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Epicardial adipose tissue (EAT) is a component of the visceral adiposity located between the heart and pericardium. It is associated with certain diseases, such as metabolic syndrome, coronary artery disease, and hypertension. Therefore, measurement of EAT thickness has recently gained importance. Examination by transthoracic echocardiography for measuring EAT thickness is preferable because of easy availability and low cost. The present review focuses on the method of measuring EAT thickness by transthoracic echocardiography as well as the issues of concern.

In acute coronary syndromes (ACS), oxidation and inflammation have very important roles and in-vitro studies have demonstrated that gamma-glutamyl transferase (GGT) participates in such oxidative and inflammatory reactions. We aimed to evaluate the prognostic value of baseline serum GGT activity on the development of major adverse cardiac event (MACE) in the follow-up of the patients with ACS in coronary care unit (CCU), after 1 and 6 month periods. We included 117 patients (mean age: 61.2+/-11.3 years, 93 males) hospitalized in CCU with the diagnosis of ACS. All had baseline serum GGT activity and were free of systemic and hepatobiliary disease. MACE was defined as the composite of mortality from cardiac causes, recurrent hospitalization with ACS and nonfatal recurrent myocardial infarction diagnoses, to need for coronary revascularization during CCU, over 1 and 6 month follow-up periods. During the follow-up of CCU, MACE occurred in 17 (14.5%) patients (two died). Serum GGT activity was significantly higher in the patients with MACE than those free of MACE (P=0.001) and GGT was found as the independent predictor of the development of MACE-CCU [relative hazard: 1.05, 95% confidence interval (CI): 1.01-1.09, P=0.007]. During the follow-up of 1 month, MACE occurred in 23 (20.0%) patients (five died). Serum GGT activity was significantly higher in patients with MACE than those free of MACE (P=0.021) and GGT was found as the independent predictor of the development of MACE-1 month (relative hazard: 1.04, 95% CI: 1.01-1.08, P=0.039). During the follow-up of 6 months, MACE occurred in 24 (21.8%) patients (two died). Again, GGT was significantly higher in patients who developed MACE than those free of MACE (P=0.001) and GGT was found as the independent predictor of the development of MACE-6 months (relative hazard 1.06, 95% CI: 1.03-1.10, P<0.001). Serum GGT activity was found to be an independent predictor of the development of MACE in the patients with ACS during CCU, over 1 and 6 month follow-up periods.