Steven K Hildemann

TL;DR: The aldosterone blocker eplerenone improved LV remodeling in rats with LV dysfunction after extensive MI by a complementary prevention of LV fibrosis, cardiac hypertrophy, and molecular alterations.

TL;DR: Spironolactone added to an ACE inhibitor normalizes NO-mediated relaxation in experimental CHF by beneficially modulating the balance of NO and superoxide anion formation.

TL;DR: In experimental CHF, the selective aldosterone antagonist EPL reduced the increased vascular superoxide formation and although a combination of TR and EPL normalised endothelium-dependent relaxation, ACE inhibition as a monotherapy was almost equally effective.

TL;DR: The results show that platelet activation was evident only in CHF rats, which was completely rescued to basal levels by combination therapy, and increased nitric oxide bioavailability can only partially explain the reduced plateletactivation by eplerenone and ACE inhibition.

TL;DR: In CHF fractalkine was increased on the endothelium and in blood serum, and platelet surface-expression of CX3CR1 was enhanced, which may indicate a novel pathophysiological mechanism contributing to impaired clopidogrel responsiveness in CHF.