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Characteristics of Coronary Atherosclerosis Related to Plaque Burden Regression During Treatment With Alirocumab: The
Leopoldo Pérez de Isla1, Jose L Díaz-Díaz2, Manuel J Romero3
1Cardiology Department, Clinico San Carlos University Hospital, Madrid, Spain (L.P.d.I.).
Insights
Intensive lipid-lowering therapy with alirocumab can reduce coronary plaque burden in familial hypercholesterolemia patients. Higher baseline plaque burden and unstable plaque content predict greater regression, suggesting targeted treatment approaches.
Area of Science:
- Cardiology
- Pharmacology
- Medical Imaging
Background:
- Intensive lipid-lowering therapy shows potential for coronary atherosclerosis regression.
- Factors influencing lipid-lowering therapy's effect on disease regression are not well understood.
- This study investigates plaque characteristics associated with greater plaque burden reduction.
Purpose of the Study:
- To determine which atherosclerotic plaque characteristics correlate with increased plaque burden (PB) reduction.
- To evaluate the efficacy of alirocumab in patients with familial hypercholesterolemia (FH).
- To assess the impact of alirocumab on coronary plaque composition and volume.
Main Methods:
- The ARCHITECT study was a 78-week, open-label, single-arm clinical trial.
- 104 patients with FH received alirocumab plus high-intensity statins.
- Coronary computed tomographic angiography was used at baseline and follow-up to assess plaque burden and characteristics.
Main Results:
- Coronary plaque burden decreased significantly by -4.6% (P<0.001).
- Unstable core plaque percentage decreased significantly by -6.6% (P<0.001).
- Greater baseline plaque burden (β=0.36, P=0.002) and higher unstable core plaque proportion (β=0.15, P<0.001) were linked to greater plaque regression.
Conclusions:
- Alirocumab combined with high-intensity statins may enhance plaque regression in FH patients.
- Patients with higher baseline plaque burden and larger unstable core components showed greater regression.
- Further research is required to confirm these findings and their clinical implications.
Background:
Intensive lipid-lowering therapy may induce coronary atherosclerosis regression. Nevertheless, the factors underlying the effect of lipid-lowering therapy on disease regression remain poorly characterized. Our aim was to determine which characteristics of atherosclerotic plaque are associated with a greater reduction in coronary plaque burden (PB) after treatment with alirocumab in patients with familial hypercholesterolemia.
Methods:
The ARCHITECT study (Effect of Alirocumab on Atherosclerotic Plaque Volume, Architecture and Composition) is a phase IV, open-label, multicenter, single-arm clinical trial to assess the effect of the treatment with alirocumab for 78 weeks on the coronary atherosclerotic PB and its characteristics in subjects with familial hypercholesterolemia without clinical atherosclerotic cardiovascular disease. Participants underwent a coronary computed tomographic angiography at baseline and a final one at 78 weeks. Every patient received alirocumab 150 mg subcutaneously every 14 days in addition to high-intensity statin therapy.
Results:
One hundred and four patients were enrolled. Median age was 53.3 (46.2-59.4) years and 54 were women (51.9%). The global coronary PB changed from 34.6% (32.5%-36.8%) at entry to 30.4% (27.4%-33.4%) at follow-up, which is -4.6% (-7.7% to -1.9%; P<0.001) reduction. A decrease in the percentage of unstable core (fibro-fatty+necrotic plaque; from 14.1 [7.9-22.3] to 8.0 [6.4-10.6]; -6.6%; P<0.001) was found. A greater PB (β, 0.36 [0.13-0.59]; P=0.002) and a higher proportion of unstable core (β, 0.15 [0.08-0.22]; P<0.001) were significantly related to PB regression.
Conclusions:
Treatment with alirocumab in addition to high-intensity statin therapy might produce a greater PB regression in patients with familial hypercholesterolemia with higher baseline PB and in those with larger unstable core. Further studies are needed to corroborate the hypothesis raised by these results.
Registration:
URL: https://www.clinicaltrials.gov; Unique identifier: NCT05465278.
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