A study of patients with pulmonary hypertension suggests a reconsideration of the accepted benchmark for pulmonary vascular hypertension as a predictor of heart failure may be warranted.
An elevated pulmonary vascular resistance of 3.0 Wood units or greater has been used as a prognostic marker for death and heart failure in pulmonary hypertension subgroups. But a large, multiyear study of a veterans population suggests that shifting that threshold to 2.2 Wood units in patients with right-heart catheterization may be justified.
of the Veterans Affairs Boston Healthcare System and Brigham and Women’s Hospital and Harvard Medical School, Boston, and colleagues evaluated 40,082 veterans in the VA Clinical Assessment, Reporting and Tracking (CART) program who had right-heart catheterization (RHC) in the VA system from Oct. 1, 2007, to Sept. 30, 2016.
“To our knowledge, these data provide the first evidence-based information on the continuum of clinical risk related to PVR in patients with elevated pulmonary artery pressure,” the researchers wrote. Their report was published online in Lancet Respiratory Medicine (2020 Jul 27.).
The retrospective cohort study found that all-cause mortality hazard ratio (HR), when adjusted for clinical variables, and mean pulmonary artery pressure (mPAP) increased progressively beginning at around 2.0 Wood units (WU). Clinically significant mortality HR emerged at 2.2 WU, with an adjusted risk 9% greater than a PVR of 2.1 Wood units (P < .0034), which the study considered the upper limit of normal PVR in health adults of a similar age range (61.5 to 73.5 years) as the study cohort. The researchers noted that a PVR of 3.0 WU has been the standard for forecasting outcomes in pulmonary hypertension (PH) ().
“Overall, these results suggest that reconsidering the hemodynamic parameters that define pulmonary hypertension in patients with cardiopulmonary disease is warranted, and they identify a need for early detection strategies to capture this large and vulnerable population,” the researchers wrote.
A subsequent analysis focused on patients with an mPAP of >19 mm HG (n = 32,725) and found that all-cause death when adjusted over a wide range of clinical variables that included PVR of 2.2 WU increased to a 25% HR. “However,” the researchers added, “a median cardiac output of < 4.0 L/min, which has been shown to be independently associated with adverse outcome, was present only when PVR was more than 4.0 Wood units.”
For a PVR of 2.2-3.0 WU, the median cardiac output was 4.87 L/min; for > 3.0 WU, it was 4.13 L/min. Among the patients with PVR > 2.2 WU (n = 15,780), 13.6% (n = 2,147) had an mPAP of 19-24 mm Hg.
In all patients with mPAP > 19 mm HG, pulmonary artery wedge pressure (PAWP) became a determining risk factor, with 15 mm HG the demarcation between low and high PAWP. At PVR of 2.2 WU, low-PAWP patients had a 52% greater adjusted risk of death and high-PAWP a 23% greater risk. At 4.0 WU, those adjusted risks rose dramatically – to 272% and 58%, for the low- and high-PAWP subgroups, respectively (P < .0001).
“Stratification of patients by PAWP had a major effect on outcome estimates in our study, illustrating the limitations of using the same PVR level to define clinical risk between precapillary and postcapillary pulmonary hypertension,” the researchers wrote.
They called for further study into how these findings impact people with PH but lower levels of cardiopulmonary disease than the cohort. “Overall, these findings support reconsidering the combination of hemodynamic variables used to identify patients with pulmonary hypertension,” the researchers stated.
The analyses of the VA CART database makes this “an interesting study,” said G. Hossein Almassi, MD, FCCP, of the Medical College of Wisconsin and Zablocki VA Medical Center in Milwaukee. “Within its limitation as a retrospective cohort study, the findings of a lower PVR and a lower mean PAP of > 19 mm being associated with increased risk of all-cause mortality and HF hospitalization are significant.”
He added: “Time will tell whether this will be an impetus for the clinicians to consider earlier therapeutic interventions in addition to lifestyle modification such as smoking cessation in this group of patients.”
Dr. Maron disclosed a financial relationship with Actelion.
SOURCE: Maron BA et al. Lancet Respir Med. 2020 Jul 27.