The Importance of Right Ventricular Lead Positioning in Determining Outcomes of Cardiac Resynchronization Therapy.

Cardiac resynchronization therapy is known to improve clinical outcomes in patients with heart failure and left ventricular dyssynchrony. However, the optimal positioning of the right ventricular lead is unknown, and there is conflicting data on the acute hemodynamic effects and long-term outcomes. Here, we present a case of a patient who underwent implantation of a dual-chamber pacemaker for complete heart block, but who after three months, still had symptoms consistent with New York Heart Association (NYHA) Class IV heart failure. After optimal medical therapy failed and a left ventricular lead was placed, he still remained symptomatic, so the right ventricular lead was repositioned from the right ventricular outflow tract to the right ventricular apex. Afterwards, the patient's symptoms improved from NYHA Class IV to NYHA Class II, and his left ventricular ejection fraction improved from 20% to 45%.

A novel genetically-obese rat model with elevated 11 beta-hydroxysteroid dehydrogenase type 1 activity in subcutaneous adipose tissue.

11 ß-hydroxysteroid dehydrogenase type 1 (11 ß-HSD1) catalyzes the conversion of inactive glucocorticoids to active glucocorticoids and plays an important role in the development of obesity and metabolic syndrome. 11 ß-HSD1 activity is lower in liver and higher in omental adipose tissue of obese rodent models like obese zucker rats, Ob/Ob and db/db mice. Here, we report the 11 ß-HSD1 activity in liver and adipose tissue of lean and obese rats of WNIN/Ob strain, a new genetic rat model of obesity. 11 ß-HSD1 activity in liver, omental and subcutaneous adipose tissues of 3 month-old male WNIN/Ob lean and obese rats was assayed. As observed in other rodent models, 11 ß-HSD1 activity was lower in liver and higher in omental adipose tissue. In contrast to other rodent obese models, WNIN/Ob obese rats had elevated 11 ß-HSD1 activity in subcutaneous adipose tissue, which is in line with the observation in human obesity. Here, we conclude that dysregulation of 11 ß-HSD1 in WNIN/Ob obese rat model is identical to human obesity, which makes it an excellent model for studying the effect of 11 ß-HSD1 inhibitors in ameliorating obesity and metabolic syndrome.