Accelerated biological aging is characterized by an expedited deterioration of physiological systems. Phenotypic age (PA) derived from chronological age and 9 clinical biomarkers serves as a robust measure of this process, and phenotypic aging acceleration (PAA) was the discrepancy between phenotypic and chronological age. However, its association with major adverse cardiovascular events (MACEs) in stable coronary artery disease (SCAD) remains unclear.

This cohort study enrolled 8672 patients with SCAD who underwent initial percutaneous coronary intervention (PCI). Accelerated biological aging was assessed using phenotypic aging calculations, and MACEs were defined as death (all-cause and cardiac mortality), non-fatal myocardial infarction (MI), non-fatal stroke, and unplanned revascularization. A cox proportional hazard model was employed for analysis.

Overall, the subjects were 64.7 ± 6.5 years old while the PA were 62.7 ± 12.3 years and the PAA was −2.8 (−6.4, 1.5) years. During overall 2.2 (1.4, 3.1) follow up years, 1147 MACEs were documented (165 all-cause mortality, 47 cardiac mortality, 918 unplanned revascularization, 43 non-fatal MI and 80 non-fatal strokes). Compared with phenotypically younger group (PAA < 0), phenotypically older group (PAA ≥ 0) showed higher risk for MACEs and components (all P values < 0.05). A positive dose-response association was identified between PAA and MACEs. For each 1-year PAA, there were 2.80%, 8.80%, 10.80%, 1.20%, 5.80%, 4.50% higher risk of MACEs, all-cause mortality, cardiac mortality, unplanned revascularization, non-fatal MI and non-fatal stroke, respectively (all P values < 0.05). Robust results were demonstrated in subgroup analysis.

In SCAD patients undergoing PCI, accelerated biological aging is associated with an increased risk of MACEs, particularly death (all-cause and cardiac mortality) and unplanned revascularization.