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LDL subfractions in patients with myocardial infarction: effect of smoking and beta-blocker treatment

T G Theodoraki1, D C Tsoukatos, S A Karabina

  • 1Biochemistry Laboratory, Evangelismos Hospital, Athens, Greece.

Annals of Clinical Biochemistry
|May 19, 2000
PubMed

Insights

Patients surviving myocardial infarction have more small, dense low-density lipoprotein (LDL). Smoking and beta-blockers worsen this atherogenic LDL subfraction profile, increasing risk.

Area of Science:

  • Cardiology
  • Lipidology
  • Biochemistry

Background:

  • Myocardial infarction (MI) survivors often exhibit altered lipid profiles.
  • Low-density lipoprotein (LDL) heterogeneity is implicated in cardiovascular disease.
  • The influence of lifestyle factors and medications on LDL subfractions requires further elucidation.

Purpose of the Study:

  • To quantify LDL heterogeneity in myocardial infarction survivors.
  • To assess the impact of smoking and beta-blocker therapy on LDL subfractions.
  • To determine the association between dense LDL and MI risk.

Main Methods:

  • Case-control study design.
  • Density gradient ultracentrifugation for LDL subfraction analysis.
  • Logistic regression to calculate odds ratios for high LDL3.

Main Results:

  • MI survivors showed a predominance of small, dense LDL compared to controls.
  • Beta-blocker treatment and smoking were associated with a more atherogenic LDL profile.
  • High LDL3 proportion correlated with triglyceride levels and BMI in beta-blocker patients.
  • Dense LDL was prevalent in patients regardless of smoking or beta-blocker status.
  • High LDL3 indicated a 7.5-fold increased risk of MI, unaffected by other factors.

Conclusions:

  • Small, dense LDL particles are abundant in patients post-myocardial infarction.
  • Smoking and beta-blocker treatment exacerbate atherogenic LDL profiles.
  • Dense LDL, specifically LDL3, is a significant risk factor for myocardial infarction.

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