Unsuccessful transjugular intrahepatic portosystemic shunt for a patient with right heart failure and portal hypertension.

A 60-year-old women with a history of congenital pulmonary valve stenosis developed right heart failure, cardiac cirrhosis and end-stage renal disease requiring renal replacement therapy. Cirrhosis was complicated by portal hypertension, resulting in intractable gastro-intestinal bleedings despite optimal treatment with beta-blockers and endoscopic band ligation. Because of fears for worsening right heart failure, a decision for placement of a transjugular intrahepatic portosystemic shunt (TIPS) was initially turned down.

Loop diuretic down-titration in stable chronic heart failure is often achievable, especially when urinary chloride concentration is low.

Background: This study investigates spot urinary chloride concentration in euvolemic chronic heart failure (CHF) patients.

Methods: This prospective cohort study included 50 ambulatory CHF patients on maintenance loop diuretics without recent hospital admission, clinical signs of volume overload, or adjustment in neurohumoral blocker or diuretic therapy. Spot urinary samples were collected immediately after loop diuretic intake.

Long-Term Performance of the Riata/ST Implantable Cardioverter-Defibrillator Lead.

Riata and Riata ST implantable cardioverter-defibrillator leads are prone to structural and electrical failure (EF). Our objective was to evaluate Riata/ST lead performance over a long-term follow-up. Of 184 patients having undergone Riata/ST and Riata ST Optim lead implantation from September 2003 to June 2008, 154 patients were evaluated for EF and radiographic conductor externalization (CE).

Increased cardiovascular risk in patients with rheumatoid arthritis: an overview.

Patients with established rheumatoid arthritis (RA) have a higher cardiovascular morbidity and mortality in comparison with the general population. It is considered to be an independent risk factor for cardiovascular disease. The purpose of this article is to describe the mechanisms responsible for accelerated atherogenesis in RA patients and to give an overview of the effects of different RA therapies (methotrexate, TNF antagonists and other biologicals).