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Article, see p 1796 There is a complex relationship between pulmonary vascular remodeling and pulmonary hypertension with structural and functional changes in the vasculature being causal for, or occurring as a consequence of, elevated filling pressures in the cardiopulmonary system. Owing to this interplay, the primary pathology (pulmonary vascular versus cardiac) and resultant pulmonary hypertensive hemodynamic profile may both be key determinants of the location and the extent of architectural changes in the pulmonary vasculature. Although the pulmonary arterial and venous vessels form a contiguous unobstructed structure, it is well recognized that the genetic, molecular, and metabolic factors or exposures that initiate pulmonary vascular remodeling have a propensity to target either the arteries or the veins, preferentially.1,2 For example, in pulmonary arterial hypertension, the distal pulmonary arteries develop intimal and medial hypertrophy, fibrosis, inflammation, and thrombosis in situ, while the pulmonary veins are spared.1,2 In contrast, in pulmonary veno-occlusive disease, these pathological changes are restricted to pulmonary veins with the observed effect on pulmonary arteries considered a secondary finding.1,2 The aberrant structural remodeling characteristic of these pulmonary vascular diseases creates a segment of increased resistance in the cardiopulmonary circuit that ultimately leads to the hemodynamic findings consistent with pulmonary hypertension, which are discoverable clinically during invasive interrogation. These elevated filling pressures, in turn, may modulate disease progression via pressure- or flow-related compensatory remodeling in previously unaffected parts of the pulmonary vascular tree, as well as the right ventricle. Thus, while pulmonary arterial hypertension and pulmonary veno-occlusive disease are diseases of the pulmonary arteries and pulmonary veins, respectively, they are illustrative of the fact that vascular remodeling and cardiopulmonary hemodynamics serve as interrelated …