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Do patients with mild echocardiographic pulmonary hypertension have worse right ventricular function and mortality than patients with pulmonary pressures in the normal range?
In this cohort study of 47 784 patients, those with mild echocardiographic pulmonary hypertension (right ventricular systolic pressure of 33 to 39 mm Hg) had higher mortality, reduced right ventricular function, and impaired right ventricular–pulmonary arterial coupling compared with patients with right ventricular systolic pressure less than 33 mm Hg.
In a clinical referral population, mildly elevated pulmonary pressures were associated with adverse right ventricular compensation and increased adjusted mortality.
Current guidelines recommend evaluation for echocardiographically estimated right ventricular systolic pressure (RVSP) greater than 40 mm Hg; however, this threshold does not capture all patients at risk.
To determine if mild echocardiographic pulmonary hypertension (ePH) is associated with reduced right ventricular (RV) function and increased risk of mortality.
Design, Setting, and Participants
In this cohort study, electronic health record data of patients who were referred for echocardiography at Vanderbilt University Medical Center, Nashville, Tennessee, from March 1997 to February 2014 and had recorded estimates of RVSP values were studied. Data were analyzed from February 2017 to May 2019.
Mild ePH was defined as an RVSP value of 33 to 39 mm Hg. Right ventricular function was assessed using tricuspid annular plane systolic excursion (TAPSE), and RV–pulmonary arterial coupling was measured using the ratio of TAPSE to RVSP.
Main Outcomes and Measures
Associations of mild ePH with mortality adjusted for relevant covariates were examined using Cox proportional hazard models with restricted cubic splines.
Of the 47 784 included patients, 26 758 of 47 771 (56.0%) were female and 6040 of 44 763 (13.5%) were black, and the mean (SD) age was 59 (18) years. Patients with mild ePH had worse RV function compared with those with no ePH (mean [SD] TAPSE, 2.0 [0.6] cm vs 2.2 [0.5] cm; P < .001) and nearly double the prevalence of RV dysfunction (32.6% [92 of 282] vs 16.7% [170 of 1015]; P < .001). Compared with patients with RVSP less than 33 mm Hg, those with mild ePH also had reduced RV–pulmonary arterial coupling (mean [SD] ratio of TAPSE to RVSP, 0.55 [0.18] mm/mm Hg vs 0.93 [0.39] mm/mm Hg; P < .001). An increase in adjusted mortality began at an RVSP value of 27 mm Hg (hazard ratio, 1.32; 95% CI, 1.02-1.70). Female sex was associated with increased mortality risk at any given RVSP value.
Conclusions and Relevance
Mild ePH was associated with RV dysfunction and worse RV–pulmonary arterial coupling in a clinical population seeking care. Future studies are needed to identify patients with mild ePH who are susceptible to adverse outcomes.
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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.
Accepted for Publication: July 28, 2019.
Corresponding Author: Evan L. Brittain, MD, MSCI, Division of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, 2525 West End Ave, Ste 300-A, Nashville, TN 37203 (email@example.com).
Published Online: September 18, 2019. doi:10.1001/jamacardio.2019.3345
Author Contributions: Dr Brittain had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Study concept and design: Huston, Hemnes, Brittain.
Acquisition, analysis, or interpretation of data: Huston, Maron, French, Huang, Thayer, Farber-Eger, Wells, Choudhary, Brittain.
Drafting of the manuscript: Huston, Maron, Thayer, Brittain.
Critical revision of the manuscript for important intellectual content: Huston, French, Huang, Thayer, Farber-Eger, Wells, Choudhary, Hemnes, Brittain.
Statistical analysis: French, Huang, Thayer, Brittain.
Obtained funding: Brittain.
Administrative, technical, or material support: Huston, French, Thayer, Farber-Eger, Wells.
Study supervision: Huston, Hemnes, Brittain.
Conflict of Interest Disclosures: Dr Choudhary has received grants from Novartis. Dr Hemnes has received grants from the Cardiovascular Medical Research and Education Fund and the National Institutes of Health as well as personal fees from Actelion Pharmaceuticals, Bayer, Complexa, and United Therapeutics and has a patent issued for Annamometer. Dr Brittain has received personal fees from Bayer. No other disclosures were reported.
Funding/Support: This research was supported by grants U01 HL125212-01 (Dr Hemnes), K08HL111207-01A1 (Dr Maron), and R01HL146588 (Dr Brittain) from the National Institutes of Health, grants 13FTF16070002 (Dr Brittain) and 15GRNT25080016 (Dr Maron) from the American Heart Association, the Gilead Scholars Program in Pulmonary Arterial Hypertension (Dr Brittain), the Cardiovascular Medical Research and Education Foundation (Dr Maron), and the Klarman Foundation at Brigham and Women’s Hospital (Dr Maron). The datasets used for the analyses described were obtained from Vanderbilt University Medical Center’s Synthetic Derivative, which is supported by institutional funding, the 1S10RR025141-01 instrumentation award, and by the Clinical and Translational Science Award grant UL1TR000445 from the National Center for Advancing Translational Sciences and National Institutes of Health.
Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
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