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Impact of electronegative low-density lipoprotein on angiographic coronary atherosclerotic burden

Giampaolo Niccoli1, Marco Bacà, Marco De Spirito

  • 1Istituto di Cardiologia, Facoltà di Medicina e Chirurgia, Università Cattolica del Sacro Cuore, Rome, Italy. gniccoli73@hotmail.it

Atherosclerosis
|May 30, 2012
PubMed

Insights

Electronegative low-density lipoproteins (LDL(-)) are linked to more severe coronary artery disease (CAD). Higher LDL(-) levels correlate with greater CAD extent and multi-vessel disease, suggesting a proatherogenic role.

Area of Science:

  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Low-density lipoproteins (LDL) are key in cholesterol transport.
  • Electronegative LDL (LDL(-)) is implicated in endothelial dysfunction.
  • The association between LDL(-) and coronary artery disease (CAD) severity requires further investigation.

Purpose of the Study:

  • To assess the relationship between serum LDL(-) levels and the severity and extent of angiographically defined CAD.
  • To compare LDL(-) levels in patients with stable angina (SA), non-ST-elevation acute coronary syndrome (NSTE-ACS), and normal coronary arteries (NCA).

Main Methods:

  • Prospective enrollment of 47 patients with angiographic CAD (SA, NSTE-ACS) or normal coronary arteries (NCA).
  • Measurement of baseline serum LDL(-) levels.
  • Assessment of CAD extent using the Bogaty extent index and severity by evaluating multi-vessel disease.

Main Results:

  • LDL(-) levels were significantly higher in SA (21%) and NSTE-ACS (22%) patients compared to NCA (6%) patients.
  • Patients with multi-vessel disease exhibited higher LDL(-) levels than those with single-vessel disease (p = 0.002).
  • LDL(-) levels significantly correlated with CAD extent (r = 0.38, p = 0.03), unlike total LDL levels.

Conclusions:

  • Serum LDL(-) levels are associated with the angiographic severity and extent of CAD.
  • These findings suggest a potential proatherogenic role for LDL(-).
  • Further large-scale studies are warranted to confirm these results and elucidate the role of LDL(-) in atherosclerosis.
Abstract

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