Key result
Familial hypercholesterolemia is linked to ~70% higher non-culprit plaque macrophage prevalence in ACS.
Why the study?
Patients with familial hypercholesterolemia experience ACS at a younger age and have a higher risk of recurrent coronary events, but the morphological characteristics of their coronary plaques including macrophage status were unclear.
Does familial hypercholesterolemia alter coronary plaque morphology and increase macrophage activity in patients with acute coronary syndrome?
Observational (n=259)
Does familial hypercholesterolemia alter coronary plaque morphology and increase macrophage activity in patients with acute coronary syndrome?
ACS patients with familial hypercholesterolemia have increased macrophage activity and more layered plaques in non-culprit segments, which may partly explain their higher risk of recurrent coronary events.
Should not change FH-ACS management; leaves open whether macrophage-targeted therapies reduce recurrent events.
Patients with familial hypercholesterolemia (FH) experience acute coronary syndrome (ACS) at a younger age and have a higher risk of recurrent coronary events. The study aimed to elucidate the morphological characteristics of coronary plaques including the status of macrophages in patients with FH. This study included 259 patients with ACS who underwent optical coherence tomography (OCT) imaging of culprit plaques requiring percutaneous coronary intervention. The characteristics of culprit plaques and non-culprit plaques in the same coronary artery were compared between patients with and without FH. A total of 23 patients (8.9%) were clinically diagnosed with FH. In culprit plaques, the prevalence of both plaque with macrophages (69.6% vs. 49.6%, p =0.081) and plaque with greater macrophage activity (macrophage grade ≥2) (65.0% vs. 43.9%, p =0.099) was numerically higher in patients with FH than in those without FH. In non-culprit plaques, the prevalence of both plaque with macrophages (71.4% vs. 42.0%, p =0.046) and plaque with greater macrophage activity (42.9% vs. 16.0%, p =0.021) was significantly higher in patients with FH than in those without FH. The higher prevalence of layered plaques (78.6% vs. 37.8%, p =0.008) in patients with FH than in those without FH was observed in non-culprit plaques. FH patients with ACS had more coronary plaques with macrophages, particularly in non-culprit segments, which may partly explain the increased risk of recurrent coronary events. • 8.9% of ACS patients were clinically diagnosed with FH. • ACS patients with FH had an increased macrophage activity and more layered plaques in non-culprit plaques. • The present results may partly elucidate the pathogenesis of recurrent coronary events in patients with FH.
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Iwaya et al. (2025) conducted an observational in Acute coronary syndrome (n=259). Familial hypercholesterolemia vs. Without familial hypercholesterolemia was evaluated on Prevalence of plaque with macrophages in non-culprit plaques (p=0.046). Among ACS patients, familial hypercholesterolemia was associated with a higher prevalence of macrophages in non-culprit coronary plaques compared to those without FH (71.4% vs. 42.0%, p=0.046).
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