This review examines how histopathological patterns across the five WHO pulmonary hypertension (PH) groups — including arterial, capillary, and venous remodelling — shape pathophysiology, treatment response, and prognosis, drawing on experimental models and human tissue studies.
Group-specific vascular signatures were identified: venule-predominant remodelling in Group 2 PH, dense occlusive venous fibrosis in PVOD, arterial-dominant lesions in Group 1 PAH, and mixed arterial-venous changes in CTEPH — each with distinct therapeutic implications (e.g., vasodilators effective in pre-capillary disease but risk pulmonary oedema in venous-predominant phenotypes).
Direct correlations between non-invasive markers (e.g., TAPSE/RVSP, exercise hemodynamics) and histopathology remain limited; experimental models (monocrotaline, hypoxia) do not fully replicate human disease; review does not include primary data.
Identifying the vascular compartment driving PH (arterial vs. venous) is critical before initiating vasodilator therapy — vasodilators carry a real risk of pulmonary oedema in venous-predominant disease such as PVOD or Group 2 PH. Integrating hemodynamic phenotyping with emerging non-invasive surrogates may help target treatment more precisely without requiring biopsy.
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