Dysregulation of Autonomic Nervous System in Chagas' Heart Disease Is Associated with Altered Adipocytokines Levels.

Autor: Barbosa-Ferreira JM; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Mady C; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Ianni BM; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Lopes HF; Hypertension Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil; Universidade Nove de Julho-UNINOVE, São Paulo, Brazil., Ramires FJ; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Salemi VM; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Grupi CJ; Electrocardiology Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Hachul DT; Clinical Arrhythmia Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil., Fernandes F; Cardiomyopathy Unit of the Heart Institute (InCor), do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2015 Jul 06; Vol. 10 (7), pp. e0131447. Date of Electronic Publication: 2015 Jul 06 (Print Publication: 2015).
DOI: 10.1371/journal.pone.0131447
Abstrakt: Background: Chagas disease (CD) induces autonomic dysfunction and inflammatory activity, which may promote metabolic abnormalities. We studied metabolism and his correlation with Autonomic Nervous System (ANS) and inflammation in CD.
Methods and Results: Sixty subjects were divided into 4 groups: control group (CG), IF (indeterminate form) group; ECG group (ECG abnormalities and normal left ventricular systolic function), and LVD group (left ventricular sistolic dysfunction). Levels of adiponectin, leptin, insulin, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) were assayed in serum samples by ELISA. ANS was assessed by heart rate variability in frequency domain in 24-hour Holter and postural tilt test (rest and orthostatic position). High frequency (HFr) component values were used to estimate parasympathetic activity and low frequency (LFr) component, sympathetic activity. Analyzes were made of the correlations of each of the metabolic parameters (leptin and adiponectin) with the inflammatory cytokines (interleukin-6 and TNF- alpha) and with the ANS assessment measurements. No significant differences were observed in leptin and insulin levels. Adiponectin was higher in ECG and LVD groups: [CG = 4766.5 (5529.5), IF = 4003.5 (2482.5), ECG = 8376.5 (8388.5), LVD = 8798 (4188.0) ng/mL, p<0.001)]. IL-6 and TNF-alpha were higher in LVD group: [IL-6: CG = 1.85 (6.41); IF = 1.58 (1.91); ECG = 1.0 (1.57); LVD= 31.44 (72.19) pg/ml; p = 0.001. TNF-alpha: CG = 22.57 (88.2); IF = 19.31 (33.16); ECG = 12.45 (3.07); LVD = 75.15 (278.57) pg/ml; p = 0.04]. Adiponectin levels had a positive association with the HFr component (r = 0.539; p = 0.038) and an inverse association with the LFr component (r = - 0.539; p = 0.038) in ECG group. Leptin levels had a negative association with the HFr component (r= - 0.632; p = 0.011) and a positive association with the LFr component (r = 0.632; p = 0.011) in LVD group.
Conclusions: We found increased adiponectin levels in Chagas' heart disease with systolic dysfunction and in patients with ECG abnormalities and normal systolic function at rest. Adipocytokines levels (adiponectin and leptin) were associated with ANS parameters in Chagas' heart disease.
Databáze: MEDLINE
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