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Circulation, Vol 83, 1028-1037, Copyright © 1991 by American Heart Association
SE Litwin, CM Litwin, TE Raya, AL Warner and S Goldman
BACKGROUND. Previous studies have shown that global left ventricular
function is depressed after myocardial infarction. However, little is known
about the effects of myocardial infarction on contractility and the
passive-elastic properties of residual myocardium. METHODS AND RESULTS. We
evaluated isometric function and passive myocardial stiffness in isolated,
noninfarcted left ventricular papillary muscle from rats 6 weeks after sham
operation or myocardial infarction. Maximal developed tension and peak rate
of tension rise (+dT/dt) were significantly decreased in untreated rats
with large myocardial infarction compared with controls (3.3 +/- 1.1 versus
4.3 +/- 0.6 g/mm2 and 49.5 +/- 17.5 versus 72.5 +/- 10.5 g/mm2/sec,
respectively). Time to peak tension was prolonged (120 +/- 8 versus 102 +/-
4 msec) and myocardial stiffness was increased in untreated myocardial
infarction rats compared with controls (35.2 +/- 4.9 versus 24.2 +/- 3.7).
Rats with smaller myocardial infarctions differed from controls only with
respect to a prolongation of time to peak tension. Papillary muscle myocyte
cross-sectional area was increased by 44% (p less than 0.05), and
myocardial hydroxyproline content was increased by 160% (p less than 0.05)
in rats with large myocardial infarctions compared with controls. To
determine whether treatment that improves left ventricular function after
myocardial infarction also improves myocardial function, rats were treated
with captopril beginning 3 weeks after myocardial infarction and continuing
for 3 weeks. Treatment with captopril attenuated the prolongation in time
to peak tension in the myocardial infarction rats; however, developed
tension, +dT/dt, and muscle stiffness remained abnormal. Compared with
untreated myocardial infarction rats, captopril-treated myocardial
infarction rats had a 9% decrease in myocyte cross-sectional area (p = 0.1)
but a persistent increase in myocardial collagen content. In summary, large
myocardial infarction in rats causes contractile dysfunction, increased
stiffness, myocyte hypertrophy, and increased collagen content in the
residual noninfarcted myocardium. Treatment with captopril alters the
process of cardiac remodeling and hypertrophy and improves one parameter of
contractility in noninfarcted myocardium; however, myocardial collagen
content and myocardial stiffness remain abnormal. CONCLUSIONS. These
findings suggest that angiotensin converting enzyme inhibition in the rat
infarct model of heart failure improves global cardiac performance via
combined effects on myocardial function and the peripheral circulation.
ARTICLES
Contractility and stiffness of noninfarcted myocardium after coronary ligation in rats. Effects of chronic angiotensin converting enzyme inhibition
Department of Internal Medicine, Tucson Veterans Administration Medical Center, AZ 85723.
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