Author + information
- Karl T. Weber, MD, FACC∗
- ↵∗Address for reprints: Karl T. Weber, MD, Michael Reese Hospital, Lake Shore Drive at 31st Street, Chicago, Illinois 60616.
Composed of type I and III collagens, the valve leaflets, chordae tendineae and collagen matrix of the myocardium form a structural continuum. Synthesized by cardiac fibroblasts, these fibrillar collagens support and tether myocytes to maintain their alignment, whereas their respective tensile strength and resilience resist the deformation, maintain the shape and thickness, prevent the rupture and contribute to the passive and active stiffness of the myocardium. An acquired or congenital defect in this collagen network can lead to abnormalities in myocardial architecture, mechanics or valve function. In the hypertrophic process that accompanies a pressure overload, for example, increased collagen synthesis, fibroblast proliferation and a structural and biochemical remodeling of the matrix are seen. This includes distinctive patterns of reparative and reactive myocardial fibrosis, each of which alters diastolic and systolic myocardial stiffness and may lead to pathologic hypertrophy. Alternatively, a loss of collagen tethers or decline in matrix tensile strength can be responsible for regional or global transformations in myocardial architecture and function seen in the reperfused (“stunned”) myocardium and in dilated (idiopathic) cardiopathy. Inherited disorders in the transcriptional and posttranslational processing of collagen can also alter the biophysical properties of the network.
Future studies into collagen gene regulation, gene switching events and the control of collagen synthesis and degradation are needed to develop a more complete understanding of the relation between the collagen network and acquired and inherited forms of heart disease and to utilize therapeutics that will prevent, retard or regress abnormal collagen matrix remodeling.
☆ This study was supported in part by Grant No. R01-HL-31701 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
☆☆ This article is part of a series of informal teaching reviews devoted to subjects in basic cardiology that are of particular interest because of their high potential for clinical application. The intent of the series is to help the clinician keep abreast of important advances in our understanding of the basic mechanisms underlying normal and abnormal cardiac function.
- Received December 12, 1988.
- Accepted January 24, 1989.