Circulation, Vol 84, 2123-2134, Copyright © 1991 by American Heart Association
P Whittaker, DR Boughner and RA Kloner
BACKGROUND. We sought to determine if damage to the myocardial collagen
network was the cause of infarct expansion. METHODS AND RESULTS. Using
polarized light microscopy, we examined sections from rat hearts obtained
at 1, 2, 3, and 4 days after permanent coronary artery occlusion. Three
features of the collagen network likely to be important in resisting
infarct expansion were assessed: collagen quality, collagen quantity, and
collagen organization. We observed a decrease in the number of normally
birefringent collagen fibers in the infarct as early as 1 day after
infarction. This decrease correlated significantly with time (r = -0.989, p
less than 0.001). In addition, we found that the fewer normally
birefringent collagen fibers present, the greater the degree of infarct
expansion (assessed by measurement of total left ventricular
cross-sectional area). At 4 days after infarction, we noted a loss of
intermyocyte collagen struts and loss of interstitial space. These changes
coincided with the onset of pronounced infarct expansion. The loss of
collagen struts is consistent with the concept that expansion proceeds via
slippage of myocytes previously tethered by the struts. The loss of
interstitial space may represent the resolution of interstitial edema,
which could further weaken the ventricular wall. CONCLUSIONS. The
correlation of infarct expansion with collagen damage and the loss of
support provided by collagen struts suggest that collagen is important in
maintaining structural integrity after acute myocardial infarction.
ARTICLES
Role of collagen in acute myocardial infarct expansion
Heart Institute, Hospital of the Good Samaritan, Los Angeles, CA 90017.
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