Association of Borderline Pulmonary Hypertension With Mortality and Hospitalization

Study Questions:

Pulmonary hypertension (PH) is associated with increased morbidity across the cardiopulmonary disease spectrum. Is the consensus definition of PH as a mean pulmonary artery pressure (mPAP) ≥25 mm Hg adequate for identifying the populations at risk for the consequence of PH?


The authors analyzed retrospectively all US veterans undergoing right heart catheterization (RHC) (2007-2012) in the Veterans Affairs health care system (n = 21,727; 908-day median follow-up). Cox proportional hazards models were used to evaluate the association between mPAP and outcomes of all-cause mortality and hospitalization, adjusted for clinical covariates.


Mean age was 65 years, >95% were male, >75% white, and >80% had hypertension. When treating mPAP as a continuous variable, the mortality hazard increased beginning at 19 mm Hg (hazard ratio [HR], 1.183; 95% confidence interval [CI], 1.004-1.393) relative to 10 mm Hg. Patients were stratified into three groups: referent (≤18 mm Hg; n = 4,207), borderline PH (19-24 mm Hg; n = 5,030), and PH (≥25 mm Hg; n = 12,490). The adjusted mortality hazard was increased for borderline PH (HR, 1.23; p < 0.0001) and PH (HR, 2.16; p < 0.0001) compared to the referent group. The adjusted hazard for hospitalization was also increased in borderline PH (HR, 1.07; p = 0.0149) and PH (HR, 1.15; p < 0.0001). The borderline PH cohort remained at increased risk for mortality after excluding the following high-risk subgroups: patients with pulmonary artery wedge pressure >15 mm Hg, pulmonary vascular resistance ≥3.0 Wood units, or inpatient status at the time of RHC.


These data illustrate a continuum of risk according to mPAP level, and that borderline PH is associated with increased mortality and hospitalization. Future investigations are needed to test the generalizability of these findings to other populations and study the effect of treatment on outcome in borderline PH.


This is a very important clinical study that corroborates what has been suspected by PH experts, particularly in categories of patients for whom severe PH is common such as idiopathic/familial pulmonary arterial hypertension and connective tissue diseases, and structural and functional lung diseases in whom PH and right ventricular function may impact outcome. Considering the different pathobiologies of precapillary PH, the different natural history of PH by diagnosis and groups, and that treatment response to PH-specific drugs varies by diseases and triggers, the implications of the results are a bit overwhelming.

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