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Background: Aortic valve sclerosis (AVS) is closely related to hypertension and is an important predictor of coronary artery disease as well as cardiovascular morbidity and mortality. However, the mechanisms causing AVS have not yet been clarified. Therefore, we planned to investigate the influence of atherosclerosis-related risk factors including C-reactive protein (CRP), epicardial adipose tissue (EAT), carotid intima-media thickness (CIMT), pulse wave velocity (PWV), left ventricular hypertrophy, and the conventional risk parameters as well as endothelial dysfunction in untreated hypertensive patients., Methods and Results: Our study was cross-sectional and observational, and included 107 consecutive untreated hypertensive patients. All patients underwent vascular evaluation by CIMT, PWV, flow-mediated dilation (FMD%), as well as echocardiographic examinations. Age (OR = 1.180, p < 0.001), male sex (OR = 3.056, p = 0.019), waist circumference (OR = 1.082, p = 0.004), EAT (OR = 1.419, p = 0.001), smoking status (OR = 3.161, p = 0.014), FMD% (OR = 0.649, p < 0.001), mean CIMT (OR = 2.481, P < 0.001), and carotid plaque (OR = 4.692, P = 0.001) were associated with AVS in univariate analyses. Multivariate analyses revealed only age (OR = 1.144, P = 0.006) and FMD% (OR = 0.691, 0.001) as independent predictors of AVS. The presence of AVS had a high positive predictive value (100 %) but a low negative predictive value (51 %) for endothelial dysfunction (FMD < 12 %) in hypertensive patients., Conclusion: Our study supports the theory that systemic endothelial dysfunction has an initial and independent effect on AVS pathogenesis. Moreover, we demonstrated that the presence of AVS in patients with hypertension predicts endothelial dysfunction, with a high positive predictive value. Thus, AVS in hypertensive patients may urge clinicians toward aggressive risk factor modification and intensive treatment.

Background: Slow coronary flow (SCF) is an angiographic finding characterized by delayed opacification of the epicardial coronary arteries without obstructive coronary disease. Resistin, an adipocytokine, plays a major role besides low-grade inflammation in atherosclerotic vascular processes and may be of importance in other coronary pathologies such as SCF., Methods: The present study was cross-sectional and observational, consisting of 70 individuals who underwent coronary angiography and had angiographically normal coronary arteries of varying coronary flow rates. The study included 50 patients with isolated SCF and 20 control participants with normal coronary flow (NCF)., Results: There were no statistically significant differences between the SCF and NCF groups with respect to age, gender, presence of hypertension or diabetes mellitus, and smoking habit, except for increased creatinine levels (p = 0.014). The serum resistin level was significantly higher in the SCF group than in the NCF group (8.4 ± 7.2 vs. 5.4 ± 2.6 ng/ml, p = 0.014). Ln-transformed resistin levels correlated positively with left anterior descending (LAD) coronary artery TIMI frame count (TFC) (r = 0.408, p < 0.001) as well as with glucose (r = 0.340, p = 0.004), creatinine (r = 0.248, p = 0.044), and C-reactive protein (CRP; r = 0.283, p = 0.023) levels, and negatively with LAD coronary flow velocity (r = - 0.314, p = 0.009). When multivariate analyses were performed, in linear regression analysis, ln-resistin was associated with a longer TFC [beta (standardized regression coefficient): 0.404, p = 0.001] and lower coronary flow velocity (beta: - 0.280, p = 0.035); in logistic regression analysis, ln-resistin was an independent predictor of the presence of SCF (OR: 6.692, 65 %CI: 1.117-40.1, p = 0.037)., Conclusion: We demonstrated, for the first time, a significant increase in serum resistin levels in patients with SCF compared to subjects with NCF. We believe that further studies are needed to clarify the role of resistin in patients with SCF.

Background: Fragmented QRS complexes (fQRS) have been associated with increased morbidity and mortality, sudden cardiac death, and recurrent cardiovascular events. The association between left ventricular systolic and diastolic functions and presence of fragmented QRS has not been comprehensively studied to date. We tested the hypothesis that the presence of fragmented QRS is associated with left ventricular systolic and diastolic dysfunction., Methods: The study included 259 patients who were consecutively admitted to our outpatient clinic for cardiovascular risk factor management. Extensive echocardiographic parameters were obtained from all patients and these were compared with the presence and number of fQRS., Results: Patients with fQRS were of older age (58 ± 12 vs. 55 ± 13 years, p = 0.03) and had prolonged QRS time (105 ± 12 vs. 93 ± 10 ms, p < 0.001) and a higher rate of Q waves on ECG (36% vs. 11%, p < 0.001). In addition, they had worse systolic (lower LVEF%, 44 ± 17 vs. 61 ± 12, p < 0.001) and diastolic functions (DT, 177 ± 77 vs. 211 ± 59 ms, p < 0.001; IVRT, 81 ± 27 vs. 92 ± 22 ms, p = 0.001; Em, 9 ± 4 vs. 10 ± 4 cm/s, p = 0.008; E/Em ratio, 11 ± 5 vs. 8 ± 4, p < 0.001) in comparison to patients with nonfragmented QRS. There was a significant negative correlation between the number of fQRS and left ventricle systolic functions (for LVEF%, r = - 0.595, p < 0.001). After adjustment for age and gender, the number of fQRS remained significantly negatively associated with left ventricular systolic and diastolic functions., Conclusion: We found that fQRS is related to left ventricular systolic dysfunction and diastolic dysfunction. fQRS, which may be the result of myocardial ischemia or scar on myocardial electrical parameters at the cellular level, may represent inadequate systolic and diastolic functions.

Neurocardiogenic syncope comprises situations triggered by neurological reflexes resulting in abnormal responses of the neurocardiovascular system that cause loss of consciousness. A vast number of clinical conditions may cause this disorder including pain, defecation, micturition, swallowing, cough, sudden fear or excitement, exercise, and long-time standing. Treatment options for syncope prevention are not satisfactory. Several agents were used for pharmacological treatment without success. Selective inhibitors of neuronal norepinephrine transporter (NET) like duloxetine may play a role in neurally mediated syncope by increasing synaptic norepinephrine levels. Therefore, we report the effect of duloxetine in a patient with pain-induced syncope resistant to standard regimens.

Background: Macrophages in atherosclerotic plaques secrete YKL-40, a new biomarker of acute and chronic inflammation in patients with stable CAD. We hypothesized that YKL-40 may be a specific marker reflecting the burden of localized inflammation in myocardium and a predictor in patients with STEMI. In this study, we investigated the relationship of YKL-40 to in-hospital major adverse cardiac events (MACE), reperfusion parameters and its predictors in patients with STEMI., Methods: In total, 80 patients with STEMI and no history of prior coronary artery disease (CAD), who underwent primary percutaneous coronary intervention (p-PCI), were enrolled consecutively. In addition, 30 patients with normal coronary arteries (NCA) were enrolled as a control group. Cardiac biomarker levels including creatinine kinase-MB fraction (CK-MB), troponin-I, admission glucose and inflammatory markers including leukocytes and YKL-40 levels were measured as admission values., Results: In our study, YKL-40 levels correlated to high-sensitivity CRP levels (r = 0.333, p = 0.003), TIMI risk score (r = 0.445, p < 0.001), age (r = 0.477, p < 0.001), pain to balloon time (r = 0.432, p < 0.001), leukocyte and neutrophil count (r = 0.386, p < 0.001 and r = 0.430, p < 0.001, respectively), hemoglobin (r = - 0.345, p = 0.002), admission and fasting blood glucose (r = 0.388, p < 0.001 and r = 0.427, p < 0.001), creatinine levels (r = 0.395, p < 0.001) and myocardial blush grade (r = - 0.334, p = 0.004). When the patients were divided into two groups determined by presence or absence of MACE, the patients with MACE had significantly higher levels of YKL-40 in comparison to the patients without MACE and the control group (194 ± 104, 114 ± 61 and 110 ± 53 μg/L, p < 0.001, respectively). In multivariate logistic regression analysis in STEMI patients, only YKL-40 level (OR: 1.011, 95%CI: 1.002-1.019, p = 0.011) and leukocyte count (OR: 1.264, 95%CI: 1.037-1.540, p = 0.020) were the independent predictors for MACE. Sensitivity and specificity of YKL-40 to predict MACE, when 125 μg/l was accepted as a cut-off value, were 84% and 70%, respectively., Conclusion: We found that serum YKL-40 is related to older age, increased admission glucose levels, leukocyte counts and decreased hemoglobin levels; YKL-40 level and leukocyte count independently predicted MACE.