Biological Age in Coronary Artery Disease: Advancing Therapeutic Evaluation and Precision Intervention

Coronary artery disease (CAD) is a typical age-related chronic condition, with its development and progression spanning a long course of life and exhibiting significant inter-individual heterogeneity. Traditional risk assessment models based on chronological age and single risk factors are often insufficient to capture the cumulative physiological decline and the dynamic progression of disease. In this review, biological age, as a comprehensive indicator reflecting an individual’s true aging status, has gradually emerged as an important tool for understanding differences in CAD risk and disease progression. In recent years, various methods for assessing biological age have been applied in CAD research, primarily including composite biological age derived from routine clinical indicators, telomere length, and epigenetic clocks. Evidence suggests that different biological age markers provide complementary information and are suited into distinct applications. Among them, composite clinical biological age, based on routine clinical measurements, can dynamically reflect multi-system functional changes and has demonstrated feasibility and stability in CAD risk stratification, disease progression monitoring, and evaluation of intervention effects, highlighting its potential clinical utility. Telomere length and epigenetic clocks, on the other hand, provide supplementary information at the cellular and molecular regulatory levels regarding cumulative physiological burden and aging mechanisms. Looking forward, integrating molecular-level aging markers with composite clinical biological age to establish a multi-tiered assessment framework may improve early identification and precision intervention for CAD and other chronic diseases.