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C-reactive protein levels and plaque regression with evolocumab: Insights from GLAGOV
Adam J Nelson1, Rishi Puri2, Danielle M Brennan2
1South Australian Health & Medical Research Institute, Adelaide, Australia.
Insights
High-sensitivity C-reactive protein (hsCRP) levels do not affect evolocumab
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- On-treatment high-sensitivity C-reactive protein (hsCRP) levels predict atherosclerotic cardiovascular disease (ASCVD) risk.
- Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors reduce plaque burden and ASCVD events.
- The impact of systemic inflammation on PCSK9 inhibitor efficacy is unknown.
Purpose of the Study:
- To evaluate if baseline hsCRP levels influence the plaque regression effects of evolocumab in statin-treated patients.
- To determine if residual inflammation affects PCSK9 inhibitor-induced plaque burden reduction.
Main Methods:
- The GLAGOV study compared evolocumab vs. placebo over 78 weeks in statin-treated patients with coronary artery disease.
- Coronary plaque burden and composition were assessed by intravascular ultrasound.
- Patients were stratified by baseline hsCRP levels (<1, 1-3, >3 mg/L).
Main Results:
- Evolocumab treatment led to similar plaque regression across all hsCRP strata.
- The proportion of patients achieving plaque regression was consistent regardless of baseline hsCRP levels.
- No differences in plaque composition were observed based on hsCRP levels.
Conclusions:
- Evolocumab effectively reduces coronary plaque burden, irrespective of baseline systemic inflammation.
- Intensive lipid lowering with PCSK9 inhibitors is beneficial even in patients with elevated inflammatory markers.
- Residual inflammation does not attenuate the plaque-modifying effects of evolocumab.
Objective:
On-treatment levels of high sensitivity C-reactive protein (hsCRP) in statin-treated patients predict plaque progression and the prospective risk of atherosclerotic cardiovascular events. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors produce additional LDL-C lowering, reduce plaque burden and improve cardiovascular outcomes in statin-treated patients. It is unknown whether residual systemic inflammation attenuates their favorable effects on plaque burden.
Methods:
GLAGOV compared the effects of treatment for 78 weeks with evolocumab or placebo on progression of coronary atherosclerosis in statin-treated patients with coronary artery disease.Clinical demographics, biochemistry and changes in both the burden (percentage atheroma volume (PAV), total atheroma volume (TAV), n = 413) and composition (n = 162) of coronary plaque were evaluated in evolocumab-treated patients according to baseline hsCRP strata (<1, 1-3, >3 mg/L).
Results:
The study cohort comprised 413 evolocumab-treated patients (32% low [<1 mg/L], 41% intermediate [1-3 mg/L] and 27% high [>3 mg/L] baseline hsCRP levels). Patients in the highest hsCRP stratum were more likely to be female and had a higher prevalence of diabetes, hypertension, and the metabolic syndrome. LDL-C levels were similar across the groups, however participants with higher hsCRP levels had higher triglyceride and lower HDL-C levels at baseline. At follow-up, the change in PAV from baseline (-0.87% [low] vs. -0.84% [intermediate] vs. -1.22% [high], p = 0.46) and the proportion of patients experiencing any degree of regression (65.9% vs. 63.5% vs. 63.1%, p = 0.88) was similar across hsCRP strata and when evaluated by levels of achieved LDL-C. There were no serial differences in plaque composition by hsCRP strata.
Conclusion:
The ability of evolocumab to induce regression in statin-treated patients is not attenuated by the presence of enhanced systemic inflammation. This underscores the potential benefits of intensive lipid lowering, even in the presence of heightened inflammatory states.
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