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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
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Coronary endothelial dysfunction and hyperlipidemia are independently associated with diastolic dysfunction in humans

Ahmad A Elesber1, Margaret M Redfield, Charanjit S Rihal

  • 1Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN 55905, USA.

American Heart Journal
|June 2, 2007
PubMed

Insights

Coronary endothelial dysfunction and hyperlipidemia are linked to impaired heart relaxation in patients without heart failure or blocked arteries. This suggests a new pathway for developing these dysfunctions.

Area of Science:

  • Cardiology
  • Vascular Biology
  • Heart Failure Research

Background:

  • Coronary endothelial dysfunction (CED) and diastolic heart failure (DHF) are linked to myocardial ischemia and coronary artery disease (CAD) risk factors.
  • The study investigates the association between CED, CAD risk factors, and diastolic dysfunction prior to occlusive CAD or clinical heart failure.

Purpose of the Study:

  • To determine if CED and CAD risk factors are associated with diastolic dysfunction.
  • To explore potential mechanisms for endothelial and diastolic dysfunction in humans.

Main Methods:

  • Analysis of 160 patients with normal ejection fraction and nonocclusive CAD undergoing coronary endothelial function studies.
  • Assessment of left ventricular relaxation using tissue Doppler (Ea).
  • Multiple linear regression to evaluate the influence of coronary risk factors on diastolic function, adjusting for CED.

Main Results:

  • %deltaCBF was associated with higher Ea (P = .018).
  • Older age (P < .001), female sex (P = .028), higher left ventricular mass index (P = .016), and higher non-HDL cholesterol (P = .022) were associated with lower Ea.
  • CED and hyperlipidemia were independently associated with impaired relaxation.

Conclusions:

  • Coronary endothelial dysfunction and hyperlipidemia are independently linked to impaired diastolic relaxation.
  • These findings suggest a novel mechanism contributing to endothelial and diastolic dysfunction in the absence of advanced CAD or heart failure.
Abstract

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