ABC | Volume 113, Nº4, October 2019

Anatomopathological Correlation Martins et al. Cardiac failure after non-ST-elevation myocardial infarction Arq Bras Cardiol. 2019; 113(4):775-782 1. ThygesenK,Alpert JS, JaffeAS,ChaitmanBR,Bax JJ,MorrowDA,etal.Fourth Universal Definition of Myocardial Infarction (2018).J Am Coll Cardiol. 2018,72(18)2231-64. 2. Baron T, Hambraeus K, Sundström J , Erlinge D, Jernberg T, Lindahl B, et al . Type 2myocardial infarction in clinical practice Heart . 2015;101(2):101-6. 3. López-Cuenca A, Gomez-MolinaM, Flores-Blanco PJ, Sánchez-MartínezM, García-Narbon A, De Las Heras-Gómez, et al. Comparison between type-2 and type-1myocardial infarction: clinical features, treatment strategies and outcomes. J Geriatr Cardiol. 2016;13(1):15–22. 4. Saaby L, Poulsen TS, Hosbond S, Larsen TB, Diederichsen ACP, Hallas J, et al. Classification of myocardial infarction: frequency and features of type 2 myocardial infarction. Am J Med. 2013;126(9): 789–97. 5. Chapman AR , Shah ASV, Lee KK, Anand A, Francis O, Adamson P, et al. Long termoutcomes in patients with type 2myocardial infarction andmyocardial injury. Circulation. 2018;137(12):1236-45. 6. Hawatmeh A, Thawabi M, Aggarwal R, Abirami C, Vavilin I, Wasty N, et al. Implications of misclassification of type 2 myocardial infarction on clinical outcomes. Cardiovasc Revasc Med. 2019 Apr 12;Pii:S1553-8389(19)30235-0. 7. Elamm C, Fairweather D, Cooper LT. Pathogenesis and diagnosis of myocarditis. Heart.2012;98(11):835-40. 8. Vos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al.Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380(9859):2163-96. 9. MannD, Zipes D, Libby P, BonowR. Braunwald’s Heart Disease: a textbook of cardiovascular medicine, 10th ed, Saunders: Philadelphia; 2017. 10. Montera MW, Mesquita ET, Colafranceschi AS, Oliveira Junior AM, Rabischoffsky A, Ianni BM, et al. I Diretriz Brasileira de Miocardites e Pericardites. Arq Bras Cardiol. 2013;100(4 Suppl 1):1-36. 11. Tschöpe C, Cooper LT, Toree-Amione G, Van Linthout S. Management of myocarditis-relatedcardiomyopathyinadults.CircRes.2019;124(11):1568-83. 12. Johansson BB, Torsvik J, Bjørkhaug L, Vesterhus M, Ragvin A, Tjora E, et al. Diabetes and pancreatic exocrine dysfunction due to mutations in the carboxyl ester lipase gene-maturity onset diabetes of the young (CEL-MODY): a protein misfolding disease. J Biol Chem. 2011;286(40):34593-605. 13. Vesterhus M, Raeder H, Johansson S, Molven A, Njølstad PR. Pancreatic exocrine dysfunction in maturity-onset diabetes of the young type 3. Diabetes Care. 2008;31(2):306-10. 14. Kodvawala A, Ghering AB, Davidson WS, Hui DY. Carboxyl ester lipase expression in macrophages increases cholesteryl ester accumulation and promotes atherosclerosis. J Biol Chem. 2005;280(46):38592-8. 15. Hui DY, Howles PN. Carboxyl ester lipase: structure-function relationship and physiological role in lipoproteinmetabolismand atherosclerosis. J Lipid Res. 2002;43(12):2017-30. References This is an open-access article distributed under the terms of the Creative Commons Attribution License Comment This is a very unusual case, in which some points were not clarified in the necropsy. The main point concerns the fact that the patient had a lesion with microscopic appearance of a myocardial infarction with an evolution of 4 to 6 weeks, that is, compatible with the clinical history of a sudden onset heart failure, diagnosed with infarction and elevated necrosis. However, the pattern of the lesion was not usual, irregularly affecting all the walls of the left ventricle. Therefore, we came to think of myocarditis and there was no adequate explanation for the occurrence of this ischemic necrosis; Atherosclerosis was only moderate, with a single segment with severe right coronary artery injury, and there were no recent or organizing thrombi. Diabetic patients sometimes have cardiac microcirculatory lesions, but in the present case these were not significant. Another issue is that the pancreas had its exocrine portion almost completely replaced by fat, with the Langerhans islets left. There are three diagnoses to consider: cystic fibrosis, Schwachman-Diamond syndrome, and carboxyl lipase ester mutations. The former is eliminated due to the absence of cysts, whether in the pancreas, lungs or other organs. Schwachman-Diamond syndrome mainly affects young children. Therefore, the patient will most likely carry a carboxyl lipase ester mutation, which may even be responsible for delayed onset juvenile diabetes, as was the case with this patient, and influence the development of atherosclerosis. 12-15 (Dr. Paulo Sampaio Gutierrez) 782