The development and progression oflef t ventricular (LV) dysfunction and, ultimately, the clinical manifestation ofcongestive heart f (CHF) is due to the summation ofa number ofsystemic, cellular, and molecular abnormalities. The specific constellation ofabnormalities that contribute to the progression ofCHF is disease dependent, but it likely includes neurohormonal system activation, changes in LV loading conditions, defects in myocardial perfusion and metabolism, and alterations in excitation-contraction coupling. One common structural feature in the progression of the CHF process is LV myocardial remodeling. Myocardial remodeling can be defined as molecular, cellular, and interstitial changes within the myocardium that result in changes in LV size and function. One ofthe predominant geometric f eatures ofmyocardial remodeling that accompanies the CHF process is LV dilation. The progression ofLV remodeling is accompanied by alterations in the structure and function of the extracellular matrix (ECM), which in turn likely facilitates the myocardial remodeling process in CHF. Accordingly, a focused session on the myocardial ECM was held at the July 2001 Satellite Meeting ofthe XVII World Congress ofthe International Society f Heart Research: Remodeling and Progression ofHeart Failure. One goal of this session was to evaluate specific aspects ofthe myocardial ECM with respect to the LV remodeling process, to define important interfaces between the ECM and the cardiac myocyte, and to provide some avenues for future research. The purpose ofthis session was not to provide a comprehensive and exhaustive review ofpast studies. Rather, the purpose was to present a fresh perspective on a particular body ofknowledge regarding the myocardial ECM and to identify areas for future basic and clinical investigation regarding the myocardial ECM and the remodeling process. One ofthe first studies to describe the anatomic basis of the myocardial ECM was by Caufield and Borg. 1 Since that time, it has become well recognized that the ECM is not a static entity but rather a dynamic microenvironment that not only contains structural support proteins but also serves as an important interface with respect to cell-cell signaling. The first monograph, by Goldsmith and Borg, emphasizes the dynamic and diverse nature ofthe myocardial ECM. An important point made by this introductory presentation is that both biologic and physical stimuli, which are operative through the ECM, directly affect myocyte biology. The development ofLV dilation has been shown to be associated with discontinuity and disruptions ofthe supporting fibrillar collagen network, with decreases in the degree ofcollagen strut cross-linking, and with disruptions in myocyte adhesion capacity to the basement