Pelin Zeynep BEKİN SARIKAYA, Atike TEKELİ KUNT

Toraks BT'de mediastinal yağ dokusu ve aort ölçümleri: ateroskleroz ile ilişkisi var mı?

Amaç: Toraks Bilgisayarlı Tomografi (BT) görüntüleme ile mediastinal yağ dokusunun da torasik aort aterosklerozunda rol alıp almadığını sorgulamayı amaçladık. Mediastinal yağ dokusunun miktarı ve yoğunluğu ile yaş, cinsiyet ve aorta aterosklerotik plak varlığı arasındaki ilişkiyi ortaya koymaya çalıştık. Yöntemler: Bu retrospektif çalışmada 45 hastanın (21 erkek ve 24 kadın) toraks BT görüntüleri 60 yaş ve altı 23 ve 22 kişilik iki gruba ayrıldı. Aorta ve pulmoner arterin yan yana görüldüğü enine kesitten mediastendeki yağ dokusunun en geniş görüldüğü alan manuel olarak ölçüldü. Ölçülen yağ bölgesinin ortasında mediastinal yağ dokusunun yoğunluğu ölçüldü. Aortun çapı ve aortun ön kısmından sternuma olan mesafe ölçüldü. Ayrıca aort ile pulmoner arter arasındaki en dar mesafe ve aynı kesitte sternumun ön yüzünden cilt altı yağ dokusu kalınlığı ölçüldü. Aortta aterosklerotik plak varlığı ve yokluğu kaydedildi. Bulgular: Çalışmamızda cinsiyet ile aort plak varlığı arasında ilişki saptanmadı (p=0,423). Yaş grupları aterosklerotik plak varlığı ile ilişkili bulundu (p=0.001). Sternal yağ kalınlığı ile aterosklerotik plak arasında istatistiksel olarak anlamlı fark gözlendi (p=0,044). Aterosklerotik plak olmayanlarda sternal yağ kalınlığının aterosklerotik plak olmayanlara göre daha fazla olduğu görüldü. Aterosklerotik plak ile aort çapı arasında istatistiksel olarak anlamlı fark gözlendi (p=0,001). Aterosklerotik plak varlığı ile mediastinal yağ miktarı arasında istatistiksel olarak anlamlı bir fark gözlenmedi (p=0,483). Sonuç: Ateroskleroz sadece yağ dokusu fazlalığı ile artmamakta, birçok parametreye bağlı olarak artmaktadır. Aterosklerotik risk ve plak gelişimi değerlendirilirken hastanın yaşı, cinsiyeti, yağ dağılımı ve diğer hastalıkları bir bütün olarak değerlendirilmelidir. Aterosklerozun gelişiminde hala açıklanamayan multifaktöriyel parametreler olduğu akılda tutulmalıdır.

Anahtar Kelimeler:

Atherosclerosis, Aorta plaque, mediastinal fat tissue, thorax CT.

Mediastinal adipose tissue and aortic measurements in thorax CT: is it related to atherosclerosis?

Aim: We aimed to investigate whether the mediastinal adipose tissue plays a role in thoracic aortic atherosclerosis with thoracic Computed Tomography (CT) imaging. We aimed to elucidate the relationship between the amount and density of mediastinal adipose tissue, age, sex, and the presence of atherosclerotic plaque in the aorta. Material and Method: In this retrospective study, the thoracic computed tomography (CT) images of 45 patients (21 men and 24 women) were examined in two groups. There were 23 patients aged >60 years in group 1 and 22 patients aged <60 years in group 2. The measurements were manually performed from the image where the mediastinal fat tissue, located anterior compartment of the aorta and the pulmonary artery, is viewed widest. The area and density of mediastinal fat tissue, the diameter of the aorta and the distance from the anterior of the aorta to the sternum were measured. The narrowest distance between the aorta and the pulmonary artery, and the subcutaneous fat tissue thickness from the anterior of the sternum in the same section were measured. The presence and absence of atherosclerotic plaque in the aorta were also recorded. Results: We found no significant differences in demographic and clinical data between the groups. Among the patients aged >60 years (group 1) and <60 years (group 2), statistically significant differences in fat density, sternal fat thickness, and aortic diameter were found. Age was associated with the presence of atherosclerotic plaque. A statistically significant relationship was observed between sternal fat thickness and atherosclerotic plaque. The sternal fat thickness was greater in those with than in those without atherosclerotic plaques. The presence of atherosclerotic plaque was associated with aortic diameter. No statistically significant relationships were observed between the presence of atherosclerotic plaque and the amount and density of mediastinal fat, the aortosternal distance, and the aortopulmonary artery distance. Conclusion: The risk of atherosclerosis increases not only with excess adipose tissue but also depending on many other parameters. While evaluating atherosclerotic risk and plaque development, patient age, sex, fat distribution, and other diseases should also be evaluated. It should be kept in mind that atherosclerosis is still an unexplained multifactorial parameter in development.

Keywords:

Atherosclerosis, Aorta plaque, mediastinal fat tissue, thorax CT.,

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Frostegård J. Immunity, atherosclerosis and cardiovascular disease. BMC Med 2013; 11: 117.
https://www.who.int/health-topics/cardiovascular-diseases#tab=tab_1
Fan J, Watanabe T. Atherosclerosis: Known and unknown. Pathol Int 2022; 72: 151-60.
Whitlock G, Lewington S, Sherliker P, et al. Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies. Lancet 2009; 373: 1083–96.
Fuster JJ, Ouchi N, Gokce N, et al. Obesity-induced changes in adipose tissue microenvironment and their impact on cardiovascular disease. Circ Res 2016; 118: 1786–807.
Britton KA, Fox CS. Perivascular adipose tissue and vascular disease. Clin Lipidol 2011; 6: 79–91.
Mahabadi AA, Massaro JM, Rosito GA, et al. Association of pericardial fat, intrathoracic fat, and visceral abdominal fat with cardiovascular disease burden: the Framingham Heart Study. Eur Heart J 2009; 30: 850–6.
Rosito GA, Massaro JM, Hoffmann U, et al. Pericardial fat, visceral abdominal fat, cardiovascular disease risk factors, and vascular calcification in a community-based sample: the Framingham Heart Study. Circulation 2008; 117: 605–13.
Cheng CK, Bakar HA, Gollasch M, Huang Y. Perivascular adipose tissue: the sixth man of the cardiovascular system. Cardiovasc Drugs Ther 2018; 32: 481-502.
Miao CY, Li ZY. The role of perivascular adipose tissue in vascular smooth muscle cell growth. Br J Pharmacol 2012;165: 643-58.
Iacobellis G, Pond CM, Sharma AM. Different “weight” of cardiac and general adiposity in predicting left ventricle morphology. Obesity (Silver Spring) 2006; 14: 1679–84.
Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med 2005; 2: 536–43.
Fantuzzi G, Mazzone T. Adipose tissue and atherosclerosis: exploring the connection. Arterioscler Thromb Vasc Biol 2007; 27: 996–1003.
Berg AH, Scherer PE. Adipose tissue, inflammation, and cardiovascular disease. Circ Res 2005; 96: 939 –49.
Yu Y-H, Ginsberg HN. Adipocyte signaling and lipid homeostasis: sequelae of insulin-resistant adipose tissue. Circ Res 2005; 96: 1042–52.
Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab 2004; 89: 2548 –56.
Scherer PE. Adipose tissue: from lipid storage compartment to endocrine organ. Diabetes 2006; 55: 1537–45.
Vohl MC, Sladek R, Robitaille J, et al. A survey of genes differentially expressed in subcutaneous and visceral adipose tissue in men. Obes Res 2004; 12: 1217–22.
Fain JN, Madan AK, Hiler ML, Cheema P, Bahouth SW. Comparison of the release of adipokines by adipose tissue, adipose tissue matrix, and adipocytes from visceral and subcutaneous abdominal adipose tissues of obese humans. Endocrinology. 2004; 145: 2273–2282.
Bruun JM, Lihn AS, Pedersen SB, Richelsen B. Monocyte chemoattractant protein-1 release is higher in visceral than subcutaneous human adipose tissue (AT): implication of macrophages resident in the AT. J Clin Endocrinol Metab 2005; 90: 2282–9.
Wu J, et al. Origin of matrix-producing cells that contribute to aortic fibrosis in hypertension. Hypertension 2016; 67: 461–8.
Shao J-S, et al. Vascular calcification and aortic fibrosis: a bifunctional role for osteopontin in diabetic arteriosclerosis. Arterioscler Thromb Vasc Biol 2011; 31: 1821–33.
Despres JP, Lemieux I. Abdominal obesity and metabolic syndrome. Nature 2006; 444: 881–7.
Uranga AP, Levine J, Jensen M. Isotope tracer measures of meal fatty acid metabolism: reproducibility and effects of the menstrual cycle. Am J Physiol Endocrinol Metab 2005; 288: E547–55.