ABC | Volume 112, Nº4, April 2019

Anatomopathological Correlation Pereira et al Arrhythmia and heart failure Arq Bras Cardiol. 2019; 112(4):466-472 Figure 4 – Photomicrography of the left ventricular myocardium: Diffuse myocardial fibrosis (in blue). Masson’s trichrome, 50x). 1. McKennaWJ, Maron BJ, Thiene G. Classification, epidemiology, and global burden of cardiomyopathies. Circ Res. 2017;121(7):722-30 2. Trachtenberg BH, HareM. Inflammatory cardiomyopathic syndromes. Circ Res. 2017;121(7):3-18. 3. Muchtar E, Blauwet LA, Gertz MA. Restrictive cardiomyopathy. Genetic, pathogenesis, clinical manifestations, diagnosis, and therapy. Cir Res. 2017;121(7):819-37 4. Seward J.B., Casaclang-Verzosa G. Infiltrative cardiovascular diseases: cardiomyopathies that look alike. J AmColl Cardiol. 2010;55(17):1769–79. 5. Dickstein K, Cohen-Solal A, Filippatos G, McMurray JJ, Ponikowski P, Poole- Wilson PA, et al. ESCGuidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for theDiagnosis and Treatment of AcuteandChronicHeartFailure2008oftheEuropeanSocietyofCardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM). Eur Heart J. 2008;29(19):2388-442. 6. Dias JCD, Ramos Jr AN, Gontijo ED, Luquetti A, Shikanai-YasudaMA, Coura JR, et al. II Consenso Brasileiro emDoença de Chagas,2015. Epidemiol Serv Saude.2016;25(num esp):7-86. 7. MaischB,RisticAD,SeferovicP.M.Newdirections indiagnosisandtreatment of pericardial disease: a project of the Taskforce on Pericardial Disease of the World Heart Federation. Herz. 2000;25(8):769-80. 8. Babonian C, Treasure T. Meta-analysis of the association of enteroviroses with human heart disease. Heart. 1997;78(6):539-43. 9. McNally EM, Mestroni L. Dilated cardiomyopathy . Genetic determinants and mechanisms. Circ Res. 2017;121(7):731-48. 10. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, Falk V. Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology. Eur Heart J. 2016;37(27):2129-200. References used. 17 Anatomopathological 18 and coronary angiography studies 19 performed in hearts of individuals without other congenital heart malformations divide the coronary anomalies into two groups: those of anomalous arterial origin and course and intrinsic anatomical anomalies of the arteries. In the case of this patient, we observed anomalous origin of the coronary arteries, represented by the absence of the left coronary artery and independent origin in separate ostia and in the same sinus of Valsalva of the ADA and the circumflex artery. The intramyocardial course of the ADA is classified as an anatomical variation, since its occurrence in the middle segment of the ADA ranges from 5% to 80% of patients in different studies. 20 In the other coronary arteries, such an alteration is considered an anomaly, since it occurs is less than 1% of the population. The crossing of epicardial branches is an anomaly of the intrinsic anatomy of the coronary arteries and is quite rare, with few cases having been described in the literature. 20,21 One might question whether there was compression of the arterial segments involved in the epicardial crossing, but in the absence of obstructive coronary alterations and localized ischemic myocardial lesions, anatomopathological examination is limited for such evaluation. Left ventricular hypertrophy and dilatation, as well as diffuse interstitial myocardial fibrosis can be explained by the bicuspid aortic valve dysfunction. (Dr. Lea Maria Macruz Ferreira Demarchi) 471