Article history: Received 24 July 2012, Accepted 7 November 2012, Available online 29 December 2012″
“Atrial fibrillation (AF) is self-perpetuating, via mechanisms of acute electrical remodelling and ‘second factors’ acting over a longer time course. Renin-angiotensin system (RAS) blockade may inhibit AF self-perpetuation. We evaluated the effects of RAS blockade with candesartan in a burst-paced goat model of lone AF in which both mechanisms are known to operate. Bioactivity of oral candesartan was demonstrated in 10 goats by inhibition of the pressor effect NVP-LBH589 of angiotensin II. The effects of candesartan on electrical remodelling were assessed in 12 placebo and 12 candesartan-treated

goats in a 28-day burst pacing protocol. To assess the effects of candesartan on second factors Fludarabine mw (structural remodelling), 16 goats underwent further 28-day periods of burst pacing (two periods in 16 goats, three periods in eight goats) each separated by periods of sinus rhythm sufficient for electrical remodelling to reverse. There was a progressive rise in angiotensin levels in both groups. Candesartan (0.5 mg/kg/day) achieved a 76% blunting of the pressor effect of angiotensin II and had no effect on electrical remodelling; the half time for fall of atrial effective refractory period (AERP) was 22.3 +/- 4.9 h (placebo) and 22.0 +/- 3.2 h (candesartan) (p = ns). Candesartan had no effect on AF stability, which progressively

increased over successive 28-day periods (ANOVA p < 0.05). Candesartan had no effect on atrial electrical remodelling or the operation of ‘second factors’ in a goat model of lone AF. These findings suggest that any benefits of RAS blockade in patients with AF are unlikely to be due to direct effects on atrial remodelling.”
“Objectives: To investigate population trends in thoracic aortic disease (dissections YH25448 order and aneurysms) in England and Wales, with focus on the impact of thoracic endovascular aortic repair on procedure numbers and age at repair.

Materials and methods: Routine hospital

statistics of England and Wales provided admission, procedure and mortality data from 1999 to 2010. All data were age-standardised, reported per 100,000 population, by age bands (>50 years or 50-74 years versus 75+ years) and gender. Only patients 50+ years were included, to focus on degenerative disease.

Results: Between 1999 and 2010 hospital admissions for total (ascending and descending) have risen steadily for thoracic aortic dissection (TAD) from 7.2 to 8.8 and thoracic aortic aneurysm (TAA) from 4.4 to 9.0, principally attributable to increased admissions in those 75+ years. Total mortality declined steadily over the same period, for TAD from 4.4 to 3.2 and for TAA from 10.4 to 7.5. Procedure rates have risen sharply, driven by the implementation of TEVAR from 2006, for type B dissection from 0.06 to 0.53 and for descending TAA from 0.76 to 1.89.