Quantifying the Influence of Wedge Pressure, Age, and Heart Rate on the Systolic Thresholds for Detection of Pulmonary Hypertension

Author:

Amsallem Myriam12,Tedford Ryan J.3,Denault Andre4,Sweatt Andrew J.56,Guihaire Julien7,Hedman Kristofer18,Peighambari Shadi1,Kim Juyong Brian12,Li Xiao9,Miller Robert J. H.1,Mercier Olaf7,Fadel Elie7,Zamanian Roham56,Haddad Francois12

Affiliation:

1. Division of Cardiovascular Medicine Stanford University School of Medicine Stanford CA

2. Stanford Cardiovascular Institute Stanford University School of Medicine Stanford CA

3. Division of Cardiology Department of Medicine Medical University of South Carolina Charleston SC

4. Department of Anesthesiology and Division of Critical Care Montreal Heart Institute Université de Montréal Quebec Canada

5. Division of Pulmonary and Critical Care Medicine Stanford University School of Medicine Stanford CA

6. Vera Moulton Wall Center for Pulmonary Disease at Stanford University Stanford CA

7. Research and Innovation Unit INSERM U999 DHU TORINO Paris Sud University Marie Lannelongue Hospital Le Plessis Robinson France

8. Department of Medical and Health Sciences Linköping University Linköping Sweden

9. Department of Genetics Stanford University School of Medicine Stanford CA

Abstract

Background The strong linear relation between mean ( MPAP ) and systolic ( SPAP ) pulmonary arterial pressure (eg, SPAP =1.62× MPAP ) has been mainly reported in precapillary pulmonary hypertension. This study sought to quantify the influence of pulmonary arterial wedge pressure ( PAWP ), heart rate, and age on the MPAPSPAP relation. Methods and Results An allometric equation relating invasive MPAP and SPAP was developed in 1135 patients with pulmonary arterial hypertension, advanced lung disease, chronic thromboembolic pulmonary hypertension , or left heart failure. The equation was validated in 60 885 patients from the United Network for Organ Sharing ( UNOS ) database referred for heart and/or lung transplant. The MPAP / SPAP longitudinal stability was assessed in pulmonary arterial hypertension with repeated right heart catheterization. The equation obtained was SPAP =1.39× MPAP × PAWP −0.07 ×(60/heart rate) 0.12 ×age 0.08 ( P <0.001). It was validated in the UNOS cohort ( R 2 =0.93, P <0.001), regardless of the type of organ(s) patients were listed for (mean bias [−1.96  SD ; 1.96  SD ] was 0.94 [−8.00; 9.88] for heart, 1.34 [−7.81; 10.49] for lung and 0.25 [−16.74; 17.24] mm Hg for heart‐lung recipients). Thresholds of SPAP for MPAP =25 and 20 mm Hg were lower in patients with higher PAWP (37.2 and 29.8 mm Hg) than in those with pulmonary arterial hypertension (40.1 and 32.0 mm Hg). In 186 patients with pulmonary arterial hypertension , the predicted MPAP / SPAP was stable over time (0.63±0.03 at baseline and follow‐up catheterization, P =0.43). Conclusions This study quantifies the impact of PAWP , and to a lesser extent heart rate and age, on the MPAPSPAP relation, supporting lower SPAP thresholds for pulmonary hypertension diagnosis in patients with higher PAWP for echocardiography‐based epidemiological studies.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine

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