© 1999 American Heart Association, Inc.
Original Contributions |
Insulin-Like Growth Factor-1 Attenuates the Detrimental Impact of Nonocclusive Coronary Artery Constriction on the Heart
From the Department of Medicine, New York Medical College, Valhalla, NY.
Correspondence to Piero Anversa, Department of Medicine, Vosburgh Pavilion-Room 302, New York Medical College, Valhalla, NY 10595.
Abstract—Coronary artery
narrowing (CAN) induces tissue injury, which may involve myocyte
necrosis and apoptosis. Insulin-like growth factor (IGF)–1 may
counteract cell death, modifying the detrimental effects of myocardial
ischemia. On this basis, CAN was produced in female
FVB.Igf+/– mice and nontransgenic littermates, and the
animals were euthanized 7 days later. CAN consisted of an 82%
reduction in the vessel luminal cross-sectional area in both groups of
mice. Severe left ventricular dysfunction was present
in CAN nontransgenic and transgenic mice, but heart and left
ventricular weights increased more in littermates than in
FVB.Igf+/– mice. Similarly, the changes in chamber
volume and diastolic wall stress were greater in
nontransgenic mice. Subacute tissue injury, represented
by foci of replacement fibrosis, was 2.6-fold higher in CAN littermates
than in FVB.Igf+/– mice. Ongoing myocyte necrosis was
5-fold greater in nontransgenic mice, whereas apoptosis was low
and did not differ in the 2 groups of mice. In CAN nontransgenic mice,
myocyte necrosis was 12-fold more frequent than apoptosis but,
in CAN transgenic mice, these 2 types of cell death were comparable.
-Myosin and ß-myosin isoform mRNAs were affected by CAN, but
-myosin mRNA was reduced more in nontransgenic mice. In conclusion,
myocyte necrosis and replacement fibrosis are the prevailing forms of
myocardial damage induced by CAN. Constitutive overexpression of IGF-1
attenuates myocyte necrosis and tissue injury, having no effect on cell
apoptosis. These factors limit ventricular
dilation, myocardial loading, cardiac hypertrophy, and
alterations in - and ß-myosin isoform expression.
Key Words: myocardial ischemia • myocyte death • ventricular remodeling • myosin isoform • insulin-like growth factor-1 transgenic mice
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