Figure 6.

The pathophysiology and risk associated with mild pulmonary hypertension (PH). (A) Compared with normal controls, pulmonary arterioles from patients with mild PH and hypertrophic cardiomyopathy demonstrate increased fibrosis and hypertrophy on Masson trichrome and elastin staining, respectively. Scale bar, 50 mm. Reproduced with permission from Reference 175. (B) When modeling mean pulmonary artery pressure (mPAP) as a continuous variable across a national cohort of 21,727 veterans, mortality risk that is associated with increases in mPAP emerges at 19 mm Hg. Subtle increases in mPAP between 19 and 24 mm Hg are associated with a much greater change in mortality, suggesting an opportunity to modulate clinical risk in the range of mild rather than severe PH. Reproduced with permission from Reference 65. (C) Increased mortality in an Australian national cohort of patients with mild PH suggested by echocardiography is associated with pathogenic changes to RA and right ventricular (RV) geometry. Reprinted with permission from Reference 92. (D) The pathogenicity of mild PH is suggested further by evidence of impaired tricuspid annular plane of systolic excursion (TAPSE) and surrogate for RV-pulmonary arterial coupling (TAPSE/RVSP). Reprinted with permission from Reference 91. ePH = echocardiographic PH; eRVSP = estimated right ventricular systolic pressure; H/E = hematoxylin and eosin; RA = right atrial; RVSP = right ventricular systolic pressure.