Heat Induced Changes in the Mechanics of Soft Tissue

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9634109 Humphrey Advances in laser, microwave, radio-frequency, and similar technologies continue to promote new applications of heat to treat various pathologies. yet, most clinical studies are motivated by the advances in device technology, not a fundamental understanding of the underlying thermo- biomechanics, which at present remains poorly understood. Exploiting the potential of heat-therapy will, therefore, require quantification of the effects of clinically controllable parameters such as the temperature level, heating history, and the mechanical load state during heating. In general, there are two primary irreversible effects of heat treatment, cell necrosis and denaturation of structural proteins. Thus, to design and eventually optimize a heat-therapy, one must be able to predict (spatially and temporally) the concomitant irreversible effects on cell viability and connective tissue integrity for a given heating device. Rather than studying a specific clinical application, the overall goal of this work is to establish a theoretical basis for quantifying irreversible heat-induced changes in the nonlinear, anistropic behavior of soft tissue -- our specific aim is to develop and validate phenomenological thermomechanical damage relations for three different tissues that will be exposed to a broad range of temperatures (from 45 to 85oC), both isothermally and non-isothermally), hearing periods (from seconds to hours), and mechanical load states during heating (isometric, isotonic, and cyclic stretching). The proposed tissues are bovine chordae tendineae, epicardium, and endocardium. In addition to a gel matrix, chordae consists primarily of uniaxially oriented collagen, epicardium of a 2- D network of collagen, and endocardium of a 2-D network of collagen and elastin. These three tissues were selected because they have increasingly more constituents and microstructural complexity, and they admit rigorously performed and interpreted uniaxial or in-pl ane biaxial testing -- this will allow the development of 1-D and then 2- D relations of increasing complexity. There are no comparable data or constitutive relations for thermal-damage in the literature. The PIs recently showed that the effects of temperature level and heating period are coupled in heat-induced collagen denaturation: there exists a "time-temperature equivalency" in the form of an exponential relation in traction free, isothermal shrinkage tests on chordae. A similar relation exists in heat-induced cell death. The PIs hypothesize that an analogous equivalency exists in tissues under more general conditions (e.g., multiaxial, non- isothermal loading), which will simplify quantification in terms of a load and temperature-dependent scaled heating time. Concepts from finite strain damage mechanics and irreversible continuum thermodynamics will be extended to determine the dependence of the Helmholtz free energy and the damage evolution equation on the current finite strain and prior thermal-damage, the latter of which likely depends on an accumulative scaled heating time. Such quantification will allow tissue-level engineering analysis of potential heat-therapies, and hopefully optimization thereof. ***