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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.
Background:
Although low high-density lipoprotein cholesterol (HDL-C) level has been reported as an independent risk factor for coronary artery disease, few studies addressed the direct relationship between the presence of thin-cap fibroatheroma (TCFA) that is considered as vulnerable plaque in pathology and HDL-C level. The aim of this study was to investigate whether lesion vulnerability is related to HDL-C level in patients with acute coronary syndrome (ACS).
Methods And Results:
A total of 261 patients with ACS who underwent optical coherence tomography prior to percutaneous coronary intervention, were enrolled. Patients were divided into a TCFA group (n=124) and a non-TCFA group (n=137). TCFA was defined as a lipid plaque (lipid content in ≥1 quadrant) covered with <70 μm-thickness fibrous caps. There were no differences in patient characteristics and clinical results between the 2 groups except for HDL-C level, low-density lipoprotein cholesterol (LDL-C) level, and high-sensitive C-reactive protein (hs-CRP) level. On multivariate regression analysis, low HDL-C level (β coefficient: 0.302, P<0.001), high LDL-C level (β coefficient: -0.172, P=0.008), hs-CRP level (β coefficient: -0.145, P=0.017), and current smoking (β coefficient: -0.124, P=0.028) were identified as independent contributors to fibrous cap thickness.
Conclusions:
HDL-C is correlated with fibrous cap thickness of the culprit lesion in patients with ACS. HDL-C may be considered as a therapeutic target for plaque stabilization.
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