Background:
Recent publications suggested that epicardial adipose tissue (EAT) contributes to the pathogenesis of coronary atherosclerosis. Although some studies showed the association between EAT accumulation and left ventricular (LV) diastolic dysfunction, these associations are not fully understood.
Methods:
We evaluated 153 patients without coronary artery disease who underwent coronary computed tomography (CT) angiography and Doppler echocardiography. We evaluated 153 patients (mean age of 60 years and 54% men) with zero coronary artery calcium score in coronary CT. Visceral adipose tissue (VAT) area was simultaneously measured by abdominal scans, and EAT volume was also calculated. These measurements were corrected by body surface area; VAT area index (VATAI), and EAT volume index (EATVI). The early diastolic mitral annular velocity at the septal (septal E’) and lateral (lateral E’) were measured using tissue Doppler echocardiography.
Results:
The mean values of BMI, VATAI, EATVI, and LVMI were 23.7 ± 3.8 kg/m
2
, 52.6 ± 26.4 cm
2
/m
2
, 71.3 ± 29.8 cm
3
/m
2
, and 83.3 ± 17.7 g/m
2
, respectively. The mean septal E’ and lateral E’ velocities were 7.2 ± 2.2 cm/s and 9.8 ± 2.9 cm/s, respectively. Each E’ velocity was negatively correlated with EATVI (septal, R = 0.276, p < 0.001; lateral, R = 0.342, p < 0.001) and VATAI (septal, R = 0.241, p = 0.03; lateral, R = 0.255, p = 0.002; Figure). In contrast, each E’ velocity was not correlated with LVMI (septal, R = 0.161, p = 0.03; lateral, R = 0.118, p = 0.14) and BMI (septal, R = 0.182, p = 0.03; lateral, R = 0.152, p = 0.06). To determine each E’ velocity, we performed stepwise multiple regression analyses where all clinical parameters were entered. Diastolic blood pressure (p = 0.014), statin use (p = 0.011), LVMI (p = 0.003), and EATVI (p = 0.004) were independently correlated with septal E’ velocity, and statin use (p = 0.024), LVMI (p = 0.011), and EATVI (p < 0.001) were independently correlated with lateral E’ velocity.
Conclusion:
An increase in EATVI was associated with the decrease of early diastolic mitral annular velocity along each side of the left ventricle in patients with coronary calcium score of zero. These findings indicate that EAT accumulation may cause LV diastolic dysfunction in the early phase of coronary artery disease.
Secretory Type II Phospholipase A2 Is Produced and Secreted by Epicardial Adipose Tissue and Overexpressed in Patients with Coronary Artery Disease
