ReviewEuropean heart journal open2026
The role of inflammation on coronary microvascular dysfunction and potential therapeutic targets.
Review in European heart journal open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
6 authors.
Funding
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Abstract
Coronary microvascular dysfunction (CMD) is a major underlying cause of myocardial ischaemia and is associated with adverse cardiovascular outcomes. It occurs both in the presence of obstructive coronary artery disease (CAD) and in patients with non-obstructive CAD. Emerging evidence highlights chronic inflammation as a key factor in CMD pathogenesis. This review conceptualizes inflammation as a driver, amplifier, or consequence of CMD, depending on the underlying clinical phenotype. Pro-inflammatory pathways impair endothelial function and enhance immune cell infiltration within the coronary microcirculation, leading to myocardial ischaemia. Moreover, several chronic inflammatory conditions such as diabetes mellitus, obesity, and autoimmune diseases are linked with CMD. These conditions promote elevated circulating levels of pro-inflammatory cytokines, including high-sensitivity C-reactive protein, interleukins, tumour necrosis factor-α, and markers of monocyte activation. Inflammatory mechanisms of tissue damage-including adipose tissue inflammation, endothelial glycocalyx degradation, pericyte dysfunction, microvascular-specific immune cell infiltration, inflammasome signalling, microRNA dysregulation, and shear stress-induced inflammation-have been implicated in CMD. Recent advances in molecular and imaging biomarkers provide new opportunities for detecting and characterizing inflammation-driven CMD, although inflammation-specific diagnostic tools remain limited. While several therapies with anti-inflammatory or pleiotropic effects, including statins and sodium-glucose cotransporter-2 inhibitors, have demonstrated cardiovascular benefit, robust trials specifically evaluating coronary microvascular endpoints are scarce. This narrative review focuses on the chronic inflammatory mechanisms contributing to CMD, the available diagnostic techniques, and potential therapeutic strategies aimed at modulating inflammation to improve coronary microvascular function and cardiovascular outcomes.
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