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Cardiovascular Research 1998 37(1):123-129; doi:10.1016/S0008-6363(97)00217-4
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Differential myocardial abundance of collagen type I and type III mRNA in dilated cardiomyopathy: effects of myocardial inflammation

Matthias Pauschingera,*, Andrea Doernera, Andrew Remppisb, Roman Tannhäusera, Uwe Kühla and Heinz-Peter Schultheissa

aDepartment of Cardiology, Universitätsklinikum Benjamin Franklin der Freien Universität Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany
bDepartment of Cardiology, Medizinische Klinik II, University Lübeck, Ratzeburger Allee 160, D-23538 Lübeck, Germany

* Corresponding author. Fax +49-30-8445-3565.

Objective: The collagen subtypes I (Col I) and III (Col III) are essential components of the cardiac extracellular matrix (ECM) maintaining the functional integrity of the heart. Histological, immunohistological, and biochemical studies, however, demonstrate characteristical changes of the ECM in dilated cardiomyopathy, myocarditis, ischemic cardiomyopathy, and hypertensive heart disease. Methods: In order to investigate possible effects of inflammatory processes on mRNA abundance of Col I and Col III, we examined 24 patients with the presumptive clinical diagnosis of dilated cardiomyopathy (EF=30±11%). 12 Patients were classified as idiopathic dilated cardiomyopathy without any evidence of myocardial inflammation; the remaining 12 patients were classified as inflammatory cardiomyopathy due to the immunohistologically documented inflammatory myocardial process. Results: Quantification of reverse transcription polymerase chain reaction (RT–PCR) products revealed significant differences as to the mRNA abundance ratio Col III/Col I between subgroups of patients with inflammatory cardiomyopathy (1.16±0.18) and idiopathic dilated cardiomyopathy (2.77±0.65) regardless of left ventricular dysfunction (p≤0.05). Conclusion: It is not yet known, whether different Col III/Col I ratios differentially influence diastolic compliance. Our data suggest that inflammatory mechanisms seen in inflammatory cardiomyopathy influence the mRNA abundance of collagen subtypes I and III.

KEYWORDS Dilated cardiomyopathy; Inflammatory cardiomyopathy; Collagen mRNA abundance; Extracellular matrix


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