Peripheral and Coronary Sinus Catecholamine Levels in Patients with Severe Congestive Heart Failure due to Chagas&amp;rsquo; Disease

Bestetti, R. B.; Coutinho‐Netto, Joaquim; Staibano, L.; Pinto, Lucimara Z.; Muccillo, Gerson; Oliveira, João Samuel Meira de

doi:10.1159/000176874

Cited by 42 publications

(32 citation statements)

References 15 publications

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“…Similar conclusions have been drawn by investigators studying neurohormonal imbalances resulting from deficient parasympathetic control in Chagas disease (Oliveira 1985, Bestetti et al 1995, Ribeiro et al 2002. Of particular interest in this regard has been the report by Davila et al (1998) that sympathetic and parasympathetic abnormalities are actually preceded by myocardial damage and left ventricular dysfunction.…”

Section: The Neurogenic Hypothesissupporting

confidence: 65%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

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Chagas disease, caused by the obligate unicellular parasite Trypanosoma cruzi, presents itself in a diverse collection of clinical manifestations, ranging from severe, fatal heart and digestive tract pathologies to unapparent or minor alterations that do not compromise survival. Over the years, a number of mechanisms have been proposed to explain the pathogenesis of chagasic tissue lesions, all of which have faced some criticism or been received with skepticism. This article excludes the autoimmunity hypothesis for Chagas disease because it has been extensively reviewed elsewhere, and summarizes the various alternative hypotheses that have been advanced over the years. For each of these hypotheses, an outline of its main tenets and key findings that support them is presented. This is followed by the results and comments that have challenged them and the caveats that stand on their way to wider acceptance. It is hoped that this writing will draw attention to our shortcomings in understanding the pathogenesis of Chagas disease, which, unfortunately, continues to figure among the most serious health problems of the American continent.

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Section: The Neurogenic Hypothesissupporting

confidence: 65%

Mechanisms of pathogenesis in Chagas disease

Kierszenbaum

2007

Acta Parasitologica

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“…The presence of myocardial inflammatory cells are capable of producing TNF and interleukin 6, which are increased in serum of Chagas but not in IDC patients, and are prognostic markers of unfavorable outcome 24 . Furthermore, the sympathetic myocardial overactivity seen only in Chagas cardiomyopathy patients may worsen the remodeling process 25 . The presence of microvascular spasm can elicit myocardial ischemia and the presence of alterations in interstitial matrix 26 can further worsen myocardial ischemia, thus stimulating ventricular remodeling 21 in Chagas cardiomyopathy patients, a phenomenon not yet detected in patients with IDC.…”

Section: Discussionmentioning

confidence: 99%

Comparação do desfecho entre a cardiopatia chagásica e a miocardiopatia dilatada idiopática

Barbosa¹,

Neto²,

Otaviano³

et al. 2011

Arq. Bras. Cardiol.

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“…However, there are also similarities between Chagas cardiomyopathy pathophysiology and the mechanisms described in heart failure syndrome in general. Specifically, authors have reported that intracardiac sympathetic overactivity seems to occur in patients with Chagas disease and chronic heart failure, 26 and that catecholamines levels are increased in patients with Chagas disease and correlated with disease severity, 27 suggesting that the sympathetic activity play a significant role in the disease progression. 11 In resonance with this rationale, our results do support the use of ␤-blockers therapy in patients with Chagas cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

β-Blocker Therapy and Mortality of Patients With Chagas Cardiomyopathy

Issa

Amaral

Cruz

et al. 2010

Circ: Heart Failure

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Background-Peculiar aspects of Chagas cardiomyopathy raise concerns about efficacy and safety of sympathetic blockade. We studied the influence of ␤-blockers in patients with Chagas cardiomyopathy. Methods and Results-We examined REMADHE trial and grouped patients according to etiology (Chagas versus non-Chagas) and ␤-blocker therapy. Primary end point was all-cause mortality or heart transplantation. Altogether 456 patients were studied; 27 (5.9%) were submitted to heart transplantation and 202 (44.3%) died. compared with those who received ␤-blockers. Survival was lower in patients with Chagas heart disease as compared with other etiologies. When only patients under ␤-blockers were considered, the survival of patients with Chagas disease was similar to that of other etiologies. The survival of patients with ␤-blockers was higher than that of patients without ␤-blockers. In Cox regression model, left ventricle end-diastolic diameter (hazard ratio, 1.78; CI, 1.15 to 2.76; Pϭ0.009) and ␤-blockers (hazard ratio, 0.37; CI, 0.14 to 0.97; Pϭ0.044) were associated with better survival. Conclusions-Our study suggests that ␤-blockers may have beneficial effects on survival of patients with heart failure and Chagas heart disease and warrants further investigation in a prospective, randomized trial. Clinical Trial Registration-clinicaltrials.gov. Identifier: NCT00505050.(Circ Heart Fail. 2010;3:82-88.)

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Peripheral and Coronary Sinus Catecholamine Levels in Patients with Severe Congestive Heart Failure due to Chagas’ Disease

Cited by 42 publications

References 15 publications

Mechanisms of pathogenesis in Chagas disease

Mechanisms of pathogenesis in Chagas disease

Comparação do desfecho entre a cardiopatia chagásica e a miocardiopatia dilatada idiopática

β-Blocker Therapy and Mortality of Patients With Chagas Cardiomyopathy

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