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High-density lipoprotein cholesterol level is associated with fibrous cap thickness in acute coronary syndrome

Yuichi Ozaki1, Atsushi Tanaka, Kenichi Komukai

  • 1Department of Cardiovascular Medicine, Wakayama Medical University.

Insights

Low high-density lipoprotein cholesterol (HDL-C) is linked to thinner fibrous caps on vulnerable plaques in acute coronary syndrome (ACS) patients. This suggests HDL-C may be a target for stabilizing coronary artery disease plaques.

Area of Science:

  • Cardiology
  • Vascular Biology
  • Biochemistry

Background:

  • Low high-density lipoprotein cholesterol (HDL-C) is an independent risk factor for coronary artery disease (CAD).
  • The direct relationship between HDL-C levels and thin-cap fibroatheroma (TCFA), a vulnerable plaque type, is not well-established.
  • This study investigates the association between HDL-C and lesion vulnerability in patients with acute coronary syndrome (ACS).

Purpose of the Study:

  • To determine if lesion vulnerability, specifically the presence of TCFA, is related to HDL-C levels in ACS patients.
  • To explore the correlation between HDL-C and fibrous cap thickness in culprit lesions of ACS patients.

Main Methods:

  • 261 ACS patients undergoing optical coherence tomography (OCT) before percutaneous coronary intervention (PCI) were enrolled.
  • Patients were categorized into TCFA (n=124) and non-TCFA (n=137) groups based on OCT findings.
  • TCFA was defined as lipid plaque with <70 μm fibrous cap thickness.

Main Results:

  • No significant differences in patient characteristics were observed between TCFA and non-TCFA groups, except for HDL-C, LDL-C, and hs-CRP levels.
  • Multivariate regression analysis identified low HDL-C (β=0.302, P<0.001) as an independent contributor to thinner fibrous cap thickness.
  • High LDL-C, elevated hs-CRP, and current smoking were also independently associated with reduced fibrous cap thickness.

Conclusions:

  • HDL-C levels are significantly correlated with the fibrous cap thickness of culprit lesions in ACS patients.
  • These findings suggest that HDL-C may play a role in plaque stabilization.
  • Targeting HDL-C could be a potential therapeutic strategy for managing vulnerable plaques in CAD.
Abstract

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