Samim Emet

Serum Endocan Level and the Severity of Coronary Artery Disease A Pilot Study

Endothelial-specific molecule 1 (endocan) is expressed in endothelial cells. We investigated the relationship between acute coronary syndrome (ACS) and serum endocan levels. We included 30 individuals as a control group and 53 patients diagnosed with ACS. The severity of coronary artery disease was assessed by a modified Gensini stenosis and SYNTAX scoring system. There was a significant difference in serum endocan levels between the control group and the ACS group (0.75 ± 0.13 vs 0.86 ± 0.25 ng/mL, P = .014). There was also a significant difference in serum endocan levels between diabetic patients with ACS and nondiabetic patients with ACS (1.02 ± 0.33 vs 0.81 ± 0.21 ng/mL, P = .016). There was no significant correlation between serum endocan level, Gensini, and SYNTAX score (r = .11, P = .53 and r = .16, P = .37). Endocan, a new biomarker of endothelial pathology, is significantly increased in patients with ACS.

Effect of Glycemic Regulation on Endocan Levels in Patients With Diabetes: A Preliminary Study.

Endothelial-specific molecule 1 (endocan) is expressed by endothelial cells and may have a major role in the regulation of cell adhesion and in the pathogenesis of inflammatory disorders. We aimed to assess change in endocan levels after 3 months of lifestyle change recommendations and guideline-based treatment. Diabetic patients (n = 77) who had neither chronic kidney disease nor chronic inflammatory disease were included. After baseline evaluation, the patients were advised lifestyle changes, and their medical treatment was determined individually according to recommendations of the American Diabetes Association (ADA) guidelines. At the end of third month patients were reevaluated. Baseline endocan levels were significantly increased in the study group compared with the control group. The third-month laboratory workup showed significant reductions in hemoglobin A1c, urinary albumin-to-creatinine ratio (UACR), and endocan levels. Only δ-UACR was independently correlated with δ-endocan in multivariate linear regression analysis. Our findings suggest that serum endocan concentrations are elevated in patients with type 2 diabetes and decrease following anti-hyperglycemic treatment. Furthermore, decrease in endocan concentrations might be associated with improved glycemic control and reductions in UACR.

Combined analysis of unipolar and bipolar voltage mapping identifies recurrences after unmappable scar-related ventricular tachycardia ablation

AIMS Scars causing ventricular tachycardia can extend deep to and beyond bipolar low-voltage areas (LVAs) and they may be a reason for endocardial ablation failure. Analysis of endocardial unipolar voltage maps has been used to detect scar transmurality and epicardial scar. We hypothesized that endocardial unipolar LVA around the overlying bipolar LVA may predict endocardial ablation recurrence in patients with structural heart disease undergoing substrate modification. METHODS AND RESULTS Twenty consecutive patients with structural heart disease (11 ischaemic and 9 non-ischaemic cardiomyopathy) and undergoing substrate modification due to unmappable ventricular tachycardia (VT) (18 males, 51 ± 11 age, LVEF: 36 ± 7%) were retrospectively reviewed. Bipolar LVA defined as <1.5 mV and unipolar LVA defined as <8.3 mV, respectively, on electro-anatomic mapping system. Peripheral unipolar LVA (pUni-LVA) surrounding bipolar LVA was measured and compared patients with and without VT recurrence at 6-month follow-up period. : Mean unipolar voltage and mean bipolar voltage was 6.26 ± 4.99 and 1.90 ± 2.30 mV, respectively. Bipolar voltage and unipolar voltage in corresponding points were correlated (r = 0.652, P = 0.0001). In all patients, unipolar LVAs were larger than the bipolar LVAs. Bipolar LVA (91.1 ± 93.5 vs. 87.5 ± 47.5 cm(2), P = 0.91) and unipolar LVA (148.1 ± 96.3 vs. 104.7 ± 44.2 cm(2), P = 0.21) were similar in patients with and without VT recurrence, respectively. Peripheral unipolar LVA was significantly larger in patients with VT recurrence than without (57.0 ± 40.4 vs. 17.2 ± 12.9 cm(2), P = 0.01). CONCLUSION In patients with structural heart disease and unmappable VT, pUni-LVA surrounding bipolar scar predicts recurrence of VT ablation. The results of this pilot study highlight the importance of intramural/epicardial substrate on endocardial VT ablation outcome.

Identification of gene variants related to the nitric oxide pathway in patients with acute coronary syndrome

Dysfunction of vascular endothelium is known to have an essential role in the atherosclerotic process by releasing mediators including nitric oxide (NO). Nitric oxide maintains endothelial balance by controlling cellular processes of vascular smooth muscle cells. Evidence suggests that variations in the NO pathway could include atherosclerotic events. The objective of this study was to determine the possible effects of genes on the nitric oxide pathway in the development of acute coronary syndrome (ACS). The blood samples of 100 patients with ACS and 100 controls were collected at Istanbul University, Department of Cardiology. DNA samples were genotyped by using Illumina Cyto-SNP-12 BeadChip. The additive model and Correlation/Trend Test were selected for association analysis. Afterwards, a Q-Q graphic was drawn to compare expected and obtained values. A Manhattan plot was produced to display p-values that were generated by -log10(P) function for each SNP. The p-values under 1×10(-4) were selected as statistically significant SNPs while p-values under 5×10(-2) were considered as suspicious biomarker candidates. Nitric oxide pathway analysis was then used to find the single nucleotide polymorphisms (SNPs) related to ACS. As a result, death-associated protein kinase 3 (DAPK) (rs10426955) was found to be most statistically significant SNP. The most suspicious biomarker candidates associated with the nitric oxide pathway analysis were vascular endothelial growth factor A (VEGFA), methionine sulfoxide reductase A (MSRA), nitric oxide synthase 1 (NOS1), and GTP cyclohydrolase I (GCH-1). Further studies with large sample groups are necessary to clarify the exact role of nitric oxide in the development of disease.

An Unexpected Result of Obesity Treatment: Orlistat-Related Acute Pancreatitis.

Orlistat is a pancreatic lipase inhibitor which is used to treat obesity. Due to the increasing prevalence of obesity, orlistat use is thought to rise progressively. We report an interesting case caused by orlistat use caught in the early stages of acute pancreatitis through imaging; in addition, the case had significantly elevated serum amylase levels. A 54-year-old male who had a history of orlistat treatment started 7 days before was admitted to the emergency department with complaints of abdominal pain, nausea and vomiting lasting for 24 h. Abdominal computed tomography revealed peripancreatic fat tissue edema and a heterogeneous appearance of the pancreas. Based on these findings, it was concluded that edematous pancreatitis was in its initial stage. Orlistat is a drug that is increasingly widespread use due to obesity. More attention must be paid when planning to prescribe orlistat to patients if there are risk factors for acute pancreatitis (alcohol use, height, serum calcium and lipid levels).

GALECTIN-3: A NOVEL BIOMARKER PREDICTS SUDDEN CARDIAC DEATH IN HYPERTROPHIC CARDIOMYOPATHY

Background: Hypertrophic cardiomyopathy is a primary cardiac disease characterized by left ventricular hypertrophy, myocyte hypertrophy and irregularities and interstitial fibrosis in the absence of any cardiac or systemic diseases and may lead to sudden cardiac death (SCD). Galectin‐3 is a &bgr;‐galactoside‐binding lectin that has been associated with cardiac fibrosis and inflammation. In this study, we aimed to investigate the relationship between serum galectin‐3 levels and the criteria for 5‐year sudden death risk, recently defined in the European Society of Cardiology guidelines (2014), in patients with hypertrophic cardiomyopathy. Materials and Methods: A total of 52 hypertrophic cardiomyopathy patients were enrolled in the study. Patients were questioned for sudden death risk predictors as outlined in the 2014 European Society of Cardiology guideline. A standardized clinical evaluation was carried out on the basis of previously described prognostic variables to calculate the 5‐year risk of SCD. Blood samples were taken from all patients to measure serum galectin‐3 levels. A statistical significance level of P < 0.05 was accepted in all tests. Results: We found that there was a significant correlation between the estimated 5‐year risk of SCD and serum levels of galectin‐3. Conclusions: Galectin‐3 may be an inexpensive and easily accessible parameter to predict arrhythmia risk. In addition, it can be used to determine antiarrhythmic prophylaxis as a predictor of an arrhythmia storm in implantable cardioverter defibrillator‐implanted patients who are not available for magnetic resonance imaging.

Unexpected effect of mad honey poisoning on accessory pathway

Mad honey poisoning can occur by the ingestion of mad honey extracted from the flowers and leaves of Rhododendron species grown on the mountains of the eastern Black Sea region in Turkey, and also in some regions of North America, Europe, Japan, Nepal, and Brazil. The toxin responsible for the poisoning is called the grayanotoxin (GTX).1 GTX binds to the alpha subunits of the voltage-gated sodium channel leading to hyperpolarization. Also, M2-muscarinic receptors are involved in this process and they are responsible for findings like hypotension, bradycardia, atrioventricular (AV) node blockage, and respiratory depression which can occur in a patient exposed to GTX in a dose-dependent manner.2,3 Here, we are reporting a case of mad honey poisoning in which the patient had electrical blockage of the heart in not only the AV node but also through the accessory pathway. To best of our knowledge, this is the first case report presenting a blockage in accessory pathway of the heart due tomad honey poisoning.

T wave peak-to-end interval in COPD

Introduction The interval from the peak to the end of the electrocardiographic (ECG) T wave (Tp–Te) can estimate cardiovascular mortality and ventricular tachyarrhythmias. Objectives In this study, we aimed to define a new ECG parameter in patients with COPD. Methods This was a cross-sectional observational study that included COPD patients who were diagnosed previously and followed up in the outpatient clinic. All data of the patients’ demographic features, history, spirometry, and electrocardiographs were analyzed. Results We enrolled 134 patients with COPD and 40 healthy volunteers as controls in our study. Patients already known to be having COPD who were under follow-up for their COPD and diagnosed as having COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria were included. Men comprised 82.8% of the COPD group and 73.2% of controls. The mean age in the COPD and control group was 60.2±9.4 and 58.2±6.7 years, respectively. There was no significant difference between the groups for age or sex (p=0.207, p=0.267, respectively). There were 46 (34.3%) patients in group A, 23 (17.2%) patients in group B, 26 (19.4%) patients in group C, and 46 (29.1%) patients in group D as COPD group. There was a significant increase in Tp–Te results in all precordial leads in the COPD group compared with the control group (p<0.05). Precordial V4 lead has the most extensive area under the curve (0.831; sensitivity 76.5%, specificity 89.6%). Conclusion We present strong evidence that Tp–Te intervals were increased in patients with COPD, which suggests that there may be an association between COPD and ventricular arrhythmias and cardiac morbidity.

A Case of Aortopulmonary Window: Asymptomatic until the First Pregnancy.

The aortopulmonary window (APW) is an abnormal communication between the ascending aorta and the pulmonary trunk in the presence of two separate semilunar valves. It is a rare congenital malformation which represents 0.1% of all congenital cardiac diseases. Herein, we report a very rare case of 27-year-old patient with unrepaired APW causing Eisenmenger syndrome and pulmonary hypertension who was asymptomatic until her first pregnancy. The median survival of uncorrected APW is 33 years. Aortopulmonary window is a very rare congenital anomaly. To our knowledge, asymptomatic adult case has not been reported until now. APW should be considered in the differential diagnosis of the severe pulmonary hypertension also in adult patients.

A case of an atypically located cardiac hydatid cyst.

Thirty five year old female patient with complaints of chest pain, numbness in the left arm and presyncopy was admitted to the cardiology clinic. There were no significant findings on cardiac examination. Electrocardiography (ECG) revealed T negativity in leads aVL, D1 and V1-5. Her blood tests were creatinine: 1.1 mg/dL, BUN: 33, Na: 144 mmoL/L, K: 4.4 mmoL/L, glucose: 110 mg/dL, pro-BNP: 117 pg/mL, fT4: 14, TSH: 2.34, AST: 16 U/L, ALT: 14 U/L, LDH: 266 U/L, CRP: 3 mg/L, sedimentation rate: 32 mm/h, hs-troponin: 6 pg/mL (<13 pg/mL), Hgb: 12.6/dL, WBC 7,400/mm3, platelets: 296,000 mm3. Three dimensional transthoracic and transoesophageal echocardigraphy of the patient revealed a cystic mass in size of 4.6 x 4.2 cm in the interventricular septum (Video 1, Fig. 1, 2). A preliminary diagnosis of hydatid cyst was thought so indirect hemagglutination test was requested and it resulted as positive. In Cardiac MRI,