data in the literature regarding the association between hyperlipidemia and heart rate variability (HRV). The aim of the present study is to investigate the association between HRV and hyperlipidemia by retrospectively evaluating the recordings of subjects free of any apparent cardiovascular or systemic disease. Patients and Methods: Medical records of patients to whom 24 hour-Holter recording was performed in our clinic between January 2012 and May 2013 were retrospectively examined. Data of subjects who were determined to be free of any cardiovascular or systemic disease were used in the analysis. Results: Data of 37 subjects were used. There were 20 subjects with hyperlipidemia (10 male, age: 44.5 ± 11.1 years) and 17 subjects with normal lipid profi le (5 male, age: 33.4 ± 10.6 years; p= 0.18 for gender and p=0.004 for age). Majority of HRV parameters were found to be signifi cantly depressed in group with hyperlipidemia; however, there were no signifi cant difference between groups regarding prevalence of arrhythmias. Out of components of the lipid profi le, linear regression analysis revealed serum triglyceride level to be independently associated variable with RMSSD, PNN50 and LF/HF ratio (in respective order; beta=-0.40, p= 0.02; beta=-0.41, p= 0.012 and beta=-0.31, p= 0.05). Conclusion: Subjects with hyperlipidemia were observed to have signifi cantly depressed HRV compared to subjects with normal lipid profi le in our retrospective study. Based on our observations, it may be suggested that patients with hyperlipidemia, in particular with hypertriglyceridemia display higher subtle cardiac sympathetic activity which may be associated with increased cardiovascular morbidity and mortality.

Atrial fibrillation (AF) is an important risk factor for cardioembolic stroke. Warfarin is an effective treatment in reducing the risk of cardioembolic stroke in patients with AF. New anticoagulants have been widely using for stroke prophylaxis in patients with nonvalvular AF. Previous studies have suggested that thrombolytic therapy is effective treatment choice in patients with pulmonary embolisms. Warfarin therapy is also effective on prevention or treatment of cardiac thrombus in patients with AF. However, there are no evidence-based data on treatment of cardiac thrombus with new oral anticoagulants in patients with AF. In our case report, we reported an AF patient with cardiac thrombus and pulmonary embolism under dabigatran therapy.