International journal of clinical and experimental medicine · 2014
Epicardial adipose tissue thickness is increased in patients with cardiac syndrome X.
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Gedikli Omer, Ozturk Mustafa, Turan Oguzhan Ekrem, Ilter Abdusselam, Hosoglu Yusuf, Kiris Gulhanim
Аннотация
BACKGROUND: Cardiac syndrome X (CSX) is defined as normal coronary arteries with angina pectoris and a positive stress test. Epicardial adipose tissue (EAT) plays an important role in inflammatory process in cardiovascular system, therefore EAT may affect the pathogenesis of different cardiovascular disease. The aim of this study was to investigate the EAT thickness in patients with CSX and compare normal subjects.
METHODS: We prospectively enrolled 30 consecutive patients with CSX. The control group consisted of 30 age and sex-matched individuals with anginal chest pain and a negative treadmill or myocardial perfusion scan test. EAT thickness was measured by transthoracic echocardiography.
RESULTS: There were no differences in baseline clinical, biochemical and echocardiographic characteristics between CSX patients and the control group. Patients with CSX had significantly increased EAT thickness than those of the controls (3.43 ± 0.88 vs. 2.34 ± 0.89 mm, p=0.0001).
CONCLUSION: We found that EAT thickness is increased in patients with CSX. This finding suggests that EAT may contribute to the etiopathogenesis of the CSX.
METHODS: We prospectively enrolled 30 consecutive patients with CSX. The control group consisted of 30 age and sex-matched individuals with anginal chest pain and a negative treadmill or myocardial perfusion scan test. EAT thickness was measured by transthoracic echocardiography.
RESULTS: There were no differences in baseline clinical, biochemical and echocardiographic characteristics between CSX patients and the control group. Patients with CSX had significantly increased EAT thickness than those of the controls (3.43 ± 0.88 vs. 2.34 ± 0.89 mm, p=0.0001).
CONCLUSION: We found that EAT thickness is increased in patients with CSX. This finding suggests that EAT may contribute to the etiopathogenesis of the CSX.