POINT: Is It Time to Lower the Cut-off for Increased Pulmonary Vascular Resistance? Yes

Abstract

For decades, pulmonary hypertension (PH) used to be defined by a mean pulmonary artery pressure (mPAP) ≥25 mm Hg; however, this criterion was not based on data that were systematically collected. With the availability of contemporary datasets however, it was evident that the upper limit of normal mPAP was ∼20 mm Hg, which is also the level of mPAP above which adverse outcomes increase. In addition, it is now evident that the specificity of mPAP >20 mm Hg to denote precapillary pulmonary vascular disease could be enhanced by adding pulmonary vascular resistance (PVR) to the precapillary PH definition. Finally, after characterizing large groups of normal individuals, akin to observations for mPAP, it was recently demonstrated that a PVR of ∼2.0 Wood units (WU) is the upper limit of normal, and the lower level associated with all-cause mortality in at-risk patients. The current hemodynamic criteria for PH are positioned to capture more patients compared to the classical definition, with particular implications for earlier diagnosis. Importantly, pulmonary vasodilator therapies have not been tested adequately in patients with mPAP <25 mm Hg or PVR between 2 to 3 WU and, thus, should not be administered in these patients. Mild PH is an active focus of clinical trial design; at present, these patients should be referred to expert PH centers earlier for individualized therapeutic planning. The revised definition of precapillary PH uses a PVR threshold of >2 WU. This value is evidence-based, and exceeding this threshold is associated with adverse clinical outcomes. This revision places focus on early diagnosis, close monitoring, and consideration for certain treatments. Further studies are needed that test the efficacy and safety of pulmonary arterial hypertension-specific therapy in precapillary PH patients with PVR 2 to 3 WU.