Endometriosis and cardiovascular disease

Benjamin Marchandot, Anais Curtiaud, Anaïs Curtiaud, Kensuke Matsushita, Antonin Trimaille, Host A, Aline Host, Faller E, Emilie Faller, Émilie Faller, O. Garbin, Olivier Garbin, Garbin O, Chérif Akladios, Laurence Jesel, Jesel L, Olivier Morel
European heart journal open · 2022 · vol. 2(1) , pp. oeac001 · doi:10.1093/ehjopen/oeac001 · PMID:35919664 · PMC9242051 · W4210895284
article OA: gold CC0 ⤵ 26 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

This review explores the systemic hormonal, inflammatory, and immunologic processes of endometriosis and presents clinical evidence linking it to cardiovascular risk factors and disease, which remains an understudied area.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-17 · read from full text ⓘ

This paper is a focused review examining evidence for shared mechanisms and epidemiologic links between endometriosis and atherosclerotic cardiovascular disease, contextualizing overlapping biological pathways such as systemic inflammation, pro-angiogenic signaling, oxidative stress, and endothelial dysfunction, and summarizing how cardiovascular risk factors and clinical evidence have been studied. It notes that robust mechanistic understanding and clear cardiovascular associations are limited by the scarcity of strong datasets and that historically most endometriosis data come from women with surgical diagnoses, alongside additional limitations such as delayed diagnosis and nonspecific symptoms that overlap with other conditions. The review describes overlaps in immune-endocrine and molecular features (e.g., cytokines, DAMPs, VEGF, microvesicles, and enhanced local estradiol/estrogen receptor signaling) that have known relevance to atherosclerosis, and cites reported associations including increased arterial stiffness and impaired flow-mediated dilation as well as genetic susceptibility signals at loci such as CDKN2B-AS. This paper is centrally about endometriosis — [endometriosis–cardiovascular disease] review of shared mechanisms and clinical/genetic evidence linking endometriosis with cardiovascular risk and adverse outcomes.

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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.
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Lead

Dr Benjamin Marchandot is a general cardiologist in the Cardiac Care Unit (CCU) at Strasbourg University Hospital, France. He is a member of Strasbourg Cardiovascular Research Group—GERCA (Groupe pour l’Enseignement et la Recherche Cardiovasculaire en Alsace), a multidisciplinary research team involved in the field of CVD, thrombosis, and haemostasis. Conflict of interest: The authors declare that there is no conflict of interest regarding the publication of this article. O.M. received institutional research grants from Fondation Coeur et Vaisseaux, AstraZeneca and Boehringher Ingelheim. K.M. received a grant from Edwards Lifesciences (THV-F20-142). The manuscript has been read and approved for submission by all authors. The authors take responsibility for all aspects of the reliability and freedom from bias of the data presented and their discussed interpretation.

Funding

This work was supported by Groupe pour l Enseignement, la Pr赥ntion et la Recherche Cardiologique en Alsace (GERCA). Data availability: No new data were generated or analysed in support of this research.

Summary

Cardiovascular disease remains the leading cause of mortality among women, causing 1 in 3 deaths each year, 130 whereas endometriosis affects 1 in 10 reproductive-age women. This unequivocal epidemiological observation should be considered in the field of future cardiovascular research in women. Current clinical evidence is insufficient to implicate a strong association and potential role for endometriosis in CVD. The literature is sparse regarding the association between CVD and endometriosis ( Graphical Abstract ). The epidemiologically observed associations between the two should be interpreted with caution for several reasons. Current evidence is limited by small sample sizes, observational designs, and the specific characteristics of the population from which the samples are derived (high-income countries, cohort study of hospital-based healthcare workers, primarily Caucasian Europeans, etc.). Only small associations between endometriosis and CVD have been reported in the literature, although inconsistently. Representation of participants with endometriosis in cardiovascular clinical trials and registries is challenging, as endometriosis remains under-recognized. Endometriosis is usually diagnosed in higher socioeconomic groups and likely related to inequities in access to health care. In addition to socioeconomic impact, multiple factors can be identified as barriers to inclusion of women with endometriosis in CV studies: misdiagnosis is common; as diagnosis remains challenging and largely delayed by years; unawareness about ongoing trials, combined cardiac and gynaecologic care, and monitoring in clinical trials, etc. The chronic and heterogeneous nature of endometriosis (e.g. disease stage and lesion type) and the confounding influence of hormonal, non-hormonal, and pain-related interventions further complicate the cause-and-effect relationship in CV endpoints. Cardiovascular disease risk estimation remains challenging, especially in women with endometriosis. Further research is needed to better understand how endometriosis should be incorporated into risk prediction models alongside well-established risk factors. Indeed, the reduced quality of life and psychosocial risk factors such as depression and anxiety may overlap and help to explain the predisposition for CVD. In considering women with endometriosis, there is a need to better understand the potential associations with CVD and risk factors and to clarify the pathophysiology of the female heart at a broader level ( Graphical Abstract ). Inclusivity is therefore mandatory, and specific registries, studies, and trials are urgently needed to address the underlying biological mechanisms potentially shared between CVD and endometriosis, clarify whether endometriosis can cause CVD; assess the prognosis of endometriosis in cardiovascular patients, and finally, advance potential innovative solutions and tailored management of CVD in women with endometriosis. Multicentre case-controlled and cross-sectional studies may be of particular interest in women admitted to cardiology departments to ascertain the association between endometriosis and various CVDs (ischaemic cardiomyopathy, HF, AF, etc.) and risk factors. However, the benefits of such study designs are limited by the fact that (i) endometriosis is greatly underdiagnosed, (ii) there are asymptomatic cases, and (iii) the assessment of specific CVD phenotypes and risk factors distributions among endometriosis patients necessitates a large sample. Only international and/or national levels initiatives may have the power to address the prevalence, links, impact, and prognosis of endometriosis and CVD by analysing data from large-scale surveys. Strong evidence regarding the association between these two conditions obtained from large-scale cohorts or large population-based studies, may contribute to a change in the prevention, screening, early detection, and treatment of CV risk factors among women with endometriosis.

Introduction

Endometriosis is a chronic gynaecological disease estimated to affect 10% of reproductive-age women. 1 Recent insights have linked endometriosis to several pathological mechanisms ranging from systemic inflammation, pro-atherogenic lipid profile, and enhanced oxidative stress to endothelial dysfunction. 2 Considered as a systemic disease, the pathogenesis of endometriosis and the impact of the disease remain poorly understood. Robust knowledge is restricted to data from women surgically diagnosed with endometriosis limiting the development of multidisciplinary approaches to ameliorate the substantial cumulative burden of this condition. A focused update consensus document on gynaecological and obstetric conditions that impact cardiovascular risk in women was released in March 2021. 3 The scarcity of a strong dataset limited the ability to provide clear evidence regarding the pathophysiology, pathogenesis, and prognosis of endometriosis in cardiovascular disease (CVD). Here, we review relevant evidence regarding the relationship between endometriosis and CVD. The purpose of this review article is to further our understanding of the shared mechanisms underlying endometriosis and atherosclerotic CVD, by contextualizing biological pathways common to both diseases, addressing the association between cardiovascular risk factors and endometriosis, and finally, highlighting key clinical evidence that link endometriosis with adverse cardiovascular events.

Endometriosis

Several cardiovascular medications have been tested in animal models, with promising results on the establishment and maintenance of endometriotic lesions. However, their translation into human clinical trials has been very limited. Statins, classically known for their roles in lowering cholesterol and anti-inflammatory properties, have been shown to play a role in endometriosis by modifying cell signalling in preclinical studies using human endometriotic stromal cell cultures. Statins therapy lead to increased apoptosis, decreased proliferation, and impaired cell adhesion and motility. 118 , 119 Additionally, statins inhibited stromal cell invasion and reduced angiogenesis. 120–122 Recent findings showed that platelets play important roles in the development of endometriosis in general and in fibrogenesis in particular. 123 , 124 Antiplatelet treatment was demonstrated to impede the progressive epithelial-mesenchymal transition, fibroblast-to-myofibroblast transdifferentiation, and smooth muscle metaplasia, resulting in reduced lesion size of endometriotic lesions and fibrogenesis. 123 Low-dose aspirin, used in a preclinical setting, has lately been proposed for its ability to down-regulate progesterone resistance and a target for endometriosis-related infertility. 125 Women with endometriosis tend to have higher levels of psychological stress, which is known to promote tumour growth and metastasis. Β-Adrenergic receptor blockade in a mouse model of endometriosis completely abolished the promotional effect of chronic stress, through suppression of ADRB2 and CREB activation, thus suppressing angiogenesis and proliferation. 126 Additionally, perioperative use of propranolol in a mouse model of endometriosis significantly decelerated the growth of residual lesions that were intentionally left out during the primary surgery. 127 Similarly, telmisartan inhibited vascularization, immune cell content, and growth of murine endometriosis-like lesions. 128 , 129

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