Complicaciones vasculares en prediabetes 2

Prediabetes (defined as impaired fasting glucose [IFG] between 100 and 125 mg/dL, impaired glucose tolerance [IGT] between 140 and 199 mg/dL, or HbA1c between 5.7% and 6.4%) is a pathological state capable of causing early macrovascular and microvascular damage, rather than merely a transitional phase leading to type 2 diabetes1,2. Its rising global prevalence represents a significant cardiometabolic burden4,5. Insulin resistance and chronic hyperglycemia trigger oxidative stress via reactive oxygen species, low-grade systemic inflammation (elevated TNF-α and IL-6), and the accumulation of advanced glycation end-products (AGEs)1,3. These processes cause endothelial dysfunction, downregulation of the PI3K/Akt pathway, and reduced nitric oxide bioavailability, manifesting as impaired flow-mediated dilation (FMD)1,3. At the microvascular level, hyperglycemia promotes capillary basement membrane thickening and alters vascular reactivity, leading to subclinical retinal neurodegeneration and microalbuminuria1,2. At the macrovascular level, it accelerates atherogenesis and arterial stiffness, increasing carotid intima-media thickness (CIMT) and pulse wave velocity (PWV)1,3. Meta-analyses and prospective studies demonstrate that prediabetes independently increases the risk of cardiovascular disease, myocardial infarction, stroke, and all-cause mortality2-5. IFG and IGT—particularly when combined—are independent predictors of adverse events1,3,5. In light of the foregoing, a preventive, intensive, and multifactorial approach—focused on lifestyle changes and, if necessary, the use of medication—is warranted to achieve comprehensive metabolic control that prevents the onset of chronic complications1,4.