ArticleJournal of clinical hypertension (Greenwich, Conn.)2026
Insulin Resistance is Associated With Skin Microvascular Dysfunction and Reduced Circulating Endothelial Progenitor Cells in Hypertensive Patients.
Article in Journal of clinical hypertension (Greenwich, Conn.), 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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6 authors.
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Abstract
Microvascular dysfunction is an early manifestation of vascular damage in patients with hypertension and cardiometabolic disorders. Insulin resistance (IR) is linked closely to vascular dysfunction, and the triglyceride-glucose (TyG) index is a practical proxy marker of IR. Circulating endothelial progenitor cells (cEPCs) and microvascular reactivity have been proposed as markers of vascular health, but their relationships to IR and high-density lipoprotein functionality, assessed using the cholesterol efflux capacity (CEC), remain incompletely understood. We performed a cross-sectional study of coronary angiography registry data from 259 hypertensive patients with fasting glucose levels ≤ 125 mg/dL. cEPC [cluster of differentiation (CD) 34+/kinase insert domain receptor+/CD133+] levels, microvascular function [reflected by post-occlusive reactive hyperemia (PORH)], the CEC, and the TyG index were measured before catheterization. Weighted multivariable linear regression analyses were performed to examine variable associations. Higher TyG index values were associated independently with lower cEPC levels and impaired microvascular reactivity after adjustment for conventional cardiovascular risk factors. Each 1 standard deviation increase in the TyG index was associated with an 11% decrease in cEPCs and a 6.3% reduction in PORH. The TyG index was not associated with the CEC. These findings were consistent across diabetes and coronary artery disease subgroups. The association of the IR, as reflected by the TyG index, with reduced cEPC levels and impaired microvascular function in this high-risk hypertensive population supports a link between metabolic dysfunction and microvascular impairment; however, causal relationships could not be inferred.
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