BackgroundEpicardial fat tissue (EAT) acts as brown adipose tissue and protects the heart and coronary arteries against hypothermia. Recent studies demonstrated that EAT is a source of both anti-inflammatory and atherogenic cytokines. In this study, our aim was to investigate the association of vertical, horizontal, and area measurements of EAT thickness and their association with coronary artery disease, diastolic function, and myocardial performance index in patients who underwent coronary angiography.Material/MethodsThe study population consisted of patients who presented to our outpatient clinic with chest pain and whose non-invasive stress tests were positive between June 2015 and July 2017. Echocardiographic examinations were performed prior to the angiography. Coronary angiograms were performed using Judkins method from the femoral artery.ResultsMean vertical thickness of EAT was 0.6 cm in patients with CAD and 0.46 cm in those without CAD (p=0.0001). Mean horizontal length of EAT was 2.91 cm in patients with CAD and was 2.41 cm in the subjects without CAD (p=0.001). ROC analysis showed 81% sensitivity and 53% specificity for a cut-off value of 0.45, and 67% sensitivity and 71% specificity for a cut-off value of 0.55 for EAT vertical (cm). Multivariate analysis showed that EAT is an independent risk factor for coronary artery disease.ConclusionsEchocardiography is an inexpensive routine assessment for most patients. EAT thickness determined by echocardiography may be a useful indicator of increased CAD risk, but not diastolic dysfunction, of the left ventricle.

Background:Aortic valve stenosis (AVS) is the most common cause of left ventricular outflow obstruction, and its prevalence among elderly patients causes a major public health burden. Recently, platelet-to-lymphocyte ratio (PLR) has been recognized as a novel prognostic biomarker that offers information about both aggregation and inflammation pathways. Since PLR indicates inflammation, we hypothesized that PLR may be associated with the severity of AVS due to chronic inflammation pathways that cause stiffness and calcification of the aortic valve.Materials and Methods:We retrospectively enrolled 117 patients with severe degenerative AVS, who underwent aortic valve replacement and 117 control patients in our clinic. PLR was defined as the absolute platelet count divided by the absolute lymphocyte count. Severe AVS was defined as calcification and sclerosis of the valve with a mean pressure gradient of >40 mmHg.Results:PLR was 197.03 ± 49.61 in the AVS group and 144.9 ± 40.35 in the control group, which indicated a statistically significant difference (P < 0.001). A receiver operating characteristic (ROC) curve analysis demonstrated that PLR values over 188 predicted the severity of aortic stenosis with a sensitivity of 87% and a specificity of 70% (95% confidence interval = 0.734–0.882; P < 0.001; area under ROC curve: 0.808).Conclusion:We suggest that the level of PLR elevation is related to the severity of degenerative AVS, and PLR should be used to monitor patients' inflammatory responses and the efficacy of treatment, which will lead us to more closely monitor this high-risk population to detect severe degenerative AVS at an early stage.

Objective:Left ventricular (LV) rotation and twist play an important role in LV contraction and relaxation. Left bundle branch block (LBBB) deteriorates both diastolic and systolic functions. We evaluated the LV twist in patients with LBBB and preserved ejection fraction (EF) (>50%) to determine twist as a potential marker for subtle myocardial dysfunction.Methods:This observational cross-sectional study included 34 LBBB patients with preserved EF who were free from ischemic and valvular disease (Group 1) and 36 healthy controls (Group 2). All patients underwent 2-D Doppler and 2-D speckle tracking echocardiography. LV apical, basal rotation, and twist were evaluated in both groups and compared accordingly. In addition, subjects were dichotomized considering the median twist value of the study population. Binary logistic regression analysis was performed to determine the independent variables associated with inframedian twist.Results:Baseline clinical characteristics were similar in LBBB patients and controls. Mean apical rotation (2.5°±1.9° vs. 4.4°±2.9°; p=0.002), basal rotation (-2.9°±2.3° vs. -4.1°±2.7°; p=0.05), and twist (5.4°±3° vs. 8.6°±3.3°; p<0.001) were decreased in group 1. Parameters related to intra- and interventricular mechanical dyssynchrony, such as longitudinal left ventricular dyssynchrony index (LVdys) and preejection interval of LV, interventricular mechanical delay (IVMD), and left posterior wall contractions (SPMWD) were significantly higher in the LBBB group. The median twist value of the studied population was 6.65°. Binary logistic regression analysis showed that only presence of LBBB was independently associated with inframedian twist (OR=6.250; 95% CI: 2.215–17.632; p<0.001).ConclusionThe LBBB might have induced the reduction of LV twist by diminishing the LV rotation before inducing a prominent effect on the left ventricular ejection fraction (LVEF). Therefore, twist may be considered as a marker for subtle LV dysfunction in LBBB with substantially normal EF.

Previously conducted studies revealed that smoking enhanced the efficacy of clopidogrel by increasing formation of the active metabolite (AM) from the prodrug through induction of the cytochrome CYP1A2. The expression of cytochrome enzymes depends on genotype and no data exists in literature conducted in Turkish patients comparing the clopidogrel responsiveness between active smokers and non-active smokers treated with clopidogrel. In this study, our aim was to investigate the clopidogrel responsiveness in clopidogrel-treated Turkish acute coronary syndrome (ACS) patients according to their smoking status. We retrospectively enrolled 258 patients who were hospitalized due to ACS. Clinical variables of the patients, especially smoking status were recorded. Clopidogrel resistance was evaluated by using adenosine diphosphate (ADP) induced platelet aggregometry. Clopidogrel resistance was detected as a change in maximal aggregation ≤20% from baseline. A total of 139 patients were active smokers while 12 were former smokers. 107 patients did not have a history of smoking. Ten of the smokers were hyporesponsive to clopidogrel, whereas 36 of non-smokers were hyporesponsive to clopidogrel (p < 0.001). Receiver-operating characteristic curve analysis demonstrated that Au-min value >612.5 predicted the clopidogrel resistance with a sensitivity of 60% (OR: 100.65, %95 CI = 19.996-506.615 p < 0.001). Results of this study demonstrated that ADP responses were lower in smokers receiving clopidogrel and aspirin than in non-smokers receiving the same drug regimen. This finding indicates that smoking was related to an enhanced clopidogrel responsiveness in Turkish patients hospitalized due to ACS, suggesting that "smoker's paradox" probably exists in Turkish ACS patients.

Objective Herein, we investigated the balance of thiol/disulfide, with the hypothesis that the balance between disulfides and thiols, which are natural antioxidants, might be disrupted in patients with familial hypercholesterolemia, which eventually leads to endothelial damage. Methods In this study, we evaluated 51 patients diagnosed with familial hypercholesterolemia and 81 healthy subjects. Blood samples were taken from the patients after a minimum of 12 hours of fasting; samples were immediately centrifuged, stored in Eppendorf tubes, and preserved at −80°C. Results This study found that thiol levels are significantly lower in patients with familial hypercholesterolemia, whereas disulfide levels are higher (independent of age, gender, and body mass index). This means that in such patients, the thiol/disulfide balance changes in favour of disulfide. Conclusions In this study, we found that the thiol/disulfide balance in patients with familial hypercholesterolemia is disrupted in favour of disulfide.