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Low density lipoprotein cholesterol and coronary microvascular dysfunction in hypercholesterolemia

P A Kaufmann1, T Gnecchi-Ruscone, K P Schäfers

  • 1MRC Clinical Sciences Centre, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom.

Insights

In asymptomatic individuals, elevated low-density lipoprotein (LDL) cholesterol, not total cholesterol (TC), is linked to reduced coronary flow reserve (CFR). This suggests LDL-induced coronary microvascular dysfunction contributes to heart disease development.

Area of Science:

  • Cardiology
  • Vascular Biology
  • Medical Imaging

Background:

  • Endothelial dysfunction in coronary microcirculation is observed in asymptomatic hypercholesterolemia.
  • Hypercholesterolemia is a risk factor for coronary artery disease.

Purpose of the Study:

  • To investigate the relationship between total cholesterol (TC) and its subfractions with coronary flow reserve (CFR) in asymptomatic individuals.
  • To determine if lipid profiles impact integrated coronary circulation function.

Main Methods:

  • Positron emission tomography (PET) with oxygen-15-labeled water was used to measure myocardial blood flow (MBF) at rest and during adenosine stress.
  • 80 asymptomatic, nonsmoking men were divided into normal TC (Group 1) and elevated TC (Group 2) groups.
  • Coronary flow reserve (CFR) was calculated as the ratio of stress MBF to rest MBF.

Main Results:

  • Elevated TC and LDL cholesterol were observed in Group 2 compared to Group 1 (p < 0.0005).
  • No significant differences in rest MBF, stress MBF, or CFR were found between the groups.
  • A significant inverse correlation was found between LDL cholesterol and CFR in the hypercholesterolemic group (Group 2, r = -0.61, p < 0.05).

Conclusions:

  • Low-density lipoprotein (LDL) cholesterol, but not total cholesterol (TC), is inversely correlated with coronary flow reserve (CFR) in hypercholesterolemic subjects.
  • LDL-induced coronary microvascular dysfunction may play a significant role in the pathogenesis of coronary artery disease.
Abstract

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