Since the first detailed pathological description by Brinton in 1950,1 the importance of pulmonary arterial hypertension (PAH) to excess mortality has been reproduced widely. Initial studies testing PAH pharmacotherapies aimed to salvage end-stage disease; however, progress in clinical phenotyping and increased availability of medical and surgical interventions over the ensuing decades have transformed PAH into a contemporary and treatable disease. Nevertheless, modern-era epidemiological trends suggest that long-term survival has improved incrementally,2 driven in part by late detection of incident disease. In 2018, the mean pulmonary artery pressure (mPAP) diagnostic threshold was lowered from 25 mm Hg or greater to greater than 20 mm Hg; the updated threshold provided the first evidence-based hemodynamic definition for pulmonary hypertension while offering an opportunity to capture patients with PAH earlier and thereby mitigate longitudinal disease burden.3
Maron BA, Humbert M. Finding Pulmonary Arterial Hypertension—Switching to Offense to Mitigate Disease Burden. JAMA Cardiol. 2022;7(4):369–370. doi:10.1001/jamacardio.2022.0011
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