Left and right ventricular collagen type I/III ratios and remodeling post-myocardial infarction

Citation
S. Wei et al., Left and right ventricular collagen type I/III ratios and remodeling post-myocardial infarction, J CARD FAIL, 5(2), 1999, pp. 117-126
Citations number
32
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF CARDIAC FAILURE
ISSN journal
10719164 → ACNP
Volume
5
Issue
2
Year of publication
1999
Pages
117 - 126
Database
ISI
SICI code
1071-9164(199906)5:2<117:LARVCT>2.0.ZU;2-3
Abstract
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.