Abstract 16236: Role of Epoxyeicosatrienoic Acids in Syndrome X in Women
Background: Syndrome X in women is thought to be caused by coronary microvascular dysfunction. We hypothesized that this dysfunction is associated with low circulating plasma levels of of the arachidonic acid metabolites, epoxyeicosatrienoic acids (EETs), which are potent endothelium-derived vasodilators of the coronary microcirculation.
Methods: Women with typical exertional angina, a positive stress test on imaging, but no obstructive coronary artery disease (CAD) on coronary angiography (study group, n=9), and age- and risk factor-matched chest pain-free women (control group, n=15) were enrolled. Myocardial contrast echocardiography (MCE) was performed at rest and during maximal hyperemia using 0.56 mg.kg−1 of dipyridamole. The rate of replenishment of microbubbles into the myocardium after their destruction (β) which represents myocardial blood flow velocity was quantified and βreserve determined using the equation βstress/βrest. Plasma concentrations of EETs' stable metabolite, Dihydroxyeicosatrienoic acid (DHETs), were quantified using Liquid Chromatography - Tandem Mass Spectrometry.
Results: By MCE analysis, women in study group had higher resting β compared to control group (1.4±0.9 versus 0.7±0.4, P<0.05) but lower β reserve (1.5±0.7 vs. 2.9±1.0, P <0.05). The study group also had significantly lower levels of 14,15-DHET compared to the control group (247±44 ng/ml versus 336.6±91 ng/ml, P=0.02, non-parametric rank sum test). Other substances such as lipids and sex hormones were not different between the 2 groups.
Conclusions: Although preliminary, these results are the first to describe an association between syndrome X and low circulating levels of EETs. We propose a novel mechanism that the low levels of the potent coronary vasodilators, EETs, in women with syndrome X cause a reduced vasodilatory capacity resulting in exercise-induced myocardial ischemia in the absence of CAD.
- © 2011 by American Heart Association, Inc.