The contribution of prostaglandins versus prostacyclin in ventricular remodeling during heart failure.

Although the role of Cox-2 in the heart's response to physiologic stress remains controversial (i.e. expression in myocytes versus other resident myocardial cells) the ever expanding role of prostanoids in multiple models of heart failure cannot be denied. Due to the fact that prostanoids are metabolized rather quickly (half life of seconds to minutes) it is believed these signaling mediators act in a paracrine fashion at the site of production. Evidence to date is quite convincing that these bioactive lipid derivatives are involved in physiologic homeostatic regulation as well as beneficial and maladaptive ventricular remodeling in heart failure. Thus, this review will assess the direct contribution of each PG on remodeling in the left ventricle (e.g. hypertrophy, functional effects, and fibrosis).