Disfunção autonômica e anticorpos contra receptores anti-m2 e anti-β1 em pacientes chagásicos

Thiers, Clarissa Antunes; Barbosa, João Luis; Pereira, Basílio de Bragança; Nascimento, Emília Matos do; Nascimento, José Hamilton do; Medei, Emiliano; Pedrosa, Roberto Coury

doi:10.1590/s0066-782x2012005000067

Cited by 15 publications

(3 citation statements)

References 40 publications

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“…The principal disorders reported are atrial, ventricular extrasystoles, intraventricular and/or AV conduction disturbances and primary ST-T wave changes [ 5 ]. Classically, arrhythmias have been linked to autonomic dysfunction [ 6 ], anti-adrenergic and anti-cholinergic autoantibodies [ 7 ] and to wall motion abnormalities [ 8 ]. Although, Chagas patients may present with arrhythmias and sudden death in the absence of ventricular dysfunction (known as the arrhythmogenic form) [ 9 ], the causes associated with nonstructural arrhythmias are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Evidence of Reversible Bradycardia and Arrhythmias Caused by Immunogenic Proteins Secreted by T. cruzi in Isolated Rat Hearts

et al. 2015

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RationaleChagas cardiomyopathy, caused by the protozoan Trypanosoma cruzi, is characterized by alterations in intracellular ion, heart failure and arrhythmias. Arrhythmias have been related to sudden death, even in asymptomatic patients, and their molecular mechanisms have not been fully elucidated.ObjectiveThe aim of this study is to demonstrate the effect of proteins secreted by T. cruzi on healthy, isolated beating rat heart model under a non-damage-inducing protocol.Methods and ResultsWe established a non-damage-inducing recirculation-reoxygenation model where ultrafiltrate fractions of conditioned medium control or conditioned infected medium were perfused at a standard flow rate and under partial oxygenation. Western blotting with chagasic patient serum was performed to determine the antigenicity of the conditioned infected medium fractions. We observed bradycardia, ventricular fibrillation and complete atrioventricular block in hearts during perfusion with >50 kDa conditioned infected culture medium. The preincubation of conditioned infected medium with chagasic serum abolished the bradycardia and arrhythmias. The proteins present in the conditioned infected culture medium of >50 kDa fractions were recognized by the chagasic patient sera associated with arrhythmias.ConclusionsThese results suggest that proteins secreted by T. cruzi are involved in Chagas disease arrhythmias and may be a potential biomarker in chagasic patients.

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Section: Introductionmentioning

confidence: 99%

Evidence of Reversible Bradycardia and Arrhythmias Caused by Immunogenic Proteins Secreted by T. cruzi in Isolated Rat Hearts

et al. 2015

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“…HRV is reduced in Chagas patients with and without the cardiac form (including the indeterminate form) 6 , 7 , 9 , 18 , 23 , and the reduction in its indices is correlated with levels of antimuscarinic antibodies 10 , which are increased in infected patients. The levels of these antibodies seem to be associated with clinical markers of autonomic dysfunction 24 , including the reduction of the chronotropic response to stress, suggesting clinical and physiopathological significance in Chagas disease 25 . It is controversial the existence of an association between reduced HRV autonomic dysfunction marker and severity of ventricular dysfunction or the evolutionary stage of the disease 26 - 31 .…”

Section: Discussionmentioning

confidence: 97%

Effects of Exercise Training on Heart Rate Variability in Chagas Heart Disease

Nascimento¹,

Lima²,

Nunes³

et al. 2014

Arquivos Brasileiros De Cardiologia

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Background:Heart rate variability (HRV) is a marker of autonomic dysfunction severity. The effects of physical training on HRV indexes in Chagas heart disease (CHD) are not well established.Objective:To evaluate the changes in HRV indexes in response to physical training in CHD.Methods:Patients with CHD and left ventricular (LV) dysfunction, physically inactive, were randomized either to the intervention (IG, N = 18) or control group (CG, N = 19). The IG participated in a 12-week exercise program consisting of 3 sessions/week.Results:Mean age was 49.5 ± 8 years, 59% males, mean LVEF was 36.3 ± 7.8%. Baseline HRV indexes were similar between groups. From baseline to follow-up, total power (TP): 1653 (IQ 625 - 3418) to 2794 (1617 - 4452) ms, p = 0.02) and very low frequency power: 586 (290 - 1565) to 815 (610 - 1425) ms, p = 0.047) increased in the IG, but not in the CG. The delta (post - pre) HRV indexes were similar: SDNN 11.5 ± 30.0 vs. 3.7 ± 25.1 ms. p = 0.10; rMSSD 2 (6 - 17) vs. 1 (21 - 9) ms. p = 0.43; TP 943 (731 - 3130) vs. 1780 (921 - 2743) Hz. p = 0.46; low frequency power (LFP) 1.0 (150 - 197) vs. 60 (111 - 146) Hz. p = 0.85; except for high frequency power, which tended to increase in the IG: 42 (133 - 92) vs. 79 (61 - 328) Hz. p = 0.08).Conclusion:In the studied population, the variation of HRV indexes was similar between the active and inactive groups. Clinical improvement with physical activity seems to be independent from autonomic dysfunction markers in CHD.

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“…The parasite persistence induces the recruitment and expansion of T. cruzi -specific T cells to the myocardium, particularly Th1, and an increase in cytokines concentration such as interferon-γ [ 32 , 34 ]. Additionally, in vivo murine models show that T. cruzi -infected mice display autoantibodies specific for various proteins such as cardiac myosin, desmin, actin, β1-adrenergic, and M2-muscarinic cholinergic receptors, showing the relevance of the humoral response in the development of CD [ 34 , 44 , 45 ].…”

Section: Pathophysiology Of Infectionmentioning

confidence: 99%

Chagas Cardiomyopathy: From Romaña Sign to Heart Failure and Sudden Cardiac Death

et al. 2021

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Despite nearly a century of research and accounting for the highest disease burden of any parasitic disease in the Western Hemisphere, Chagas disease (CD) is still a challenging diagnosis, primarily due to its poor recognition outside of Latin America. Although initially considered endemic to Central and South America, globalization, urbanization, and increased migration have spread the disease worldwide in the last few years, making it a significant public health threat. The international medical community’s apparent lack of interest in this disease that was previously thought to be geographically restricted has delayed research on the complex host–parasite relationship that determines myocardial involvement and its differential behavior from other forms of cardiomyopathy, particularly regarding treatment strategies. Multiple cellular and molecular mechanisms that contribute to degenerative, inflammatory, and fibrotic myocardial responses have been identified and warrant further research to expand the therapeutic arsenal and impact the high burden attributed to CD. Altogether, cardiac dysautonomia, microvascular disturbances, parasite-mediated myocardial damage, and chronic immune-mediated injury are responsible for the disease’s clinical manifestations, ranging from asymptomatic disease to severe cardiac and gastrointestinal involvement. It is crucial for healthcare workers to better understand CD transmission and disease dynamics, including its behavior on both its acute and chronic phases, to make adequate and evidence-based decisions regarding the disease. This review aims to summarize the most recent information on the epidemiology, pathogenesis, clinical presentation, diagnosis, screening, and treatment of CD, emphasizing on Chagasic cardiomyopathy’s (Ch-CMP) clinical presentation and pathobiological mechanisms leading to sudden cardiac death.

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Disfunção autonômica e anticorpos contra receptores anti-m2 e anti-β1 em pacientes chagásicos

Cited by 15 publications

References 40 publications

Evidence of Reversible Bradycardia and Arrhythmias Caused by Immunogenic Proteins Secreted by T. cruzi in Isolated Rat Hearts

Evidence of Reversible Bradycardia and Arrhythmias Caused by Immunogenic Proteins Secreted by T. cruzi in Isolated Rat Hearts

Effects of Exercise Training on Heart Rate Variability in Chagas Heart Disease

Chagas Cardiomyopathy: From Romaña Sign to Heart Failure and Sudden Cardiac Death

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