Background. After acute myocardial infarction, regional myocardial wall str
ains and stresses change and a complex cellular and biochemical response is
initiated to remodel the ventricle. This study tests the hypothesis that c
hanges in regional ventricular wall strains affect regional collagen accumu
lation and collagenase activity.
Methods. Fourteen sheep had acute anteroapical infarction that progressivel
y expands into left ventricular aneurysm within 8 weeks. In 7 sheep, infarc
t expansion was restrained by prior placement of mesh over the area at risk
. Fourteen days after infarction, and after hemodynamic and echocardiograph
ic measurements, animals were euthanized for histology, measurements of hyd
roxyproline, matrix metalloproteinase-1 (MMP-1 or collagenase) and MMP-2 (g
elatinase) activity, as well as collagen type I and III in infarcted, borde
rzone, and remote myocardium.
Results. Restraining infarct expansion does not change collagen content or
MMP-1 or MMP-2 activity in the infarct, but significantly increases the rat
io of collagen I/III. In borderzone and remote myocardium infarct, restrain
t significantly increases collagen content and significantly reduces MMP-1
activity. MMP-2 activity is reduced (p = 0.059) in borderzone myocardium on
ly. Between groups, the ratio of type I/III fibrillar collagen does not cha
nge in borderzone myocardium.
Conclusions. Fourteen days after acute myocardial infarction, restraining i
nfarct expansion increases collagen accumulation in borderzone and remote m
yocardium, which may prevent expansion of hypocontractile, fully perfused "
remodeling myocardium" adjacent to the infarct. This study demonstrates tha
t changes in regional myocardial wall strain alter the cellular and biochem
ical processes involved in postinfarction ventricular remodeling. (C) 2001
by The Society of Thoracic Surgeons.