There is increasing evidence that current thresholds for diagnosing pulmonary hypertension (PHT) underestimate the prognostic impact of PHT.
Objectives
The aim of this study was to determine the prognostic impact of increasing pulmonary pressures within the National Echocardiography Database of Australia cohort (n = 313,492).
Methods
The distribution of estimated right ventricular systolic pressure (eRVSP) was examined in 157,842 men and women. All had data linkage to long-term survival during median follow-up of 4.2 years (interquartile range: 2.2 to 7.5 years).
Results
The cohort comprised 74,405 men and 83,437 women 65.6 ± 17.7 years of age. Overall, 17,955 (11.4%), 7,016 (4.4%), and 4,515 (2.9%) subjects had eRVSP levels indicative of mild (40 to 49 mm Hg), moderate (50 to 59 mm Hg), or severe (≥60 mm Hg) PHT, respectively, assuming a right atrial pressure of 5 mm Hg. These subjects were more likely to die during long-term follow up (for severe PHT, adjusted hazard ratio: 9.73; 95% confidence interval: 8.60 to 11.0; p < 0.001). After adjustment for age, sex, and evidence of left heart disease, those subjects with eRVSP levels within the third (28.05 to 32.0 mm Hg; hazard ratio: 1.410; 95% confidence interval: 1.310 to 1.517) and fourth (32.05 to 38.83 mm Hg; hazard ratio: 1.979; 95% confidence interval: 1.853 to 2.114) quintiles had significantly higher mortality (p < 0.001) than those in the lowest quintile. Accordingly, a clear and consistent threshold of increased mortality (including 1- and 5-year actuarial mortality) around an eRVSP of 30.0 mm Hg was evident.
Conclusions
In this large and unique cohort, the prognostic impact of clinically accepted levels of PHT was confirmed. Moreover, a distinctly lower threshold for increased risk for mortality (eRVSP >30.0 mm Hg) indicative of PHT was identified. (A Longitudinal Cohort Study of Echocardiograms From Public and Private Echocardiography Laboratories From Around Australia, Linked With the National Deaths Index; ACTRN12617001387314)
The National Echo Database Australia was initially supported (database engineering and infrastructure costs) through unrestricted research grants from Actelion, Bayer, and GlaxoSmithKline. It is also supported by National Health and Medical Research of Australia funding (grant 1055214). Dr. Celermajer works at an institution that has received clinical trials funding and educational grants from Actelion. Dr. Prior has received payments for talks from Actelion. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Bradley A. Maron, MD, served as Guest Associate Editor for this paper.
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