Assessing the physiological impact of exercise intensity on pulmonary artery pressure in healthy volunteers using a novel stress echocardiography protocol
Authors: Dorobantu D , Smith M , Williams M , Haywood A J , Emirza Cilbir C , Wadey C A , Stuart A G , Pieles G E , Williams C A 
Published: January 2025

Background

Pulmonary artery pressure (PAP) response to exercise is frequently investigated in a wide range of heart disease. Yet, there remains a grey area, especially in special groups such as athletes, where normal PAP response to exercise is not well defined. This is mainly due to how current ESE protocols do not account for individual variability in cardiorespiratory fitness and exercise tolerance, which introduces biases. Additionally, non-invasive estimation of PAP at exercise is technically challenging, especially at peak exertion.

Aims

This study aims to describe the normal PAP response to exercise in relation to physiological exercise intensity, reducing bias from individual cardiorespiratory fitness variation, and evaluate the feasibility of non-invasive estimation methods during exercise stress echocardiography (ESE).

Methods

A total of 115 healthy children and adults between (mean age 38 ± 16 years, range 10-65) were included. Participants underwent resting echocardiography, then a maximal CPET followed by ESE consisting of two 6-minute stages: 1. Moderate intensity (M-Int) at 90% of the work rate at the gas exchange threshold (GET) and 2. High intensity (H-Int) at 40% of the difference between GET and peak exercise. Right ventricular (RV) systolic pressure (RVsp) was estimated based on tricuspid regurgitant jet velocity and mean pulmonary artery pressure (mPAP) using the RV outflow tract pulmonary ascension time. Based on WR and HR, H-Int steps were matched 1-to-n with M-Int steps from other participants, to identify pairs with identical values at different exercise intensity. Physical activity (PA) was assessed using age-appropriate questionnaires.

Results

RVsp and mPAP estimation was possible for: 92% vs 96% (rest), 43% vs 89% (M-Int) and 50% vs 84% (H-Int). RVsp and mPAP increased significantly between rest, M-Int and H-Int, including after adjusting for HR (Figure A). There was a significant correlation between RVsp and mPAP values across the exercise (b=0.53 [0.44;0.61], p&lt;0.01, Figure B), which remained statistically significant after adjusting for exercise intensity, HR, age and physical activity level (b=0.12 [0.02;0.22], p=0.02). At identical HR, H-Int vs M-Int had higher RVsp (42 vs 34 mmHg, p&lt;0.001) and mPAP (30 vs 24 mmHg, p&lt;0.001). At identical WR, H-Int vs M-Int had higher RVsp (41 vs 33 mmHg, p&lt;0.001) and mPAP (32 vs 21 mmHg, p&lt;0.001).

Conclusion

Physiological exercise intensity, and not HR or work-rate alone, appears to drive the physiological increase in PAP during exercise. Echocardiographic estimation of RVsp is often not feasible at exercise, while that of mPAP is more feasible but not yet validated against invasive measures at ESE, being HR dependent. Translating this novel physiologically guided ESE and accompanying normative values in disease groups, with multi-parametric estimations of PAP could potentially improve diagnosis and follow-up in cases where resting data is equivocal.

Figure A

Figure B