Study Background and Disease Burden
Advanced glycation end-products (AGEs) are proteins or lipids that become nonenzymatically glycated and oxidized after exposure to sugars and oxidative stress. This chemical modification is significantly increased under hyperglycemic conditions and with aging, processes common in the elderly population. AGEs, particularly Nε-carboxymethyl-lysine (CML), accumulate in tissues including the heart and vasculature, and contribute to alterations in structural and functional integrity. These changes potentially foster the pathogenesis of cardiovascular diseases such as heart failure (HF) and atrial fibrillation (AF), conditions that impose substantial morbidity and mortality burdens in older adults. Despite established mechanistic links, prospective epidemiological data on circulating AGEs and incident HF or AF risk in aging populations have been lacking, representing a critical knowledge gap in cardiovascular geriatric care and preventive cardiology.
