Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2022 Feb 2;2(1):oeac001.
doi: 10.1093/ehjopen/oeac001. eCollection 2022 Jan.

Endometriosis and cardiovascular disease

Benjamin Marchandot  1 , Anais Curtiaud  1 , Kensuke Matsushita  1   2 , Antonin Trimaille  1   2 , Aline Host  3   4 , Emilie Faller  3   4 , Olivier Garbin  3   4 , Chérif Akladios  3   4 , Laurence Jesel  1   2 , Olivier Morel  1   2
Affiliations

Endometriosis and cardiovascular disease

Benjamin Marchandot et al. Eur Heart J Open. .

Erratum in

Abstract

Endometriosis is a chronic gynaecological disease affecting 1 in 10 reproductive-age women. It is defined as the presence of endometrium-like tissue outside the uterus. Beyond this placid anatomical definition, endometriosis is a complex, hormonal, inflammatory, and systemic condition that poses significant familial, psychological, and economic burden. The interaction between the cardiovascular system and endometriosis has become a field of interest as the underlying mutual mechanisms become better understood. On the basis of accumulating fundamental and clinical evidence, it is likely that there exists a close relationship between endometriosis and the cardiovascular system. Therefore, investigating the endometriosis-cardiovascular interaction is highly clinically significant. In this review, we highlight our current understanding of the pathophysiology of endometriosis with systemic hormonal, pro-inflammatory, pro-angiogenic, immunologic, and genetic processes beyond the peritoneal microenvironment. Additionally, we provide current clinical evidence about how endometriosis interacts with cardiovascular risk factors and cardiovascular disease (CVD). To date, only small associations between endometriosis and CVD have been reported in observational studies, inherently limited by the potential influence of unmeasured confounding. Cardiovascular disease in women with endometriosis remains understudied, under-recognized, and underdiagnosed. More detailed study of the cardiovascular-endometriosis interaction is needed to fully understand its clinical relevance, underlying pathophysiology, possible means of early diagnosis and prevention.

Keywords: Cardiovascular disease; Endometriosis; Heart disease; Women.

PubMed Disclaimer

Figures

Graphical Abstract
Graphical Abstract
Figure 1
Figure 1
Epidemiology and economic burden of endometriosis.
Figure 2
Figure 2
Molecular pathways underpinning endometriosis. Endometriotic lesions are characterized by a unique environment. The interplay between pro-inflammatory signals, pro-angiogenic signals, and a unique endocrine signature contribute to the pathogenesis of endometriosis. This schematic representation of the endometriotic lesion identifies three distinct molecular pathways that facilitate lesion growth in endometriosis. (1) Pro-inflammatory signals: increased neutrophil infiltration in the peritoneal fluid; increased macrophage populations in the peritoneal fluid and eutopic endometrium; elevated cytokine levels (IL-6, IL-8, IL-17, IL-33, TNF-a, etc.) in both the peritoneal fluid and plasma; at sites of inflammation, macrophages and mast cells drive neutrophil recruitment through the release of chemokines; impair regulatory T cells function. (2) Pro-angiogenic signals: Damage-associated molecular patterns: high-mobility group box 1, elevated IL-33 level, etc.; vascular endothelial growth factor. (3) Endocrine signals: local synthesis of oestradiol by endometriotic lesions; enhanced oestrogen receptor expression. ILs, interleukins; OR, oestrogen receptor; Treg cells, regulatory T cells; VEGF, vascular endothelial growth factor.
Figure 3
Figure 3
Summary of proposed mechanisms for endometriosis–cardiovascular interaction. Cardiovascular dysfunction in endometriosis may be caused by several mechanisms, including pro-inflammatory, pro-angiogenic, and aberrant immune-endocrine function. (? indicates that future studies are warranted.) DAMPs, damage-associated molecular patterns; ILs, interleukins; MVs, microvesicles; OR, oestrogen receptor; ROS, reactive oxygen species; Treg cells, regulatory T cells; VEGF, vascular endothelial growth factor.
See this image and copyright information in PMC

References

    1. Shafrir AL, Farland LV, Shah DK, Harris HR, Kvaskoff M, Zondervan K, Missmer SA. Risk for and consequences of endometriosis: a critical epidemiologic review. Best Pract Res Clin Obstet Gynaecol 2018;51:1–15. - PubMed
    1. Taylor HS, Kotlyar AM, Flores VA. Endometriosis is a chronic systemic disease: clinical challenges and novel innovations. Lancet 2021;397:839–852. - PubMed
    1. Maas AHEM, Rosano G, Cifkova R, Chieffo A, van Dijken D, Hamoda H, Kunadian V, Laan E, Lambrinoudaki I, Maclaran K, Panay N, Stevenson JC, van Trotsenburg M, Collins P. Cardiovascular health after menopause transition, pregnancy disorders, and other gynaecologic conditions: a consensus document from European cardiologists, gynaecologists, and endocrinologists. Eur Heart J 2021;42:967–984. - PMC - PubMed
    1. Zondervan KT, Becker CM, Missmer SA. Endometriosis. N Engl J Med 2020;382:1244–1256. - PubMed
    1. Parazzini F, Esposito G, Tozzi L, Noli S, Bianchi S. Epidemiology of endometriosis and its comorbidities. Eur J Obstet Gynecol Reprod Biol 2017;209:3–7. - PubMed