A Case of Pacemaker Lead Fracture Associated with Thoracic Outlet Syndrome

A pacemaker lead fracture in the left subclavian vein was caused by compression of the clavicle and the first rib; subsequent coil elongation at the same site on the right side was observed in the replacement lead in a patient with thoracic outlet syndrome. Venography showed narrowing of the subclavian vein at the site where the lead abnormalities were observed. This case illustrates that a lead in the subclavian vein can be easily damaged when a patient has thoracic outlet syndrome.     

Torsion of the hernia sac within a hydrocele of the scrotum in a child

Torsion of the hernia sac is a rare disease that presents as acute scrotum in children. Including the present case, only six cases have been reported in the English literature. We report a 10-year-old boy who presented with pain and swelling of his right scrotum. Ultrasonography revealed a hypoechoic region adjacent to the normal right testis. The inflammatory changes of the right scrotum deteriorated. The patient underwent surgery and a necrotic cyst was recognized within a hydrocele of the scrotum. The cyst was not connected with the testis or epididymis and was twisted at an angle of 270 degrees. The cause of the necrotic cyst observed was anatomical and pathological torsion of the hernia sac.     

Polymorphism of renin-angiotensin system genes in progressive IgA nephropathy

Summary: Clinical studies revealed that angiotensin converting enzyme (ACE) inhibitor reduces proteinuria and attenuates progressive decline in renal function in IgA nephropathy. Recent studies by us and others have demonstrated that the homozygote of the D allele (DD) of the ACE insertion/deletion (I/D) polymorphism is a potential risk factor for poor prognosis in IgA nephropathy, and that this deletion polymorphism predicts the therapeutic efficacy of ACE inhibition on proteinuria and, potentially, on progressive deterioration of renal function in patients with the nephropathy.     

Appropriate Heart Rate in a Patient with Repaired Tetralogy of Fallot

Appropriate heart rate in a failing pulmonary ventricle remains unknown, particularly in congenital heart disease with unique hemodynamics. A 71-year-old male with repaired tetralogy of Fallot and a pacemaker for a sinus node dysfunction suffered from heart failure symptoms with preserved left ventricular function. Simply changing the pacemaker’s lower rate from 60 to 75 bpm, New York Heart Association classification improved from III to II, and hemodynamic parameters drastically improved. We regarded this case as informative. Appropriate heart rate could be higher in congenital patients with failing right and non-failing left ventricles than in adults with malfunctioning LV.     

Upregulation of Angiotensin II Receptor and Connexin 43 in Increased Suburothelial Myofibroblasts in the Rat Inflammatory Bladder

Objectives: Signaling pathways in suburothelial layer are involved in the bladder sensory response. The expression of angiotensin II type 1 (AT1) receptors and connexin 43 (Cx43) in suburothelial myofibroblasts was investigated in an acute bladder inflammation model. Methods: Adult female Wistar rats underwent urethral catheterization and received 0.2 mL intravesical infusion of 0.4 M HCl to establish acute bladder inflammation model or 0.2 mL of sterile saline as control (n = 10 rats/group). Eight days after treatment, cystometry was performed. Suburothelial myofibroblasts were also collected and subjected to immunohistochemical staining to examine AT1 receptor and Cx43 expression. Results: Eight days after treatment with HCl to induce acute bladder inflammation, the frequency and basal pressure of the bladder was significantly increased compared with those in control rats. The number of suburothelial myofibroblasts was significantly increased in acute bladder inflammation rats, as was the expression of AT1 receptor and Cx43. Conclusion: These results suggest that the increased number of suburothelial myofibroblasts, upregulation of AT1 receptor and Cx43 expression may be associated with the pathogenesis of hyperactivation of bladder sensory signaling pathways in acute inflammatory bladder.