Background: Types I and III collagen have different physical properties, an
d an increase of type I/III ratio can have a deleterious impact on myocardi
al compliance and left and right ventricular diastolic function. Post-myoca
rdial infarction, these changes in collagen types may be relevant to the re
modeling process and the development of heart failure.
Methods and Results: In the rat coronary ligation heart failure model, we s
tudied the time course of changes in types I and III and total collagen lev
els over 10 weeks postinfarction. Collagen types were separately quantified
in the left (LV) and right ventricles (RV) by computerized morphometry and
standard immunohistochemistry techniques, and also by hydroxyproline analy
sis, and these were correlated with hemodynamic changes. Compared with sham
-operated rats, total collagen level increased 2.5- to 2.9-fold and 1.7- to
2.9-fold in the noninfarcted areas (NIAs) of the LV and RV, respectively,
over the 10-week period and showed a good relation with changes in hydroxyp
roline content (r(2) = 0.62; P < .0001). In the NIAs of both the LV and RV,
type III collagen level showed a transient twofold increase at 2 weeks, wh
ich declined to normal at 4 weeks. Type I collagen level increased twofold
at 4 weeks in the NIA of the LV and remained elevated at 10 weeks. In the R
V, type I collagen level increased 2.7-fold to a peak at 4 weeks and declin
ed gradually to 1.7 times baseline at 10 weeks. The patterns of change in t
ype I collagen level in the RV correlated with the changes in LV end-diasto
lic pressure (r = 0.73; P < .0001) and RV weight to body weight ratio (r =
0.73; P < .0001).
Conclusion: There is a relative greater increase of type I collagen level i
n the NIA and RV postinfarction, and this may lead to left and right ventri
cular dysfunction. Separate mechanisms might be involved in the induction o
f the different types of collagen deposition, with type I collagen levels a
pparently closely correlating with hemodynamic stress.