Myocardial infarction (MI) initiates adaptive tissue remodeling, which is essential for heart function (such as
infarct healing) but is also important for maladaptive remodeling (for example, reactive
fibrosis and left ventricular dilation). The effect of
aldosterone receptor antagonism on these processes was evaluated in Sprague-Dawley rats using
eplerenone, a selective
aldosterone receptor antagonist.
Infarct healing and
left ventricular remodeling were evaluated at 3, 7, and 28 days after MI by determination of the diastolic pressure-volume relationship of the left ventricle, the
infarct-thinning ratio, and the
collagen-volume fraction.
Eplerenone did not affect reparative
collagen deposition as was evidenced by a similar
collagen volume fraction in the infarcted myocardium between
eplerenone and vehicle-treated groups at 7 and 28 days post-MI. In addition, the thinning ratio, which is an index of
infarct expansion, was comparable between the
eplerenone and vehicle-treated animals at 7 and 28 days post-MI. A protective effect of
eplerenone was demonstrated at 28 days post-MI, where reactive
fibrosis in the viable myocardium was reduced in
eplerenone-treated animals compared with vehicle-treated animals. Thus
aldosterone receptor antagonism does not retard
infarct healing but rather protects against maladaptive responses after MI.