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Updated: Jul 14, 2026
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Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research
Published on: October 22, 2014
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
Summary
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.
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