New research widens continuum of risk associated with PVR in pulmonary hypertension

New data expand the range of pulmonary vascular resistance associated with mortality and heart failure in patients at risk for pulmonary hypertension undergoing right heart catheterization.

“Data from this study show that risk for adverse outcome associated with [pulmonary vascular resistance] in pulmonary hypertension emerges at around 2.2 Wood units, which is well below the [pulmonary vascular resistance] associated with the disease state in clinical practice. We identified patients with precapillary pulmonary hypertension at the time of right heart catheterization as particularly vulnerable,” Bradley A. Maron, MD, cardiovascular medicine specialist at Brigham and Women’s Hospital and assistant professor of Medicine at Harvard University, and colleagues wrote in The Lancet Respiratory Medicine.

Researchers conducted a retrospective cohort study of 40,082 patients (median age, 66.5 years; 96.7% male) undergoing right heart catheterization in the U.S. Veterans Affairs healthcare system from October 2007 through September 2016. Patients were included if they had complete right heart catheterization and were followed for at least 1 year. Fifty-eight percent of patients had a history of heart failure and 33.3% had a history of COPD. Eighty-one percent of patients were at risk for pulmonary hypertension based on an elevated mean pulmonary artery pressure (mPAP) of at least 19 mm Hg.

The primary outcome was time to all-cause mortality assessed by the Veteran Affairs vital status file. Results showed that the all-cause mortality hazard for pulmonary vascular resistance (PVR) was increased at 2.2 Wood units compared PVR of 1.0 Wood unit, when modeled as a continuous variable.

When the researchers compared PVR of 2.2 Wood units or more vs. less than 2.2 Wood units in patients with mPAP of at least 19 mm Hg and pulmonary artery wedge pressure of 15 mm Hg or less, the adjusted HR for mortality was 1.71 (95% CI, 1.59-1.84; P < .0001) and adjusted HR for heart failure hospitalization was 1.27 (95% CI, 1.13-1.43; P = .0001), according to the results.

Maron and colleagues also analyzed the relationship between PVR and clinical outcomes in a validation cohort of 3,699 patients (median age, 60.4 years; 50.3% male) that included 77.6% of patients with mPAP of at least 19 mm Hg. In this cohort, the researchers reported the adjusted HR for mortality was 1.81 (95% CI, 1.33-2.47; P = .0002) for the patients with mPAP of at least 19 mm Hg, PVR of 2.2 Wood units or more and pulmonary artery wedge pressure of 15 mm Hg or less.

This study provides the first evidence-based determination of the appropriate vascular resistance levels used clinically to guide risk assessment in patients with pulmonary hypertension, Maron told Healio.

“These data clarify and widen the range of data from clinical tests that are used to identify and assess risk for patients with pulmonary hypertension. Findings from this study provide much-needed evidence to inform clinicians at point-of-care on who is at risk for major adverse events, including heart failure hospitalization and death,” Maron told Healio. “This, in turn, provides an opportunity to capture a novel and substantial subpopulation of vulnerable patients that heretofore was considered normal.”

Further, Maron noted that “adherence to risk factor modification and standard-of-care lung and cardiac therapy will become increasingly important in the patients identified in this study. Most importantly, these data provide a roadmap for identifying pulmonary hypertension early.”

The researchers noted several limitations of the study, including a primarily male cohort, cohorts from a single country and exclusion of patients with incomplete records.

Maron and colleagues noted that further analyses are warranted.

“Additional research is needed that validates our findings in other pulmonary hypertension populations that are followed prospectively, and studies the effect of treatment on outcome in patients with pulmonary hypertension using the pulmonary artery pressure and pulmonary vascular levels used in our work,” Maron told Healio.

For more information:

Bradley A. Maron, MD, can be reached at bmaron@bwh.harvard.edu.