ABC | Volume 111, Nº2, August 2018

Original Article Sympathetic Dysautonomia in Heart Failure by 123 I-MIBG: comparison between Chagasic, non-Chagasic and heart transplant patients Viviane Santuari Parisotto Marino, 1 Sandra Monetti Dumont, 1 Luciene das Graças Mota, 1 Daniela de Souza Braga, 2 Stephanie Saliba de Freitas, 2 Maria da Consolação Vieira Moreira 3 Departamento de Anatomia e Imagem da Faculdade de Medicina da Universidade Federal de Minas Gerais, 1 Belo Horizonte, MG - Brazil Hospital das Clínicas da Universidade Federal de Minas Gerais, 2 Belo Horizonte, MG - Brazil Departamento de Clínica Médica da Faculdade de Medicina da Universidade Federal de Minas Gerais, 3 Belo Horizonte, MG - Brazil Mailing Address: Viviane Santuari Parisotto Marino • Alameda Serra da Canastra, 284. Condomínio Vila del Rey. Postal Code 34007-206, Nova Lima, MG - Brazil E-mail: parisottoviviane@yahoo.com.br Manuscript received November 17, 2017, revised manuscript March 21, 2018, accepted March 23, 2018 DOI: 10.5935/abc.20180124 Abstract Background: Heart failure (HF) is a severe public health problem because of its high morbidity and mortality and elevated costs, thus requiring better understanding of its course. In its complex and multifactorial pathogenesis, sympathetic hyperactivity plays a relevant role. Considering that sympathetic dysfunction is already present in the initial phases of chronic Chagas cardiomyopathy (CCC) and frequently associated with a worse prognosis, we assumed it could be more severe in CCC than in cardiomyopathies of other etiologies (non-CCC). Objectives: To assess the cardiac sympathetic dysfunction ( 123 I-MIBG) of HF, comparing individuals with CCC to those with non-CCC, using heart transplant (HT) patients as denervated heart parameters. Methods: We assessed 76 patients with functional class II-VI HF, being 25 CCC (17 men), 25 non-CCC (14 men) and 26 HT (20 men), by use of cardiac 123 I-metaiodobenzylguanidine ( 123 I-MIBG) scintigraphy, estimating the early and late heart-to-mediastinum ratio (HMR) of 123 I-MIBG uptake and cardiac washout (WO%). The 5% significance level was adopted in the statistical analysis. Results: The early and late HMR values were 1.73 ± 0.24 and 1.58 ± 0.27, respectively, in CCC, and 1.62 ± 0.21 and 1.44 ± 0.16 in non‑CCC (p = NS), being, however, higher in HT patients (p < 0.001). The WO% values were 41.65 ± 21.4 (CCC), 47.37 ± 14.19% (non-CCC) and 43.29 ± 23.02 (HT), p = 0.057. The late HMR values showed a positive weak correlation with left ventricular ejection fraction (LVEF) in CCC and non-CCC (r = 0.42 and p = 0.045; and r = 0.49 and p = 0.015, respectively). Conclusion: Sympathetic hyperactivity ( 123 I-MIBG) was evidenced in patients with class II-IV HF, LVEF < 45%, independently of the HF etiology, as compared to HT patients. (Arq Bras Cardiol. 2018; 111(2):182-190) Keywords: Heart Failure; Primary Dysautonomies; Chagas Cardiomyopathy; Myocardial/radionuclide imaging; 123 I-metaiodobenzylguanidine ( 123 I-MIBG). Introduction Heart failure (HF) currently represents a public health problem because of its epidemic proportions (worldwide prevalence greater than 23 million individuals), its high morbidity and mortality, and, consequently, high health expenditures. 1 A large variety of cardiac conditions can result in HF, whose prevalence differs when comparing developed and developing countries. 2 In Brazil, the ischemic etiology accounts for 34.1% of the HF cases, being followed by the Chagasic (21.4%) and hypertensive (13.2%) etiologies, the Chagasic being associated with a worse prognosis. 3-6 Previous studies have suggested that the pathogenesis of HF is complex and multifactorial, 7 sympathetic dysautonomia playing a relevant role in the process. 8-11 In the initial phase of HF, the sympathetic nervous system activation would modulate the pump function; however, over time, its action would become deleterious, leading to myocardial remodeling and restructuring, with progressive decline of the cardiac function. 10,12,13 In such patients, sympathetic dysfunction would be characterized by a significant reduction in the presynaptic uptake of norepinephrine, with consequent elevation in its serum levels and reduction in the postsynaptic density of β -adrenoreceptors. 10,13,14 In chronic Chagas cardiomyopathy (CCC), early impairment of the parasympathetic nervous system has been well established, 15,16 and sympathetic dysfunction, although not totally established, is believed to be present in the initial phases of the disease, 11,17-19 when the cardiac pump function is preserved and potentially associated with malignant arrhythmias and sudden death. 20-22 Because cardiac autonomous dysfunction is present early in CCC and the incidence of malignant arrhythmias and sudden death is elevated in those patients, 15,16,20-22 this 182