Background-Postinfarction left ventricular remodeling (LVR) is associated w
ith reductions in myocardial high-energy phosphate (HEP) levels, which are
more severe in animals that develop overt congestive heart failure (CHF). D
uring high work states, further HEP loss occurs, which suggests demand-indu
ced ischemia. This study tested the hypothesis that inadequate myocyte oxyg
en availability is the basis for these HEP abnormalities.
Methods and Results-Myocardial infarction was produced by left circumflex c
oronary artery ligation in swine. Studies were performed in 20 normal anima
ls, 14 animals with compensated LVR, and 9 animals with CHF. Phosphocreatin
e (PCr)/ATP was determined with P-31 NMR and deoxymyoglobin (Mb-delta) with
H-1 NMR in myocardium remote from the infarct, Basal PCr/ATP tended to be
decreased in postinfarct hearts, and this was significant in animals with C
HF. Infusion of dobutamine (20 mu g.kg(-1).min(-1) IV) caused doubling of t
he rate-pressure product in both normal and LVR hearts and resulted in comp
arable significant decreases of PCr/ATP in both groups. This decrease in PC
r/ATP was not associated with detectable Mb-delta, In CHF hearts, rate-pres
sure product increased only 40% in response to dobutamine; this attenuated
response also was not associated with detectable Mb-delta.
Conclusions-Thus, the decrease of PCr/ATP during dobutamine infusion is not
the result of insufficient myocardial oxygen availability. Furthermore, in
CHF hearts, the low basal PCr/ATP and the attenuated response to dobutamin
e occurred in the absence of myocardial hypoxia, indicating that the HEP an
d contractile abnormalities were not the result of insufficient oxygen avai
lability.