Mohamed Hassan1, Karim Said1, Hussien Rizk2, Fatma ElMogy3, Mohamed Donya4, Mohamed Houseni5, Magdi Yacoub6. 1. Division of Cardiology, Aswan Heart Centre, Aswan, Egypt Cardiology Department, Cairo University, Cairo, Egypt. 2. Cardiology Department, Cairo University, Cairo, Egypt. 3. Chemical Pathology Department, Cairo University, Cairo, Egypt. 4. Division of Radiology, Aswan Heart Centre, Aswan, Egypt. 5. National Liver Institute, Menofia University, Menofia, Egypt. 6. Division of Cardiothoracic Department, Aswan Heart Centre, Aswan, Egypt Imperial College, London, UK m.yacoub@imperial.ac.uk.
Abstract
AIMS: Epicardial adipose tissue (EAT) has been proposed to modulate underlying coronary plaque features. The study aimed to determine the relation between segmental EAT (sEAT) volume, assessed by cardiac magnetic resonance (CMR), and underlying coronary plaque characteristics, as estimated by multidetector computed tomography (CT) (MDCT). METHODS AND RESULTS: The study included 32 male patients with stable angina pectoris and 11 age-matched healthy controls. For each CAD patient, sEAT volume around 8 coronary segments (3 in left anterior descending artery, 3 in right coronary artery, and 2 in left circumflex artery) was quantified by CMR. By MDCT, plaques in each coronary segment were characterized in terms of plaque volume, type, CT attenuation, and severity of luminal stenosis. Serum levels of adipokines were measured. Total EAT volume was significantly higher in CAD patients than in control group. Serum resistin showed significant correlation with EAT volume (r = 0.69, P < 0.001). Analysis of 256 coronary segments showed larger sEAT volume with increasing luminal stenosis of the corresponding segment (mild: 8.2 cm(3); moderate: 11 cm(3); severe: 11.8 cm(3), P < 0.001). sEAT volume was larger in segments with mixed than those with calcified or non-calcified plaques (12.1 vs. 10.2 vs. 9.5 cm(3), respectively, P = 0.015). sEAT volume was larger in segments with low CT attenuation non-calcified plaques compared with non-calcified plaques with CT attenuation >30 HU (10.5 vs. 8.2 mm(3), P < 0.001). CONCLUSION: Peri-coronary epicardial adipose tissue volume is significantly associated with the extent and severity of coronary atherosclerosis and may be a determinant of plaque vulnerability. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Epicardial adipose tissue (EAT) has been proposed to modulate underlying coronary plaque features. The study aimed to determine the relation between segmental EAT (sEAT) volume, assessed by cardiac magnetic resonance (CMR), and underlying coronary plaque characteristics, as estimated by multidetector computed tomography (CT) (MDCT). METHODS AND RESULTS: The study included 32 male patients with stable angina pectoris and 11 age-matched healthy controls. For each CAD patient, sEAT volume around 8 coronary segments (3 in left anterior descending artery, 3 in right coronary artery, and 2 in left circumflex artery) was quantified by CMR. By MDCT, plaques in each coronary segment were characterized in terms of plaque volume, type, CT attenuation, and severity of luminal stenosis. Serum levels of adipokines were measured. Total EAT volume was significantly higher in CAD patients than in control group. Serum resistin showed significant correlation with EAT volume (r = 0.69, P < 0.001). Analysis of 256 coronary segments showed larger sEAT volume with increasing luminal stenosis of the corresponding segment (mild: 8.2 cm(3); moderate: 11 cm(3); severe: 11.8 cm(3), P < 0.001). sEAT volume was larger in segments with mixed than those with calcified or non-calcified plaques (12.1 vs. 10.2 vs. 9.5 cm(3), respectively, P = 0.015). sEAT volume was larger in segments with low CT attenuation non-calcified plaques compared with non-calcified plaques with CT attenuation >30 HU (10.5 vs. 8.2 mm(3), P < 0.001). CONCLUSION: Peri-coronary epicardial adipose tissue volume is significantly associated with the extent and severity of coronary atherosclerosis and may be a determinant of plaque vulnerability. Published on behalf of the European Society of Cardiology. All rights reserved.