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In contrast, the increase in stiffness that occurs due to changes in extracellular matrix (ECM) content and arterial geometry during disease progression ( ) is referred to as remodeling-induced stiffening. To describe this mechanism in simple terms, we and others have referred to the nonlinearly elastic response of arteries that gives rise to increased stiffness at increased strain as strain-induced stiffening ( ). Using acute pulmonary embolization, PA stiffening was investigated through the arterial nonlinear elastic response of the tissue during mechanical testing.

However, since arteries are nonlinearly elastic materials, the increase in stiffness measured clinically may be due to the elevation in pressure, which increases vessel stretch or chronic remodeling-induced changes in extracellular matrix (ECM) content and arterial geometry ( ), or a combination of these effects.Common large animal models of PH employ acute or chronic pulmonary embolization to elevate PA pressures ( ). Clinical studies have demonstrated that large pulmonary artery (PA) stiffening is a robust predictor of patient mortality in PH ( ). IntroductionPulmonary hypertension (PH) is a debilitating vascular disease that causes increased pulmonary vascular resistance and decreased pulmonary vascular compliance. The ability to differentiate between strain- and remodeling-induced stiffening in vivo may lead to tailored clinical treatments for PA stiffening in PH patients. Remodeling-induced stiffening was evident from a significant increase in the constitutive model stress parameter, which correlated with increased PA collagen content and decreased PA elastin content as measured histologically. Strain-induced stiffening was evident from mechanical testing as nonlinear elasticity in both directions and computationally by a high correlation coefficient between the mechanical data and model (R 2=0.89). To do this, circumferential and axial tissue strips of large extralobar PAs from control and CTEPH tissues were tested in uniaxial tension, and data were fit to a phenomenological constitutive model.

Here, we used an established constitutive model to demonstrate and differentiate between strain-induced stiffening, which is due to nonlinear elasticity, and remodeling-induced stiffening, which is due to ECM and geometric changes, in a canine model of chronic thromboembolic PH (CTEPH). Remodeling can alter arterial nonlinear elastic properties via chronic changes in extracellular matrix (ECM) content and geometry.

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