| Summary: | 碩士 === 國立臺灣大學 === 臨床醫學研究所 === 103 === The metabolic syndrome is usually associated with insulin resistance and visceral fat distribution, which appear to play a direct role in the development of diabetes and cardiovascular disease (CVD). Insulin resistance and increased visceral adipose tissue are also associated with an abnormal ectopic accumulation of lipids in non-adipocytes to cause organ failure, like steatosis hepatitis. The epicardial adipose tissue (EAT), in a similar fashion as visceral intra-abdominal fat, might directly affect the pathophysiology of cardiac vessels and function of the heart. Accordingly, ectopic accumulation of fat within cardiac muscle cells can impair the heart function and predispose to heart failure (HF). The echocardiography-based epicardial adipose tissue (EAT) measurement has been recognized to be related to several metabolic abnormalities and increase the risk of cardiovascular diseases. However, clinical data on the EAT’s association with HF with preserved ejection fraction (HFpEF) are limited.
We measured the echocardiography-based EAT thickness in 254 subjects (female/male 165/89 and mean age 65.7± 9.8 years) divided into 3 group: Those with HF (HFpEF group, n = 55), those with ≥1 cardiometabolic risks (at-risk group, n = 150), and normal controls (n = 49). HFpEF group showed significantly greater amount of EAT than both normal and at-risk groups (p=0.000, p= 0.002 separately). Logistic regression was used to estimate the cross-sectional association of the EAT, metabolic syndrome and HFpEF. Models were adjusted for age, sex, body mass index (BMI), LV mass, and related biomarkers. The echocardiography-based EAT thickness was significantly related in multivariate analysis to MS (OR 8.02, 95% CI 1.3- 49.7), and HFpEF (OR 53.95, 95% CI 0.7- 18.2).
Our study suggests that EAT can be an important factor correlated with LV diastolic dysfunction and the heart structural change. Moreover, the heart itself is covered by fat. The EAT, a metabolically active fat depot with no physical barrier separating it from the adjacent myocardium and coronary arteries, plays an important local metabolic role by a paracrine effect, related to inflammation and the secretion of related adipokines. Confirm the relationships between cardiac fat burden, cardiometabolic risk factors and diastolic heart failure may contribute to identify and treatment of diastolic heart failure risk individuals earlier and more appropriately.
Conclusions - These results indicate a strong, consistent relationship of the EAT with prevalent metabolic syndrome and HFpEF.
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