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The Relationship of Cardiac Output to Alveolar-Capillary Expansion in Response to Exercise to Identify and Track PAH Patients

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A6142 - The Relationship of Cardiac Output to Alveolar-Capillary Expansion in Response to Exercise to Identify and Track PAH Patients
Author Block: C. Wheatley1, G. M. Stewart2, G. Patangey1, K. E. Joyce1, B. Ziegler2, B. S. Cierzan2, B. D. Johnson2; 1Cardiovascular Diseases, Mayo Clinic, Scottsdale, AZ, United States, 2Cardiovascular Diseases, Mayo Clinic, Rochester, MN, United States.
Conditions such as early forms of pulmonary arterial hypertension (PAH) can be difficult to detect at rest, when it is most treatable, due to the large reserves of the lungs. But stressing the system with a stimulus such as exercise increases the interaction between cardiac and pulmonary systems and provides an excellent modality to allow for earlier detection of underlying dysfunction. Purpose: To evaluate if limitations in expansion of the pulmonary circulation with exercise exist in early and mild stages of PAH and could consequently be used as a novel, noninvasive tool for screening. Methods: Seven mild-moderate PAH (Group 1 with a mean functional class of 1.5) and fifteen healthy subjects completed four increasing stages of submaximal exercise on an ergometer (11min total). At rest and twice during each 3-min stage DLCO and pulmonary blood flow (Q) were measured, while gas exchange was continuously assessed. Results: Upon initiation of exercise there was a sharper drop in the relationship between DLCO/Q from rest to unloaded cycling for healthy participants (ΔDLCO/Q: -0.51±0.66 vs -1.29±0.63 for PAH vs. Healthy respectively, p=0.015), but plateaued at subsequent workloads in contrast to PAH where DLCO/Q steadily dropped (DLCO/Q: workload*condition interaction p=0.08). This was driven by a greater change in Q with a similar change in DLCO upon starting exercise (ΔQ: 0.8±0.9 vs. 2.0±1.0, p=0.01; ΔDLCO: 0.7±0.7 vs. 0.6±2.9, p>0.05, for PAH vs. Healthy). PAH patients also tended to demonstrate a plateau in the gas exchange estimate of pulmonary capacitance (O2pulse×PetCO2, GxCap), which did not occur for healthy participants (GxCap: 92±18, 182±53, 214±46, 212±60, 214±59 vs. 107±48, 230±88, 256±69, 272±100, 287±130, PAH vs. Healthy for rest, unloaded, stage 1, 2 and 3; workload*condition interaction p=0.22). Finally, partial pressure of mix expired CO2 (PeCO2)/partial pressure of end tidal CO2 (PetCO2) ratio as a measure of V/Q mismatching demonstrated higher ratios though not significant for PAH patients suggesting higher ventilation relative to perfusion. Conclusions: With initiation of exercise there was a reduced change in DLCO/Q relationship driven primarily by a difference in the change in Q. With PAH individuals also tending to have a blunted increase in pulmonary capacitance (GxCap) and higher V/Q mismatch (PeCO2/PetCO2 ratio) with exercise, despite effective medical management of mild disease, there appears to be a delay in recruitment/distention of pulmonary capillaries which may have the potential to be used as a tool to detect undiagnosed mild PAH earlier.
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