Paradoxical Long-Term Impact Between Serum Apolipoprotein E and High-Density Lipoprotein Cholesterol in Patients

Tatsuya Fukase1, Tomotaka Dohi1, Ryota Nishio1

  • 1Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine.

Insights

Serum Apolipoprotein E (ApoE) levels show a paradoxical impact on cardiovascular risk in coronary artery disease (CAD) patients, depending on high-density lipoprotein cholesterol (HDL-C) levels. This finding is crucial for understanding CAD progression and risk stratification.

Area of Science:

  • Cardiovascular Medicine
  • Lipid Metabolism
  • Atherosclerosis Research

Background:

  • Apolipoprotein E (ApoE) influences arteriosclerosis, with potential atheroprotective effects when combined with high-density lipoprotein cholesterol (HDL-C).
  • The interplay between serum ApoE and HDL-C levels in coronary artery disease (CAD) patients requires further elucidation.

Purpose of the Study:

  • To investigate the quantitative relationship between serum ApoE and HDL-C levels.
  • To evaluate the impact of this relationship on major adverse cardiac and cerebrovascular events (MACCE) in CAD patients.

Main Methods:

  • Inclusion of 3632 consecutive patients undergoing first intervention (2000-2016).
  • Categorization into normal and abnormal HDL-C groups, further subdivided by ApoE levels (high/low).
  • Evaluation of MACCE incidence (cardiovascular death, myocardial infarction, stroke, all-cause death) over a 6.4-year follow-up.

Main Results:

  • A statistically significant interaction between ApoE levels and HDL-C status was observed for MACCE and all-cause death.
  • In the normal HDL-C group, elevated ApoE correlated with higher MACCE incidence.
  • Conversely, in the abnormal HDL-C group, reduced ApoE correlated with higher MACCE incidence.

Conclusions:

  • Serum ApoE levels exhibit a paradoxical association with cardiovascular risk in CAD patients.
  • The impact of ApoE on future cardiovascular risk is contingent upon the patient's HDL-C status.
Abstract

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