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Divisions of Endocrinology and Pediatric Cardiology, Departments of Medicine and Pediatrics, North Shore University Hospital/New York University School of Medicine, Manhasset, New York 11030
In a rat model of acute
myocardial infarction (MI) produced by coronary artery ligation,
thyroid hormone metabolism was altered with significant reductions
(54%) in serum triiodo-L-thyronine (T3), the
cellular active hormone metabolite. T3 has profound effects
on the heart; therefore, rats were treated with T3 after acute MI for 2 or 3 wk, at either replacement or elevated doses, to
determine whether cardiac function and gene expression could be
normalized. Acute MI resulted in a 50% (P < 0.001)
decrease in percent ejection fraction (%EF) with a 32-35%
increase (P < 0.01) in compensatory left ventricle
(LV) hypertrophy. Treatment of the MI animals with either replacement
or elevated doses of T3 significantly increased %EF to 64 and 73% of control, respectively. Expression levels of several
T3-responsive genes were altered in the hypertrophied LV
after MI, including significant decreases in 
-myosin heavy chain
(MHC), sarcoplasmic reticulum calcium-activated ATPase (SERCA2), and
Kv1.5 mRNA, whereas 
-MHC and phospholamban (PLB) mRNA were
significantly increased. Normalization of serum T3 did not
restore expression of all T3-regulated genes, indicating altered T3 responsiveness in the postinfarcted myocardium.
Although -MHC and Kv1.5 mRNA content was returned to control levels,
-MHC and SERCA2 were unresponsive to T3 at replacement
doses, and only at higher doses of T3 was -MHC mRNA
returned to control values. The present study showed that acute MI in
the rat was associated with a fall in serum T3 levels, LV
dysfunction, and altered expression of T3-responsive genes
and that T3 treatment significantly improved cardiac
function, with normalization of some, but not all, of the changes in
gene expression.
triiodothyronine; left ventricular ejection fraction; myosin; calcium ATPase; cardiac gene expression
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