Impact of evolocumab on plaque phenotypic changes in patients with acute coronary syndrome and elevated lipoprotein(a) levels: a HUYGENS secondary analysis
Authors' conclusion
The ability of evolocumab to more effectively promote plaque stabilization, compared with statin monotherapy, appears more pronounced in patients with higher Lp(a) levels, suggesting that Lp(a) may help identify those who benefit most from intensive lipid-lowering therapy.
Study context
- Population
- Patients after ACS undergoing serial optical coherence tomography, by baseline Lp(a) <125 vs ≥125 nmol/LLp(a) <125: 71
- Comparison
- Evolocumab vs placebo by baseline Lp level
Methodological detailspost hoc analysis
- Post hoc analysis
Primary result
As reported in the abstract
High Lp(a): change in minimum fibrous cap thickness (FCT), Evolocumab vs Placebo (P < 0.001)
+51.6 ± 40.9 vs. +12.4 ± 23.9 μm
High Lp(a): change in lipid arc, Evolocumab vs Placebo (P = 0.008)
−60.9 ± 56.5° vs. −9.1 ± 70.8°
Low Lp(a): change in minimum FCT, Evolocumab vs Placebo (P = 0.21)
+45.9 ± 37.8 vs. +34.7 ± 36.0 μm
Low Lp(a): change in lipid arc, Evolocumab vs Placebo (P = 0.18)
−59.9 ± 50.1° vs. −44.5 ± 46.1°
Further findings
LDL-C, by Lp(a) subgroup
- High Lp(a): Evolocumab vs Placebo (P < 0.001)
- 21.7 ± 10.3 vs. 94.5 ± 22.9 mg/dL
- Low Lp(a): Evolocumab vs Placebo (P < 0.001)
- 23.3 ± 34.9 vs. 82.9 ± 46.5 mg/dL
Lp(a), by Lp(a) subgroup
- High Lp(a): Evolocumab vs Placebo (P = 0.007)
- 156.0 (136.0, 187.0) vs. 204.0 (170.5, 290.5) nmol/L
- Low Lp(a): Evolocumab vs Placebo (P = 0.01)
- 11.5 (5.8, 23.8) vs. 25.0 (13.5, 41.0) nmol/L
Original publication
Summarised from the published abstract; every number is checked against it