Association of Peak Circulatory Power with Invasive Hemodynamic Severity in Pulmonary Hypertension
- 1State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Road, Xicheng District, Beijing 100037, China
Abstract
Background: Peak circulatory power (CP), derived from peak oxygen uptake per kilogram (peak VO2/kg) and peak systolic blood pressure (SBP), has prognostic value in cardiovascular disease, but its association with invasive hemodynamic severity in pulmonary hypertension (PH) remains unclear. We examined the relationship between peak CP and mixed venous oxygen saturation (SvO2) and other hemodynamic markers in patients with PH. Methods: This retrospective cross-sectional study included 133 adults with confirmed PH who underwent cardiopulmonary exercise testing and right heart catheterization before targeted therapy. Linear regression adjusted for age and sex evaluated associations between peak CP and SvO2, pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), N-terminal pro-brain natriuretic peptide (NT-proBNP), and six-minute walk distance (6MWD). Exploratory receiver operating characteristic (ROC) analysis assessed the ability of peak CP to identify SvO2 ≤ 65%. Results: Median age was 33 years, and 62.4% were female. After adjustment for age and sex, lower peak CP was associated with lower SvO2 (B per 100-unit increase = 0.30, 95% CI: 0.10–0.50, p = 0.011), higher PVR (B = −0.20, 95% CI: −0.40 to −0.10, p = 0.001), higher mPAP (B = −0.70, 95% CI: −1.10 to −0.20, p = 0.003), higher NT-proBNP (B = −19.0, 95% CI: −30.9 to −7.0, p = 0.002), and shorter 6MWD (B = 2.40, 95% CI: 0.50–4.30, p = 0.015). Peak CP identified SvO2 ≤ 65% (15/133, 11.3%) with an AUC of 0.781 (95% CI: 0.674–0.888), similar to peak VO2/kg (AUC 0.783). Conclusions: In patients with PH not receiving targeted therapy, lower peak CP is age- and sex-adjusted associated with lower SvO2, higher PVR, higher mPAP, higher NT-proBNP, and shorter 6MWD, suggesting that peak CP reflects exercise cardiovascular reserve and hemodynamic severity. Thresholds and discriminatory estimates require prospective validation.
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BibTeX
@article{song2026association,
title = {{Association of Peak Circulatory Power with Invasive Hemodynamic Severity in Pulmonary Hypertension}},
author = {Ya Song and Chao Shi and Yan-Li Gu and Meng Li and Mig-Jing Zhao and Ting-Ting Dou and Liu Du and Ruo-Xi Li and Xue Feng and Xin-Xin Yan},
journal = {Journal of Clinical Medicine},
year = {2026},
month = oct,
doi = {10.3390/jcm15218309},
url = {https://www.mdpi.com/2077-0383/15/21/8309},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Association of Peak Circulatory Power with Invasive Hemodynamic Severity in Pulmonary Hypertension
AU - Ya Song
AU - Chao Shi
AU - Yan-Li Gu
AU - Meng Li
AU - Mig-Jing Zhao
AU - Ting-Ting Dou
AU - Liu Du
AU - Ruo-Xi Li
AU - Xue Feng
AU - Xin-Xin Yan
PY - 2026
DA - 2026/10/25
JO - Journal of Clinical Medicine
DO - 10.3390/jcm15218309
UR - https://www.mdpi.com/2077-0383/15/21/8309
AB - Background: Peak circulatory power (CP), derived from peak oxygen uptake per kilogram (peak VO2/kg) and peak systolic blood pressure (SBP), has prognostic value in cardiovascular disease, but its association with invasive hemodynamic severity in pulmonary hypertension (PH) remains unclear. We examined the relationship between peak CP and mixed venous oxygen saturation (SvO2) and other hemodynamic markers in patients with PH. Methods: This retrospective cross-sectional study included 133 adults with confirmed PH who underwent cardiopulmonary exercise testing and right heart catheterization before targeted therapy. Linear regression adjusted for age and sex evaluated associations between peak CP and SvO2, pulmonary vascular resistance (PVR), mean pulmonary arterial pressure (mPAP), N-terminal pro-brain natriuretic peptide (NT-proBNP), and six-minute walk distance (6MWD). Exploratory receiver operating characteristic (ROC) analysis assessed the ability of peak CP to identify SvO2 ≤ 65%. Results: Median age was 33 years, and 62.4% were female. After adjustment for age and sex, lower peak CP was associated with lower SvO2 (B per 100-unit increase = 0.30, 95% CI: 0.10–0.50, p = 0.011), higher PVR (B = −0.20, 95% CI: −0.40 to −0.10, p = 0.001), higher mPAP (B = −0.70, 95% CI: −1.10 to −0.20, p = 0.003), higher NT-proBNP (B = −19.0, 95% CI: −30.9 to −7.0, p = 0.002), and shorter 6MWD (B = 2.40, 95% CI: 0.50–4.30, p = 0.015). Peak CP identified SvO2 ≤ 65% (15/133, 11.3%) with an AUC of 0.781 (95% CI: 0.674–0.888), similar to peak VO2/kg (AUC 0.783). Conclusions: In patients with PH not receiving targeted therapy, lower peak CP is age- and sex-adjusted associated with lower SvO2, higher PVR, higher mPAP, higher NT-proBNP, and shorter 6MWD, suggesting that peak CP reflects exercise cardiovascular reserve and hemodynamic severity. Thresholds and discriminatory estimates require prospective validation.
SN - 2077-0383
ER -