Cardiovascular Journal of Africa: Vol 33 No 3 (MAY/JUNE 2022)

CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 3, May/June 2022 AFRICA 111 found to be significantly correlated with the severity of coronary artery disease in patients with known coronary artery disease.14 Epicardial adipose tissue has been shown to be a source of inflammatory mediators such as interleukin (IL)-1β, IL-6 and tumour necrosis factor.15 Inflammatory mediators have been shown to play a role in the pathogenesis of calcific aortic stenosis as well.16,17 A significant correlation between epicardial fat thickness and levels of pro-inflammatory cytokines and calcific aortic stenosis has been described.9 The authors indicated a strong association between epicardial fat thickness and aortic stenosis.9 Epicardial adipose tissue is an important source of several pro-inflammatory mediators and it may play a role in promoting aortic valve degeneration and calcification. Mancio et al. reported that low body mass index (BMI) was paradoxically associated with aortic valve calcification and mortality in elderly aortic stenosis patients submitted for TAVI.18 Koifman et al. also concluded that patients with BMI < 20 kg/ m2 were associated with a higher risk of mortality.19 Interestingly, in another study, the authors revealed that patients with larger epicardial adipose tissue volume had an increased all-cause one-, two- and three-year mortality rate after TAVI.20 In our study, we aimed to evaluate the association of epicardial fat thickness with post-procedural outcomes of TAVI. To the best of our knowledge, our study is the first report to focus on the relationship between epicardial fat thickness and outcomes of patients who underwent TAVI. Our results failed to reveal any significant relationship. The limitations of this study are the small sample size and retrospective design. There is no consensus on the gold standard for an in vivo quantification of epicardial adipose tissue. Volume measurement could be more accurate in the assessment of epicardial adipose tissue, however, epicardial fat thickness measurement is less time consuming and easier. Conclusion Larger trials are needed to evaluate whether epicardial fat thickness might have predictive properties and become a routine way of assessing cardiovascular risk in a clinical setting of TAVI. References 1. Iacobellis G, Corradi D, Sharma AM. Epicardial adipose tissue: anatomic, biomolecular and clinical relationships with the heart. Nat Clin Pract Cardiovasc Med 2005; 2: 536–543. 2. Jazet IM, Pijl H, Meinders AE. Adipose tissue as an endocrine organ: impact on insulin resistance. Neth J Med 2003; 61: 194–212. 3. Demircelik MB, Yilmaz OC, Gurel OM, Selcoki Y, Atar IA, Bozkurt A, et al. Epicardial adipose tissue and pericoronary fat thickness measured with 64-multidetector computed tomography: potential predictors of the severity of coronary artery disease. Clinics (Sao Paulo) 2014; 69: 388–392. 4. Dey D, Nakazato R, Li D, Berman DS. Epicardial and thoracic fat – noninvasive measurement and clinical implications. Cardiovasc Diagn Ther 2012; 2: 85-93. 5. Alexopoulos N, McLean DS, Janik M, Arepalli CD, Stillman AE, Raggi P. Epicardial adipose tissue and coronary artery plaque characteristics. Atherosclerosis 2010; 210: 150–154. 6. Cheng VY, Dey D, Tamarappoo B, Nakazato R, Gransar H, MirandaPeats R, et al. Pericardial fat burden on ECG-gated noncontrast CT in asymptomatic patients who subsequently experience adverse cardiovascular events. J Am Coll Cardiol Cardiovasc Imaging 2010; 3: 352–360. 7. Tamarappoo B, Dey D, Shmilovich H, Nakazato R, Gransar H, Cheng VY, et al. Increased pericardial fat volume measured from noncontrast CT predicts myocardial ischemia by SPECT. J Am Coll Cardiol Cardiovasc Imaging 2010; 3: 1104–1112. 8. Al Chekakie MO, Welles CC, Metoyer R, Ibrahim A, Shapira AR, Cytron J, et al. Pericardial fat is independently associated with human atrial fibrillation. J Am Coll Cardiol 2010; 56: 784–788. 9. Parisi V, Rengo G, Pagano G, D’Esposito V, Passaretti F, Caruso A, et al. Epicardial adipose tissue has an increased thickness and is a source of inflammatory mediators in patients with calcific aortic stenosis. Int J Cardiol 2015; 186: 167–169. 10. Wang TD, Lee WJ, Chen MF. Epicardial adipose tissue measured by multidetector computed tomography: Practical tips and clinical implications. Acta Cardiol Sin 2010; 26: 55–68. 11. Kappetein AP, Head SJ, Généreux P, Piazza N, van Mieghem NM, Blackstone EH, et al; Valve Academic Research Consortium-2. Updated standardized endpoint definitions for transcatheter aortic valve implantation: the Valve Academic Research Consortium-2 consensus document. J Thorac Cardiovasc Surg 2013; 145: 6–23. 12. 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Int J Cardiol 2009; 135: 4–13. 17. Helske S, Kupari M, Lindstedt KA, Kovanen PT. Aortic valve stenosis: an active atheroinflammatory process. Curr Opin Lipidol 2007; 18: 483–491. 18. Mancio J, Fonseca P, Figueiredo B, Ferreira W, Carvalho M, Ferreira N, et al. Association of body mass index and visceral fat with aortic valve calcification and mortality after transcatheter aortic valve replacement: the obesity paradox in severe aortic stenosis. Diabetol Metab Syndr 2017; 9: 86. 19. Koifman E, Kiramijyan S, Negi SI, Didier R, Escarcega RO, Minha S, et al. Body mass index association with survival in severe aortic stenosis patients undergoing transcatheter aortic valve replacement. Catheter Cardiovasc Interv 2016; 88(1): 118–124. 20. Eberhard M, Stocker D, Meyer M, Kebernik J, Stähli BE, Frauenfelder T, et al. Epicardial adipose tissue volume is associated with adverse outcomes after transcatheter aortic valve replacement. Int J Cardiol 2019; 286: 29–35.

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