The mechanisms leading to elevations in precapillary pulmonary vascular resistance are complex and likely involve multiple pathways, but the histopathologic sequelae of these processes are restricted to a few findings, primarily neoangiogenesis, intimal and smooth muscle proliferation, vasoconstriction, and/or in situ thrombosis. Regardless of the etiology of pulmonary hypertension, abnormalities in endothelial function are often observed and likely play a central role in mediating structural changes.
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http://dx.doi.org/10.1177/1089253207301732 | DOI Listing |
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