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Objectives: This study aimed to determine the risk factors for the occurrence of arrhythmias after either transcatheter or surgical closure of atrial septal defect. Methods: This prospective study included 150 patients admitted for transcatheter or surgical closure of atrial septal defect. Transthoracic echocardiography together with a twelve-leads ECG were done during 1 and 3 months follow up. The paired T, chi-square and Logistic regression tests were used to detect any association between any arrhythmias and factors that may affect its occurrence. Results: One-hundred and twenty-three patients had percutaneous device closure while the remaining 27 patients had surgical closure. The youngest and oldest of the studied patients being 3 & 50 years old respectively with female (108) over male (42) predominance in incidence. After closure, 8 patients at one month and another 3 patients at three months follow up out of the total 150 patients had supraventricular arrhythmias in the form of frequent premature atrial contractions (6 patients), atrioventricular nodal re-entrant tachycardia (2 patients), and paroxysmal Atrial fibrillation (3 patients). No conduction abnormalities nor ventricular arrhythmias occurred. Multivariate analysis showed that age, P wave dispersion, systolic myocardial velocity of right ventricle, and systolic pulmonary artery pressure were independently associated with the occurrence of atrial arrhythmia after atrial septal defect repair. Conclusion: Age, P wave dispersion, Systolic pulmonary artery pressure, and systolic myocardial velocity of the right ventricle are independent risk factors to develop arrythmias in patients after atrial septal defect closure.
RESUMO
BACKGROUND: Endothelial dysfunction (ED) is closely linked to cardiovascular disease and outcome in patients with chronic kidney disease (CKD). Visfatin is an adipocytokine that recently generated much interest; however, its role in CKD remains to be clarified. This study aimed to assess visfatin in correlation with markers of ED and inflammation in Egyptian patients with CKD. METHODS: The study included 40 non-diabetic, clinically stable CKD patients and 20 healthy volunteers. Serum levels of visfatin, markers of ED (intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) and markers of inflammation (interleukin-6 (IL-6), and C-reactive protein (CRP)) were measured. Endothelial function was evaluated using brachial artery flow-mediated dilatation (FMD). RESULTS: Serum visfatin, ICAM-1, VCAM-1, CRP, and IL-6 levels were significantly elevated and FMD% was decreased in CKD patients as compared to controls. Visfatin correlated positively with ICAM-1, VCAM-1, CRP, and IL-6 and negatively with FMD% in CKD patients. In a multiple regression model, visfatin was strongly and independently associated with FMD (Beta=-0.02, P<0.001) in CKD patients. CONCLUSIONS: Serum visfatin is strongly associated with endothelial adhesion molecules and FMD%, suggesting that visfatin is an important promising biomarker for prediction of ED and future cardiovascular risk in CKD patients. Moreover, the relationship between visfatin and IL-6 indicates that circulating visfatin may reflect the sub-clinical inflammatory status. Thus, visfatin might be involved in the complex interactions between ED, inflammation, and atherosclerosis and their major clinical consequences; however, further prospective studies are required to prove this hypothesis.