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Pulmonary Arterial Stiffness: Toward a New Paradigm in Pulmonary Arterial Hypertension Pathophysiology and Assessment

  • Blood Pressure Monitoring and Management (J Cockcroft, Section Editor)
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Abstract

Stiffening of the pulmonary arterial bed with the subsequent increased load on the right ventricle is a paramount feature of pulmonary hypertension (PH). The pathophysiology of vascular stiffening is a complex and self-reinforcing function of extracellular matrix remodeling, driven by recruitment of circulating inflammatory cells and their interactions with resident vascular cells, and mechanotransduction of altered hemodynamic forces throughout the ventricular-vascular axis. New approaches to understanding the cell and molecular determinants of the pathophysiology combine novel biopolymer substrates, controlled flow conditions, and defined cell types to recapitulate the biomechanical environment in vitro. Simultaneously, advances are occurring to assess novel parameters of stiffness in vivo. In this comprehensive state-of-art review, we describe clinical hemodynamic markers, together with the newest translational echocardiographic and cardiac magnetic resonance imaging methods, to assess vascular stiffness and ventricular-vascular coupling. Finally, fluid-tissue interactions appear to offer a novel route of investigating the mechanotransduction processes and disease progression.

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Grant Support

NIH Program Project Grant (5 P01 HL014985-40A1); NIH Axis Grant (1R01HL114887-03); NIH RO1 (R01 HL125827-01) and NIH T32 HL007171

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Correspondence to Kurt R. Stenmark.

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Drs. Schäfer, Myers, Brown, Frid, Tan, Hunter, and Stenmark have no conflicts of interest.

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This article is part of the Topical Collection on Blood Pressure Monitoring and Management

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Schäfer, M., Myers, C., Brown, R.D. et al. Pulmonary Arterial Stiffness: Toward a New Paradigm in Pulmonary Arterial Hypertension Pathophysiology and Assessment. Curr Hypertens Rep 18, 4 (2016). https://doi.org/10.1007/s11906-015-0609-2

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