فهرست مطالب ramin behrozian

There is no obvious etiology for cardiac syndrome X (CSX). Some mechanisms, such as endothelial dysfunction and estrogen deficiency have been involved. In this study, we tried to find the association between Helicobacter pylori (HP) infection and cardiac syndrome X. In this case control study in year 2007, 54 cardiac syndrome X-affected patients and 168 referred patients to the Taleghani hospital for elective surgery were included. Data were collected by interview physical examination, laboratory and angiographic findings. Then, Serum anti-Helicobacter pylori antibody (IgG) was determined by enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed using Chi-square, and Mantel- Hanzel tests with SPSS software. According to the results of this study, 54 patients were considered as case group and meeting diagnostic criteria for cardiac syndrome X. The mean age of subjects was 54.54±8.99 years (range=38 to 72 years). From the total 54 case group patients, 44 patients (81.5%) were positive for helicobacter pylori and from 168 control patients, 95 patients (56.5%) were positive (P<0.001). There was no significant difference between history of diabetes and blood pressure in H.pylori-positive cardiac syndrome X-affected patients According to the results of this study, a probable role for HP infection seems to be involved in the pathogenesis of CSX.

There are two kinds of ascites, cirrhotic and malignant. The conventional diagnostic method to differentiate them is paracentesis. This is an invasive and time consuming method. However, ultrasonography is an easy and available method to provide valuable results in a short period of time. The aim of this study was to evaluate gallbladder wall thickness in differentiating cirrhotic ascites from malignant ones. In our study, gallbladder wall thickness was measured by ultrasonography (3.5-5 MHZ curve linear ultrasound probe) in 100 patients with portal hypertension induced ascites and in 100 patients with peritoneal carcinomatosis induced ascites. The mean gallbladder wall thickness was 3.9±0.6 mm in cirrhotic patients and 2.2±0.6 mm in non-cirrhotic patients. Gallbladder wall thickening was significantly more frequent in patients with cirrhotic ascites than in patients with non-cirrhotic ascites (p‹0.001). This study revealed that the ultrasound finding of gallbladder wall thickening in patients with ascites could be highly predictive for portal hypertension induced ascites.