We would like to emphasize that SA is mono-articular, frequently localized in the knee, hip and ankle in 85% of patients, joint fluid culture was positive in 55% of patients, bacteria was isolated from one or more cultures of blood, joint fluid, pus or bone in 70% of patients and the most common isolated micro-organism was S. aureus. In addition, it must be pointed out that children younger than 2 years of age with fever, a positive trauma history and/or abnormal joint findings should be carefully examined for SA because the rate of SA was lower (7.5%) than expected in this age group. We also found that the mortality of SA was not influenced by age, joint involvement and bacterial agents, and there was no significant difference in symptoms on admission, the history of trauma and antibiotic use, sex, age, fever, joint involvement,anemia, leukocytosis and micro-organisms isolated from joint fluid and blood between patients with SA
The study aimed to investigate the intermediate-term effects of transcatheter atrial septal defect (ASD) closure on cardiac remodeling in children and adult patients. Between December 2003 and February 2009, 117 patients (48 males, 50 adults) underwent transcatheter ASD closure with the Amplatzer septal occluder (ASO). The mean age of the patients was 15 years, and the mean follow-up period was 25.9 +/- 12.4 months. New York Heart Association (NYHA) class, electrocardiographic parameters, and transthoracic echocardiographic (TTE) examination were evaluated before the ASD closure, then 1 day, 1 month, 6 months, 12 months, and yearly afterward. Transcatheter ASD closure was successfully performed for 112 (96%) of the 117 patients. The mean ASD diameter measured by transesophageal echocardiography (TEE) was 14.0 +/- 4.2 mm, and the mean diameter stretched with a sizing balloon was 16.6 +/- 4.8 mm. The mean size of the implanted device was 18.6 +/- 4.9 mm. The Qp/Qs ratio was 2.2 +/- 0.8. The mean systolic pulmonary artery pressure was 40 +/- 10 mmHg. At the end of the mean follow-up period of 2 years, the indexed right ventricular (RV) end-diastolic diameter had decreased from 36 +/- 5 to 30 +/- 5 mm/m(2) (p = 0.005), and the indexed left ventricular (LV) end-diastolic diameter had increased from 33 +/- 5 to 37 +/- 6 mm/m(2) (p = 0.001), resulting in an RV/LV ratio decreased from 1.1 +/- 0.2 to 0.8 +/- 0.2 (p = 0.001). The New York Heart Association (NYHA) functional capacity of the patients was improved significantly 24 months after ASD closure (1.9 +/- 0.5 to 1.3 +/- 0.5; p = 0.001). At the 2-year follow up electrocardiographic examination, the P maximum had decreased from 128 +/- 15 to 102 +/- 12 ms (p = 0.001), the P dispersion had decreased from 48 +/- 11 to 36 +/- 9 ms (p = 0.001), and the QT dispersion had decreased from 66 +/- 11 to 54 +/- 8 ms (p = 0.001). Five of six patients experienced resolution of their preclosure arrhythmias, whereas the remaining patient continued to have paroxysmal atrial fibrillation. A new arrhythmia (supraventricular tachycardia) developed in one patient and was well controlled medically. Transcatheter ASD closure leads to a significant improvement in clinical status and heart cavity dimensions in adults and children, as shown by intermediate-term follow-up evaluation. Transcatheter ASD closure can reverse electrical and mechanical changes in atrial myocardium, resulting in a subsequent reduction in P maximum and P dispersion times.
Objective:The clinical use of doxorubicin, which is a strong antineoplastic agent, is limited due to its cardiotoxic side effects. Metformin is a drug with antihyperglycemic effects, and it has been shown to have a cardioprotective effect on left ventricular function in experimental animal models of myocardial ischemia. The present study investigated the cardioprotective effect of metformin in rats with doxorubicin cardiotoxicity.Methods:Wistar albino rats were used in the study. Forty male, 10-week-old Wistar albino rats were randomly divided four groups. The control group rats were intraperitoneally administered saline solution twice a week, four doses in total. The doxorubicin group rats received doxorubicin (4 mg/kg, twice a week, cumulative dose: 16 mg/kg) intraperitoneally. The metformin group rats received metformin (250 mg/kg/day, every day for 14 days) via gavage. The doxorubicin + metformin group rats received doxorubicin and metformin at the same dose. Left ventricular functions were evaluated by using M-mode echocardiography one day after the last dose of doxorubicin. Heart tissue samples were histopathologically examined. Cardiomyocyte apoptosis was detected using in situ terminal deoxynucleotide transferase assay (TUNEL). Serum brain natriuretic peptide and C-type natriuretic peptide levels were measured. Catalase, superoxide dismutase, glutathione peroxidase, and tumor necrosis factor alpha levels were analyzed in the heart tissue. The assumptions of equality of variances and normal distribution were checked for all variables (Shapiro-Wilk test and Q-Q graphics). To identify intergroup differences, one-way variant analysis or the Kruskal-Wallis test was used. A p<0.05 value was accepted as statistically significant.Results:Our results showed that doxorubicin treatment caused significant deterioration in left ventricular functions by echocardiography, histological heart tissue damage, and increase in cardiomyocyte apoptosis. Doxorubicin + metformin group showed protection in left ventricular function, elimination of histopathologic change, and reduced of cardiomyocyte apoptosis.Conclusion:The present study provided evidence that metformin has cardioprotective effects against doxorubicin cardiotoxicity.
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