Reviews in cardiovascular medicine · 2026
The Extent and Phenotype of Coronary Artery Disease in Diabetes and Prediabetes: Insights From Imaging Studies and Potential Therapeutic Implications.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gurgoglione Filippo Luca, Navacchi Rebecca, Ristagno Alessia, Benatti Giorgio, Solinas Emilia, Tadonio Iacopo, Denegri Andrea, Donelli Davide, Magnani Giulia, Torlai Triglia Laura, Bianconcini Michele, Barocelli Federico, Covani Marco, De Gregorio Mattia, Dei Cas Alessandra, Bonadonna Riccardo C, Vignali Luigi, Niccoli Giampaolo
Аннотация
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder that is associated with a markedly increased risk of coronary artery disease (CAD) and cardiovascular (CV) mortality compared with the general population. Prediabetes, a heterogeneous intermediate glycemic state defined by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT), and/or glycated hemoglobin (HbA1c) levels between 5.7% and 6.4%, is likewise associated with a significantly higher CV risk than normoglycemia. Over the past decade, both overall CAD burden and specific plaque morphologic features have been established as robust predictors of future adverse CV events using invasive and non-invasive coronary imaging modalities. More recently, growing evidence has highlighted the influence of glycemic abnormalities on the extent, progression, and phenotype of CAD, underscoring the interplay between metabolic dysfunction and atherosclerotic vulnerability. Therefore, this review aims to (i) elucidate the pathophysiological mechanisms linking T2DM and prediabetes with atherogenesis, (ii) summarize findings from coronary imaging studies in these populations, and (iii) evaluate therapeutic strategies designed to promote plaque stabilization and regression.