BACKGROUND AND OBJECTIVES: Coronary artery ectasia (CAE) is an angiographic finding characterized by dilation of an arterial segment with a diameter at least 1.5 times that of its adjacent normal coronary artery. Fragmented QRS (fQRS) complexes are electrocardiographic signals which reflect altered ventricular conduction around regions of a myocardial scar and/or ischaemia. In the present study, we aimed to evaluate the presence of fQRS in patients with CAE. SUBJECTS AND METHODS: The study population included 100 patients with isolated CAE without coronary artery disease (CAD) and 80 angiographically normal controls. fQRS was defined as the presence of an additional R wave or notching of R or S wave or the presence of fragmentation in two contiguous leads corresponding to a major coronary artery territory. RESULTS: The two groups were similar in terms of age, sex, hypertension, dyslipidemia, and family history of CAD. The presence of fQRS was significantly (p<0.05) higher in the CAE group than that in the normal coronary artery group (29% vs. 6.2%, p=0.008). Isolated CAE were detected most commonly in the right coronary artery (61%), followed by left anterior descending artery (52%), left circumflex artery (36%), and left main artery (9%). Multivariate stepwise logistic regression analysis showed that CAE {odds ratio (OR) 1.412; 95% confidence interval (CI) 1.085-1.541; p=0.003} and diabetes (OR 1.310; 95% CI 1.025-1.482; p=0.041) were independently associated with fQRS. CONCLUSION: The presence of fragmented QRS associated with increased risk for arrhythmias and cardiovascular mortality was significantly higher in patients with CAE than in patient with normal coronary artery. Further studies are needed to determine whether the presence of fragmented QRS is a possible new risk factor for patients with CAE.
Angiography ; Arrhythmias, Cardiac ; Arteries ; Cicatrix ; Coronary Artery Disease ; Coronary Vessels* ; Dilatation, Pathologic* ; Dyslipidemias ; Electrocardiography* ; Humans ; Hypertension ; Logistic Models ; Mortality ; Risk Factors

Patients with diabetes have an increased risk for development of cardiomyopathy, even in the absence of well known risk factors like coronary artery disease and hypertension. Diabetic cardiomyopathy was first recognized approximately four decades ago. To date, several pathophysiological mechanisms thought to be responsible for this new entity have also been recognized. In the presence of hyperglycemia, non-enzymatic glycosylation of several proteins, reactive oxygen species formation, and fibrosis lead to impairment of cardiac contractile functions. Impaired calcium handling, increased fatty acid oxidation, and increased neurohormonal activation also contribute to this process. Demonstration of left ventricular hypertrophy, early diastolic and late systolic dysfunction by sensitive techniques, help us to diagnose diabetic cardiomyopathy. Traditional treatment of heart failure is beneficial in diabetic cardiomyopathy, but specific strategies for prevention or treatment of cardiac dysfunction in diabetic patients has not been clarified yet. In this review we will discuss clinical and experimental studies focused on pathophysiology of diabetic cardiomyopathy, and summarize diagnostic and therapeutic approaches developed towards this entity.
Calcium ; Cardiomyopathies ; Coronary Artery Disease ; Diabetes Mellitus ; Diabetic Cardiomyopathies* ; Fibrosis ; Glycosylation ; Heart Failure ; Humans ; Hyperglycemia ; Hypertension ; Hypertrophy, Left Ventricular ; Reactive Oxygen Species ; Risk Factors

PURPOSE: The β3-adrenergic receptor (ADRB3) is expressed in visceral adipose tissue and has been speculated to contribute to lipolysis, energy metabolism, and regulation of the metabolic rate. In this study, we aimed to investigate the association of polymorphism of the ADRB3 gene with the sex of children with obesity and related pathologies. METHODS: ADRB3 gene trp64arg genotyping was conducted in 441 children aged 6–18 years. Among these subjects, 264 were obese (103 boys; 161 girls) and 179 were of normal weight (81 boys; 98 girls). In the obese group, fasting lipids, glucose and insulin levels, and blood pressure were measured. Metabolic syndrome (MS) was defined according to the modified World Health Organization criteria adapted for children. RESULTS: The frequency of trp64arg genotype was similar in obese and normal weight children. In obese children, serum lipid, glucose, and insulin levels; homeostasis model assessment of insulin resistance (HOMA-IR) scores; and MS were not different between arg allele carriers (trp64arg) and noncarriers (trp64trp). In 264 obese children, genetic analysis results revealed that the arg allele carriers were significantly higher in girls than in boys (p=0.001). In the normal weight group, no statistically significant difference was found between genotypes of boys and girls (p=0.771). CONCLUSION: Trp64arg polymorphism of the ADRB3 gene was not associated with obesity and MS in Turkish children and adolescents. Although no relationships were observed between the genotypes and lipids, glucose/insulin levels, or HOMA-IR, the presence of trp64arg variant was frequent in obese girls, which can lead to weight gain as well as difficulty in losing weight in women.
Adolescent ; Alleles ; Blood Pressure ; Child ; Energy Metabolism ; Fasting ; Female ; Genotype ; Glucose ; Homeostasis ; Humans ; Insulin ; Insulin Resistance ; Intra-Abdominal Fat ; Lipolysis ; Obesity ; Pathology ; Weight Gain ; World Health Organization

Purpose: Obesity is defined as the abnormal or excessive accumulation of fat over acceptable limits. Leptin is a metabolic hormone present in the circulation in amounts proportional to fat mass. Leptin reduces food intake and increases energy expenditure, thus regulating body weight and homeostasis. Various polymorphisms are present in the leptin gene and its receptor. These polymorphisms may be associated with obesity. This study aimed to show the association of leptin (+19) AG, leptin (2548) GA, and Gln223Arg leptin receptor polymorphisms with obesity and metabolic syndrome in Turkish children aged 6–17 years, and to conduct further investigations regarding the genetic etiology of obesity. Methods: A total of 174 patients diagnosed with obesity and 150 healthy children who were treated at Tokat Gaziosmanpaşa Medical School Hospital between September 2014 and March 2015 were included in this study. The ages of the children were between 6 and 17 years, and anthropometric and laboratory results were recorded. Genotyping of leptin (+19) AG, leptin (2548) GA, and leptin receptor Gln223Arg polymorphisms was performed by polymerase chain reaction. Results: An association between leptin receptor Gln223Arg gene polymorphism and obesity was detected. Conclusion Further studies are needed to determine the role of genetic etiologies and to indicate the role of leptin signal transmission impairment in the pathogenesis of obesity. We hope that gene therapy can soon provide a solution for obesity.

Purpose: Obesity is defined as the abnormal or excessive accumulation of fat over acceptable limits. Leptin is a metabolic hormone present in the circulation in amounts proportional to fat mass. Leptin reduces food intake and increases energy expenditure, thus regulating body weight and homeostasis. Various polymorphisms are present in the leptin gene and its receptor. These polymorphisms may be associated with obesity. This study aimed to show the association of leptin (+19) AG, leptin (2548) GA, and Gln223Arg leptin receptor polymorphisms with obesity and metabolic syndrome in Turkish children aged 6–17 years, and to conduct further investigations regarding the genetic etiology of obesity. Methods: A total of 174 patients diagnosed with obesity and 150 healthy children who were treated at Tokat Gaziosmanpaşa Medical School Hospital between September 2014 and March 2015 were included in this study. The ages of the children were between 6 and 17 years, and anthropometric and laboratory results were recorded. Genotyping of leptin (+19) AG, leptin (2548) GA, and leptin receptor Gln223Arg polymorphisms was performed by polymerase chain reaction. Results: An association between leptin receptor Gln223Arg gene polymorphism and obesity was detected. Conclusion Further studies are needed to determine the role of genetic etiologies and to indicate the role of leptin signal transmission impairment in the pathogenesis of obesity. We hope that gene therapy can soon provide a solution for obesity.