We previously showed that
digitoxin prolongs the survival of rats with
heart failure due to
myocardial infarction (MI). In this study, we evaluated the effect of
digitoxin on myocardial structure, ventricular function, and
proteins involved in
calcium kinetics. Seventy-two rats with MI >35% of the left ventricle were randomly assigned to 4 treatment groups:
sham (n = 15),
digitoxin (n = 11),
infarction (n = 20), and
infarction +
digitoxin (n = 26). The rats were assessed 120 days after surgery by echocardiogram, hemodynamics, papillary muscle mechanics,
collagen content, cardiomyocyte nuclear volume, and Western blot analysis of
proteins involved in
calcium kinetics.
Digitoxin was administered via the rat chow. Two-way analysis of variance was used for comparisons.
Myocardial infarction caused inotropic impairment, pulmonary congestion, increase of nuclear volume, myocardial
collagen, and Na+/Ca2+ exchanger levels, and decreased SERCA2 and phosphorylated
phospholamban levels. Treatment with
digitoxin showed improvements in cardiac remodeling, inotropism, ventricular performance, pulmonary congestion,
collagen accumulation, nuclear volume, and
proteins involved in
calcium kinetics. In rats with
heart failure due to MI, long-term treatment with
digitoxin attenuates
congestive heart failure, mitigates myocardial remodeling and contractile impairment, and preserves myocardial levels of
proteins involved in
calcium kinetics.