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Cardiovascular disease is the leading cause of death in diabetes, driven primarily by coronary artery disease (CAD). Although female sex confers relative protection against CAD in the general population, this advantage is attenuated by diabetes. This narrative review examines CAD in women with diabetes across epidemiology, pathophysiology, clinical presentation, prognosis, and management explicitly distinguishing type 1 from type 2 diabetes. Data were synthesized from original articles, population-based cohorts, reviews, consensus statements, and cardiovascular outcome trials (CVOTs) identified through structured PubMed searches. Effect estimates for sodium-glucose cotransporter-2 (SGLT2) inhibitors, glucagon-like peptide-1 receptor agonists (GLP1-RAs), and antiplatelet and lipid-lowering agents were extracted from primary trials and meta-analyses, focusing on sex-stratified outcomes. Most, but not all, studies suggest that women with type 1 and type 2 diabetes have higher relative CAD risk than men. Shared mechanisms—endothelial and microvascular dysfunction, accelerated atherogenesis, inflammation, advanced glycation, and loss of estrogen-mediated protection—produce a female coronary phenotype with more diffuse and microvascular disease, yet the drivers, presentation, and prognosis diverge by diabetes type. In type 1 diabetes, early-onset disease, glycemic variability, and an autoimmune, pro-inflammatory milieu impose decades of cumulative vascular injury that may underlie the marked female disadvantage; CAD presents at a younger age, unexpectedly and against few conventional risk factors. In type 2 diabetes, insulin resistance and visceral adiposity dominate; CAD presents in older women with multivessel disease and silent ischemia, and the female disadvantage operates chiefly through heart failure and post-myocardial infarction outcomes. These differences argue against a single diagnostic template and call for presentation-aware strategies. Across both diabetes types, women are underdiagnosed, undertreated, and underrepresented in CVOTs; cardioprotective GLP1-RAs and SGLT2 inhibitors are effective in type 2 diabetes, whereas dedicated CVOTs lack in type 1 diabetes. Both type 1 and type 2 diabetes attenuate the cardioprotection historically observed in women. This excess risk is largely preventable—through proportional enrollment of women in trials, refinement of diagnostic tools tailored to the female coronary phenotype, and equitable delivery of guideline-directed therapy. Women with type 2 diabetes need current guidelines applied; those with type 1 diabetes need new evidence. What is currently known about this topic? •Diabetes substantially elevates the risk of coronary artery disease (CAD) in men and women. •Premenopausal women are physiologically protected against CAD. •Most studies suggest that diabetes blunts the innate cardioprotective advantage observed in women. What is the key research question? •How do type 1 and type 2 diabetes distinctly alter CAD risk, mechanisms, and outcomes in women? What is new? •Most studies report loss of female cardioprotection in both diabetes types, though findings vary. •Women are underrepresented in type 2 diabetes trials, and data are lacking in type 1 diabetes. •Cardioprotective drugs work in women with type 2 diabetes but therapeutic targets are less often met. How might this study influence clinical practice? •In women, type 1 diabetes needs new evidence, and type 2 diabetes needs current guidelines applied.
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Mohammedi et al. (2026) studied this question.
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