IJCS | Volume 31, Nº2, March / April 2018

192 1. Sabah KM, Chowdhury AW, IslamMS, Cader FA, Kawser S, Hosen MI, et al. "Graves’ disease presenting as bi-ventricular heart failure with severe pulmonary hypertension and pre-eclampsia in pregnancy–a case report and review of the literature." BMC Res Notes. 2014;7:814. doi: 10.1186/1756-0500-7-814. 2. JacobsonDL,GangeSJ,RoseNR,GrahamNM.Epidemiologyandestimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol. 1997;84(3):223-43. PMID: 9281381. 3. PearceE.Thyroiddisordersduringpregnancyandpostpartum.BestPractRes Clin Obstet Gynaecol. 2015;29(5):700-6. doi: 10.1016/j.bpobgyn.2015.04.007. 4. Nazarpour S, Ramezani Teherani F, Simbar M, Azizi F. Thyroid dysfunctions andpregnancy outcomes. Iran J ReprodMed. 2015;13(7):387- 96. PMID: 26494985. 5. Klein I, Levey GS. The cardiovascular system in thyrotoxicosis. In: Braverman LE, Utiger RD. (eds.). The thyroid. 8 th ed. Philadelphia: Lipincott-Raven; 2000. p. 596-604. 6. Klein I, Ojamaa K. Thyroid hormone and cardiovascular system. N Engl J Med. 2001;344(7):501-9. doi:10.1056/NEJM200102153440707. 7. Babenko AY, Bairamov AA, Grineva EN, Ulupova EO. Thyrotoxic cardiomyopathy: cardiomyopathies - from basic research to clinical management. 2012;255:553-80. doi: 10.5772/29331. 8. Reynolds JL, Woody HB. Thyrothoxic mitral regurgitation: A probable form of intrinsic papillary muscle dysfunction. Am J Dis Child. 1971;122(6):544-8. PMID:5156265. 9. Fadel BM, Ellahham S, Ringel MD, Lindsay J Jr, Wartofsky L, Burman KD. Hyperthyroid heart disease. Clin Cardiol. 2000;23(6):402-8. PMID: 10875028. 10. Cavros NG, Old WD, Castro FD, Estep HL. Reversible mitral regurgitation and congestive heart failure complicating thyrotoxicosis. Am J Med Sci. 1996;311(3):142-4. PMID: 8615390. References Jorge et al. Mitral regurgitation and hyperthyroidism Int J Cardiovasc Sci. 2018;31(2)190-192 Case Report by echocardiography, and who, after treatment optimization, showed complete regression. It is possible that anemia and lung infection have contributed to exacerbate the hemodynamic changes that caused the patient's high output. The development of heart failure in these patients occurs due to changes in contractility, caused by poor oxygen supply optimization and changes in the myosin isoform expression in the cardiomyocyte. 5-7 In addition, there is an increase in blood volume and in the final diastolic pressure and, therefore, increased cardiac work. 5-7 The presence of functional RM in GD may occur secondary to an accumulation of glycosaminoglycans or intrinsic papillary muscle dysfunction. 8 The patient presented elevated FT4 levels. However, the cardiovascular manifestations of hyperthyroidism may occur due to minimal changes in hormone levels and include an increased heart rate at rest, in myocardial contractility, in ventricular muscle mass and a predisposition to atrial arrhythmias. 9 HR in GD is unusual and, when it occurs, it is often due to high biventricular rate with regular or reduced pulmonary and systemic vascular resistance. It affects mostly patients at extremes of age or those with previous heart disease - conditions not presented by the patient in this case. MR in GD may be caused by ventricular dilatation. However, it is important to highlight that, unlike the case report written by NG Cravos et al. 10 , there was no evidence of such increase in this patient. The cause of MR, in this case, must be associated with an increased synthesis of glycosaminoglycans of the endocardium or with an intrinsic dysfunction of papillary muscle activity. 8 In this case, there was a relation between the levels of circulating thyroid hormone and the severity of RM and HR. The use of diuretics and antithyroid agents led to regression of the clinical picture within one week, with the disappearance of mitral regurgitation. Author contributions Conception and design of the research: Jorge AJL, MartinsWA, Almeida BM. Acquisition of data: Gripp EA, Almeida BM, Figueroa CCRP, Sabino CL. Analysis and interpretation of the data: Jorge AJL, Martins WA. Writing of the manuscript: Jorge AJL, Martins WA, Gripp EA, Almeida BM, Figueroa CCRP, Sabino CL. Critical revision of themanuscript for intellectual content: Jorge AJL, Martins WA, Gripp EA. Supervision / as the major investigador: Jorge AJL. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding There were no external funding sources for this study. Study Association This article is part of the line of research on heart failure of the Postgraduate Course in Cardiovascular Sciences of the Universidade Federal Fluminense.