Left and right ventricular collagen type I/III ratios and remodeling post-myocardial infarction.
BACKGROUND
Types I and III collagen have different physical properties, and an increase of type I/III ratio can have a deleterious impact on myocardial compliance and left and right ventricular diastolic function. Post-myocardial infarction, these changes in collagen types may be relevant to the remodeling process and the development of heart failure.


RESULTS
In the rat coronary ligation heart failure model, we studied the time course of changes in types I and III and total collagen levels 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 analysis, 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 hydroxyproline content (r2 = 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, which 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 RV, type I collagen level increased 2.7-fold to a peak at 4 weeks and declined gradually to 1.7 times baseline at 10 weeks. The patterns of change in type I collagen level in the RV correlated with the changes in LV end-diastolic pressure (r = 0.73; P < .0001) and RV weight to body weight ratio (r = 0.73; P < .0001).


CONCLUSIONS
There is a relative greater increase of type I collagen level in the NIA and RV postinfarction, and this may lead to left and right ventricular dysfunction. Separate mechanisms might be involved in the induction of the different types of collagen deposition, with type I collagen levels apparently closely correlating with hemodynamic stress.
Department of Medicine, Chinese University of Hong Kong, Prince of Wales Hospital, China.
S
S
Wei
L T
LT
Chow
I O
IO
Shum
L
L
Qin
J E
JE
Sanderson
D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D003094:Collagen / Q000032:analysis*; D004195:Disease Models, Animal; D006439:Hemodynamics; D017379:Hypertrophy, Left Ventricular / Q000473:pathology* / Q000503:physiopathology; D007150:Immunohistochemistry; D016014:Linear Models; D008297:Male; D009203:Myocardial Infarction / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000737:chemistry*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012680:Sensitivity and Specificity; D018487:Ventricular Dysfunction, Left / Q000473:pathology* / Q000503:physiopathology; D020257:Ventricular Remodeling
D015415:Biomarkers; D003094:Collagen