What question did this study set out to answer?

This study aims to evaluate the combined effect of small dense low-density lipoprotein cholesterol and Lp(a) on coronary artery disease risk.

February 8, 2026

Small dense low-density lipoprotein cholesterol potentiates the risk of Lp(a) for long-term secondary prevention in patients with stable coronary artery disease

Puntos clave

This study aims to evaluate the combined effect of small dense low-density lipoprotein cholesterol and Lp(a) on coronary artery disease risk.
Measured sdLDL-C and Lp(a) in 974 patients with stable coronary artery disease.
Monitored CAD events over 12 years, including sudden cardiac death and acute coronary syndrome.
Utilized multivariable hazards model to assess the relationship between biomarkers and CAD events.
First CAD events occurred in 279 patients over the study period.
Patients with sdLDL-C ≥32.1 mg/dL and Lp(a) ≥30 mg/dL had a significantly increased risk for CAD events (HR 2.402).
Risk prediction was greater than that provided by LDL-C, non-HDL-C, and apolipoprotein B, highlighting the importance of sdLDL-C and Lp(a) combination.

Resumen

Abstract Background Both Lp(a) and small dense low-density lipoprotein cholesterol (sdLDL-C) are individually associated with increased coronary artery disease (CAD) risk but have not been studied in combination. Purpose This study was aimed to investigate how sdLDL-C was jointly associated with the risk of Lp(a) for long-term coronary artery disease (CAD) compared with LDL-C, non-HDL-C and apolipoprotein B in patients with stable CAD. Methods sdLDL-C measured using homogenous assay and Lp(a) measured using latex agglutination immunoassay were evaluated in 744 male and 230 female patients with stable CAD who did not need urgent coronary revascularization between 2003 and 2010. CAD events defined as sudden cardiac death, onset of acute coronary syndrome, and/or need for coronary revascularization were monitored for 12 years. Cut-points of sdLDL-C and apolipoprotein B were determined by receiver operating characteristic curves. Multivariable hazards model was used to examine the relationship between Lp(a) and sdLDL-C, LDL-C, non-HDL-C or apolipoprotein B for incident risk of CAD. Results First CAD events were observed in 215 male and 64 female patients. The Kaplan–Meier event-free survival curves showed that patients with sdLDL-C ≥32.1 mg/dL and Lp(a) ≥30mg/dL had an increased risk for CAD events. The multivariable-adjusted hazard ratio (HR) was 2.402, 95% confidence interval (CI) 1.538-3.753. The HR was greater than those of LDL-C, non-HDL-C and apolipoprotein B (1.522, 1.729 and 1.915, respectively). These results remained significant in 588 patients treated with statins (HR 3.603, 95%CI 2.042-6.358). Conclusions: Combination of high sdLDL-C and high Lp(a) synergistical predicted long-term recurrence of CAD in stable CAD patients independently of LDL-C, non-HDL-C and apolipoprotein B. Concurrent measurement of sdLDL-C and Lp(a) are useful to detect high risk CAD patients.

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