Key result
Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension.
This review summarizes the clinical, physiological, and molecular changes associated with pressure and volume overload in the pulmonary circulation leading to pulmonary hypertension.
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Supports hemodynamic assessment in pulmonary hypertension; extends remodeling models but leaves open targeted interventions.
Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension. Recently, some advances have been made in our molecular understanding of the exogenous upstream stimuli that initiate hemodynamic pertubations as well as the downstream vasoactive effectors that control these responses. However, much still remains unknown regarding how these complex signaling pathways connect in order to result in these characteristic pathophysiological changes. This chapter will describe our current understanding of and needed areas of research into the clinical, physiological, and molecular changes associated with pressure/volume overload in the pulmonary circulation.
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Chan et al. (2011) conducted a review in Pulmonary Vascular Disease / Pulmonary Hypertension. Hemodynamic stress (pressure/volume overload) was evaluated. Hemodynamic stress in the pulmonary vessel is directly linked to the development of vascular remodeling and dysfunction, ultimately leading to pulmonary hypertension.
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