Mechanisms of vascular remodeling

Persistent pulmonary hypertension, whether acute in onset or chronic and slowly progressive, induces structural changes to the pulmonary arterial tree. Remodeling of pulmonary arteries is a response to high flow and high pressures and/or any underlying inflammatory or toxic process. Shear stress to vascular endothelial cells and the subsequent restructuring of their surface properties and shape are considered important factors for remodeling. Pulmonary arteriosclerosis is the most common initial alteration, presenting as a thickening and hypertrophy of smooth muscle of the vascular medial layer. An increase in connective tissue can also be observed. The consequence is a narrowing of the arterial lumen, already the major site of pulmonary vascular resistance under physiological conditions. Furthermore, a reduced compliance of the vascular wall to changing blood flows enhances the development of pulmonary hypertension. The anatomical localization of the injury is of major importance for the disease process because a destruction of alveolar vessels, as seen in severe emphysema, does not raise pulmonary vascular resistance to the same extent as obliteration of large-caliber pulmonary arteries such as segmental arteries.

The late presentation of the patient with chronic pulmonary hypertension represents a major problem in the treatment of chronic pulmonary hypertension. At this stage of the disease vascular changes are advanced and therapy is often restricted to a symptomatic therapeutic approach.

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