Relation between epicardial fat thickness and coronary flow reserve in women with chest pain and angiographically normal coronary arteries☆
Introduction
Angina-like chest pain with angiographically normal coronary arteries affects women more frequently than man [1]. Additionally an important proportion of these individuals have microvascular dysfunction [2]. Microvascular angina has been described as chest pain with normal coronary arteriograms and reduced coronary blood flow reserve (CFR) with or without ST segment depression [3]. The impairment of CFR may result from vasomotor, metabolic or structural abnormalities in the coronary microcirculation or inflammation of the microvasculature and may precede coronary atherosclerosis.
Various studies have highlighted the potential importance of adipose tissue in relation to inflammatory burden in cardiovascular diseases. Epicardial fat thickness (EFT) is clinically related to abdominal visceral adiposity [4], coronary artery disease [5], subclinical atherosclerosis [6], and metabolic syndrome [7] and seems to have high capacity of local proinflammatory activity [8]. Echocardiographic assessment of EFT is easily reproducible and showed an excellent reliability with the magnetic resonance imaging (MRI) measurements of EFT [7]. There is growing evidence that the changes in or perivascular tissues surrounding epicardial coronary arteries could alter vascular homeostasis and contribute to endothelial dysfunction, amplification of vascular inflammation, intimal lesions, plaque progression by an outside-to-inside signaling mechanism [9], [10]. Accordingly we assessed whether EFT is associated with impaired CFR in women with chest pain and angiographically normal coronary arteries.
Section snippets
Study population
Women who underwent coronary angiography and had no obstructive coronary artery disease were consecutively enrolled into our study. After exclusion of patients with diabetes mellitus (fasting plasma glucose level on three separate days >126 mg/dL), peripheral vascular disease, uncontrolled hypertension (≥140/90 mmHg), low density lipoprotein (LDL) level >160 mg/dL, high density lipoprotein (HDL) level <30 mg/dL, triglyceride level >400 mg/dL, moderate to severe valvular lesions, left ventricular
Clinical and laboratory characteristics of the study population
Echocardiographic coronary flow data could be obtained in 65 (96%) of 68 patients. Twenty-six women (40%) had reduced CFR suggestive of microvascular dysfunction (mean, 1.7 ± 0.24). Thirty-nine (60%) had normal CFR consistent with functionally intact coronary microvasculature (mean, 2.6 ± 0.48). Clinical and laboratory characteristics of women with and those without coronary microvascular dysfunction are presented in Table 1. Among these, menopause and hypertension were significantly more prevalent
Discussion
Coronary flow reserve is the magnitude of the increase in blood flow at maximal coronary vasodilatation. Since flow resistance is primarily determined by the microvasculature, CFR is a measurement of the ability of the microvasculature [13]. In patients with coronary artery disease, the extent of the reduction in CFR is directly related to the severity of stenosis, whereas in patients with angiographically normal coronary arteries it is a marker of microvascular dysfunction [14]. Other factors
Study limitations
EFT can be assessed on computerized tomography and MRI more though roughly than on echocardiography, however widespread use of these methods is not practical for a screening parameter, and echocardiography has been validated against MRI for quantitative assessment of EFT [8]. Also we did not assess invasively CFR. However transthoracic Doppler echocardiography with pharmacological stress has become very popular for the assessment of CFR and has been demonstrated to be a useful and highly
Conflict of interest
Authors have no conflict of interest.
Acknowledgement
All the financial support and equipment for this study were provided by the University of Baskent.
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This study was presented at the European Society of Atherosclerosis Congress 2008.