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Uncoupling between intravascular and distending pressures leads to underestimation of circulatory congestion in obesity
Abstract
Aims: Patients with obesity frequently present with dyspnoea. Biomarkers that reflect wall stress are often used to evaluate circulatory congestion and help determine whether dyspnoea is of cardiac causes. Patients with obesity display greater external restraint on the heart, which may alter relationships between intravascular pressures and stress markers. Methods and results: Subjects with unexplained dyspnoea ( n = 212) underwent cardiac catheterization with simultaneous echocardiography. Blood sampling was performed in a subset ( n = 58). Relationships between echocardiographic and blood biomarkers of circulatory congestion and directly‐measured haemodynamics were compared between participants with severe obesity [body mass index (BMI) ≥35 kg/m 2 , Group B) and those without (BMI <35 kg/m 2 , Group A). Circulatory congestion was assessed by pulmonary capillary wedge pressure (PCWP), and vascular distending pressure was assessed by left ventricular transmural pressure (LVTMP). As compared to Group A, participants in Group B displayed higher PCWP relative to N‐terminal pro‐B‐type natriuretic peptide, mid‐regional pro‐atrial natriuretic peptide, troponin T, and growth differentiation factor‐15 (all p < 0.01). In contrast, the relationships between LVTMP and the biomarkers were superimposable. Echocardiographic biomarkers revealed the same pattern: PCWP was higher for any E/e′ ratio in Group B compared to Group A, but the relationship between LVTMP and E/e′ was similar. In contrast, levels of C‐terminal pro‐endothelin‐1 and mid‐regional pro‐adrenomedullin were more robustly correlated with PCWP (r = 0.67 and r = 0.62, both p < 0.0001), with no differential relationship based upon BMI. Conclusions: Non‐invasive haemodynamic markers underestimate circulatory congestion in patients with obesity, an effect that appears related to uncoupling between cardiac wall stress and intravascular pressures. This may lead to systematic under‐recognition of congestion in patients with obesity.
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As compared with nonobese HFpEF, patients with obesity-related HFpEF display distinct pathophysiologic features, including greater volume expansion, more severe inflammation, increases in visceral and paracardiac adipose tissue and more severe myocardial injury.
“As compared with nonobese HFpEF, patients with obesity-related HFpEF display distinct pathophysiologic features, including greater volume expansion5,17, more severe inflammation6,7, increases in visceral and paracardiac adipose tissue5,15,18,19 and more severe myocardial injury15.”
From Effects of tirzepatide on circulatory overload and end-organ damage in heart failure with preserved ejection fraction and obesity: a secondary analysis of the SUMMIT trial (2025) · cites this paper as [15]
The “Mechanism for underestimation of filling pressures in obesity” section says obesity may increase external cardiac pressure partly through plasma volume retention, which supports the volume-expansion point attached to this citation. It does not directly establish greater blood volume in obesity-related versus nonobese HFpEF: the study compared patients with and without severe obesity who had unexplained dyspnoea, not exclusively patients with HFpEF. The other listed features have separate citations in the citing sentence. (LLM, conf=0.82)
Experimental — accuracy not yet measuredParacardiac adipose tissue in patients with obesity may impair LV relaxation and increase cardiac filling pressures.
“Paracardiac adipose tissue (epicardial and pericardial adipose tissue) in patients with obesity may also impair LV relaxation20 and increase cardiac filling pressures, owing to increases in extrinsic restraint on the heart in obesity-related HFpEF.2,6,7”
From Tirzepatide Reduces LV Mass and Paracardiac Adipose Tissue in Obesity-Related Heart Failure (2025) · cites this paper as [6]
Individuals with the obesity phenotype have higher troponin levels than those without obesity.
“Patients with HFpEF and elevated troponin have more severe elevation in filling pressures, reduced myocardial stress reserve and poorer exercise capacity compared with those without injury13, and individuals with the obesity phenotype have higher troponin levels than those without obesity15.”
Cardiac injury is greater in patients with obesity-related HFpEF compared with those without obesity.
“Notably, cardiac injury is greater in patients with obesity-related HFpEF compared with those without obesity15.”
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Citations
Cites
Projected U.S. State-Level Prevalence of Adult Obesity and Severe Obesity
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Impact of Obesity on Plasma Natriuretic Peptide Levels
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Self-citationKoepp, K. E., Obokata, M., Reddy, Y. N. V., Olson, T. P., & Borlaug, B. A. (2020) · JACC Heart Failure · doi:10.1016/j.jchf.2020.04.016 · Cited by 269
Self-citationReddy, Y. N. V., Rikhi, A., Obokata, M., Shah, S. J., Lewis, G. D., AbouEzzedine, O. F., Dunlay, S., McNulty, S., Chakraborty, H., Stevenson, L. W., et al. (2020) · European Journal of Heart Failure · doi:10.1002/ejhf.1788 · Cited by 243
Self-citationObesity, venous capacitance, and venous compliance in heart failure with preserved ejection fraction
Sorimachi, H., Burkhoff, D., Verbrugge, F. H., Omote, K., Obokata, M., Reddy, Y. N. V., Takahashi, N., Sunagawa, K., & Borlaug, B. A. (2021) · European Journal of Heart Failure · doi:10.1002/ejhf.2254 · Cited by 124
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Cited by
Sorted by citations
Heart Failure With Preserved Ejection Fraction
Borlaug, B. A., Sharma, K., Shah, S. J., & Ho, J. E. (2023) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2023.01.049 · Cited by 742
Self-citationBorlaug, B. A., Jensen, M. D., Kitzman, D. W., Lam, C. S. P., Obokata, M., & Rider, O. J. (2023) · Cardiovascular Research · doi:10.1093/cvr/cvac120 · Cited by 450
Self-citationTirzepatide Reduces LV Mass and Paracardiac Adipose Tissue in Obesity-Related Heart Failure
Kramer, C. M., Borlaug, B. A., Zile, M. R., Ruff, D., DiMaria, J. M., Menon, V., Ou, Y., Zarante, A. M., Hurt, K. C., Murakami, M., et al. (2025) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2024.11.001 · Cited by 200
Self-citationBorlaug, B. A., Zile, M. R., Kramer, C. M., Baum, S. J., Hurt, K., Litwin, S. E., Murakami, M., Ou, Y., Upadhyay, N., & Packer, M. (2025) · Nature Medicine · doi:10.1038/s41591-024-03374-z · Cited by 166
Self-citationSemaglutide and NT-proBNP in Obesity-Related HFpEF
Petrie, M. C., Borlaug, B. A., Butler, J., Davies, M. J., Kitzman, D. W., Shah, S. J., Verma, S., Jensen, T. J., Einfeldt, M. N., Liisberg, K., et al. (2024) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2024.04.022 · Cited by 95
Self-citation2025 ACC Scientific Statement on the Management of Obesity in Adults With Heart Failure
Kittleson, M. M., Benjamin, E. J., Blumer, V., Harrington, J., Januzzi, J. L., McMurray, J. J. V., & Vest, A. R. (2025) · JACC · doi:10.1016/j.jacc.2025.05.008 · Cited by 79
Zile, M. R., Borlaug, B. A., Kramer, C. M., Baum, S. J., Litwin, S. E., Menon, V., Ou, Y., Weerakkody, G. J., Hurt, K. C., Kanu, C., et al. (2025) · Circulation · doi:10.1161/circulationaha.124.072679 · Cited by 74
Self-citationKosyakovsky, L. B., Liu, E. E., Wang, J. K., Myers, L., Parekh, J. K., Knauss, H., Lewis, G. D., Malhotra, R., Nayor, M., Robbins, J. M., et al. (2024) · Circulation: Heart Failure · doi:10.1161/circheartfailure.123.011366 · Cited by 43
Verma, R., Dhingra, N. K., & Connelly, K. A. (2024) · Current Opinion in Cardiology · doi:10.1097/hco.0000000000001113 · Cited by 24
Metadata
- Authors
- Obokata, M., Reddy, Y. N. V., Melenovsky, V., Sorimachi, H., Jarolim, P., & Borlaug, B. A.
- Affiliations
- Department of Cardiovascular Diseases Mayo Clinic Rochester MN USA
- Brigham and Women's Hospital Harvard Medical School Boston MA USA
- ORCID
- Borlaug, Barry A.
- Venue
- European Journal of Heart Failure
- Publisher
- Oxford University Press (OUP)
- Published
- 2021-11-21
- Volume
- 24
- Issue
- 2
- Pages
- 353-361
- ISSN
- 1388-9842
- 1879-0844
- Cited by
- 99
- References
- 7
- Language
- en
- Funders
- Foundation for the National Institutes of Health (RO1 HL128526)
- Fukuda Foundation for Medical Technology (N/A)
- Japanese Circulation Society
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Nippon Shinyaku
- Takeda Science Foundation
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