Endometriosis as an underrecognized risk factor for heart failure: Mechanistic insights from inflammation, estrogen dysregulation, and cardiometabolic overlap
1 Department of Community Medicine and Primary Health Care, Faculty of Medicine, College of Health Sciences, Nnamdi Azikiwe University, Awka, Nigeria.
2 Department of Pharmacognosy and Phytotherapy, University of Port-harcourt, Port-harcourt, Nigeria.
3 Department of Medicine, Obafemi Awolowo University, Ile Ife, Nigeria.
4 Department of Biochemistry, Adeleke University, Ede, Nigeria.
5 Department of Medicine and Surgery, Igbinedion University, Okada, Nigeria.
6 Department of Obstetric and Gynaecology, Usmanu Danfodiyo University, Sokoto, Nigeria.
7 Department of Public Health, Anglia Ruskin University, Cambridge, UK.
8 Department of Biochemistry, Wesley University, Ondo, Nigeria
2 Department of Pharmacognosy and Phytotherapy, University of Port-harcourt, Port-harcourt, Nigeria.
3 Department of Medicine, Obafemi Awolowo University, Ile Ife, Nigeria.
4 Department of Biochemistry, Adeleke University, Ede, Nigeria.
5 Department of Medicine and Surgery, Igbinedion University, Okada, Nigeria.
6 Department of Obstetric and Gynaecology, Usmanu Danfodiyo University, Sokoto, Nigeria.
7 Department of Public Health, Anglia Ruskin University, Cambridge, UK.
8 Department of Biochemistry, Wesley University, Ondo, Nigeria
Review
International Journal of Biological and Pharmaceutical Sciences Archive, 2026, 11(02), 009-022.
Article DOI: 10.53771/ijbpsa.2026.11.2.0036
Publication history:
Received on 24 February 2026; revised on 16 April 2026; accepted on 18 April 2026
Abstract:
Endometriosis is often treated as a localised gynaecological issue, but a growing body of evidence shows it has broader systemic effects including an increase in the risk of heart failure. The condition affects roughly 10% of women of reproductive age and is linked through large cohort studies and meta-analyses to elevated rates of ischaemic heart disease (IHD), stroke and arrhythmias (adjusted hazard ratios typically 1.1 to 1.5), with heart failure emerging as a signal in several nationwide registries. The connection appears to arise from three overlapping mechanisms; Persistent low-grade inflammation releases pro-inflammatory cytokines (notably IL-6, TNF-α, and IL-1β) into the circulation which promotes endothelial dysfunction and oxidative stress, Oestrogen dysregulation which plays a paradoxical role: locally, excessive production in endometriotic lesions sustains inflammation while systemic hormonal imbalance can undermine vascular protection and contribute to pro-thrombotic or arrhythmogenic effects. Concurrent cardiometabolic disturbances such as insulin resistance, atherogenic dyslipidaemia, central adiposity and elevated cardiometabolic index further strain the myocardium and predisposes one to diastolic dysfunction particularly in the heart failure with preserved ejection fraction phenotype that disproportionately affects women. Clinically, this means endometriosis should no longer be managed in isolation. Routine cardiovascular risk assessment such as blood pressure, lipid profile, glucose tolerance and possibly selected inflammatory markers should become standard in follow-up especially for younger patients or those with long disease duration or have had prior surgery. Closer collaboration between gynaecologists and cardiologists together with prospective studies that track true heart failure incidence and evaluate targeted interventions (anti-inflammatory strategies, optimised hormonal regimens, lifestyle modification) could substantially reduce preventable cardiac morbidity in this population.
Keywords:
Endometriosis; Heart Failure; Inflammation; Estrogens; Risk Factors; Cardiovascular Diseases; Insulin Resistance; Metabolic Syndrome
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