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

Barbosa, Amanda Pires; Neto, Augusto Cardinalli; Otaviano, Ana Paula; Rocha, Bianca Faria da; Bestetti, Reinaldo B.

doi:10.1590/s0066-782x2011005000112

Cited by 43 publications

(25 citation statements)

References 30 publications

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“…It has been observed that the occurrence of myocarditis is correlated with clinical severity, ASY patients having minimal inflammation, while patients with advanced CCC display frequent and intense myocarditis [5]. Approximately 1/3 of patients developing CCC present a particularly lethal form of dilated cardiomyopathy, with shorter survival than idiopathic dilated cardiomyopathy [6]. In addition, CCC is associated with a worse prognosis and survival than other cardiomyopathies of non-inflammatory etiology (NIC) [7].…”

Section: Introductionmentioning

confidence: 99%

Myocardial Chemokine Expression and Intensity of Myocarditis in Chagas Cardiomyopathy Are Controlled by Polymorphisms in CXCL9 and CXCL10

et al. 2012

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BackgroundChronic Chagas cardiomyopathy (CCC), a life-threatening inflammatory dilated cardiomyopathy, affects 30% of the approximately 8 million patients infected by Trypanosoma cruzi. Even though the Th1 T cell-rich myocarditis plays a pivotal role in CCC pathogenesis, little is known about the factors controlling inflammatory cell migration to CCC myocardium.Methods and ResultsUsing confocal immunofluorescence and quantitative PCR, we studied cell surface staining and gene expression of the CXCR3, CCR4, CCR5, CCR7, CCR8 receptors and their chemokine ligands in myocardial samples from end-stage CCC patients. CCR5+, CXCR3+, CCR4+, CCL5+ and CXCL9+ mononuclear cells were observed in CCC myocardium. mRNA expression of the chemokines CCL5, CXCL9, CXCL10, CCL17, CCL19 and their receptors was upregulated in CCC myocardium. CXCL9 mRNA expression directly correlated with the intensity of myocarditis, as well as with mRNA expression of CXCR3, CCR4, CCR5, CCR7, CCR8 and their ligands. We also analyzed single-nucleotide polymorphisms for genes encoding the most highly expressed chemokines and receptors in a cohort of Chagas disease patients. CCC patients with ventricular dysfunction displayed reduced genotypic frequencies of CXCL9 rs10336 CC, CXCL10 rs3921 GG, and increased CCR5 rs1799988CC as compared to those without dysfunction. Significantly, myocardial samples from CCC patients carrying the CXCL9/CXCL10 genotypes associated to a lower risk displayed a 2–6 fold reduction in mRNA expression of CXCL9, CXCL10, and other chemokines and receptors, along with reduced intensity of myocarditis, as compared to those with other CXCL9/CXCL10 genotypes.Conclusions Results may indicate that genotypes associated to reduced risk in closely linked CXCL9 and CXCL10 genes may modulate local expression of the chemokines themselves, and simultaneously affect myocardial expression of other key chemokines as well as intensity of myocarditis. Taken together our results may suggest that CXCL9 and CXCL10 are master regulators of myocardial inflammatory cell migration, perhaps affecting clinical progression to the life-threatening form of CCC.

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Section: Introductionmentioning

confidence: 99%

Myocardial Chemokine Expression and Intensity of Myocarditis in Chagas Cardiomyopathy Are Controlled by Polymorphisms in CXCL9 and CXCL10

et al. 2012

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“…20,000 deaths attributable to Chagas disease occur annually, typically due to CCC [3]. Heart failure due to CCC has a worse prognosis with 50% shorter survival when compared to other cardiomyopathies of different etiologies [4,5]. …”

Section: Introductionmentioning

confidence: 99%

Genetic susceptibility to Chagas disease cardiomyopathy: involvement of several genes of the innate immunity and chemokine-dependent migration pathways

et al. 2013

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BackgroundChagas disease, caused by the protozoan Trypanosoma cruzi is endemic in Latin America. Thirty percent of infected individuals develop chronic Chagas cardiomyopathy (CCC), an inflammatory dilated cardiomyopathy that is, by far, the most important clinical consequence of T. cruzi infection. The others remain asymptomatic (ASY). A possible genetic component to disease progression was suggested by familial aggregation of cases and the association of markers of innate and adaptive immunity genes with CCC development. Migration of Th1-type T cells play a major role in myocardial damage.MethodsOur genetic analysis focused on CCR5, CCL2 and MAL/TIRAP genes. We used the Tag SNPs based approach, defined to catch all the genetic information from each gene. The study was conducted on a large Brazilian population including 315 CCC cases and 118 ASY subjects.ResultsThe CCL2rs2530797A/A and TIRAPrs8177376A/A were associated to an increase susceptibility whereas the CCR5rs3176763C/C genotype is associated to protection to CCC. These associations were confirmed when we restricted the analysis to severe CCC, characterized by a left ventricular ejection fraction under 40%.ConclusionsOur data show that polymorphisms affecting key molecules involved in several immune parameters (innate immunity signal transduction and T cell/monocyte migration) play a role in genetic susceptibility to CCC development. This also points out to the multigenic character of CCC, each polymorphism imparting a small contribution. The identification of genetic markers for CCC will provide information for pathogenesis as well as therapeutic targets.

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“…RBBB and left anterior fascicular block are found in about 40 % of patients with Chagas heart failure, which is higher than that seen in CHF due to other types of cardiomyopathy. 17,18,21 The association between RBBB and left anterior fascicular block, which is more frequent in patients with Chagas cardiomyopathy, 22 should alert physicians to the possibility of Chagas heart failure. In contrast, the prevalence of left bundle branch block (LBBB), which is frequently found in patients with non-Chagas cardiomyopathy, 23 is lower in Chagas heart failure.…”

Section: Peculiarities Of Subsidiary Testsmentioning

confidence: 99%

Chagas Heart Failure in Patients from Latin America

Bestetti

2016

Cardiac Failure Review

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Physicians working in Europe and the United States should suspect Chagas heart failure in every patient coming from Latin America with chronic heart failure. Diagnosis should be confirmed by positive serology. Right bundle branch block and left anterior fascicular block on 12-lead electrocardiogram, enlarged cardiac silhouette with no pulmonary congestion on chest X-ray and left ventricular apical aneurysm on echocardiography are the distinctive features of this condition. The clinical course is poorer than that of non-Chagas heart failure; however, medical treatment is similar. Implantable cardioverter-defibrillators are useful in the primary and secondary prevention of sudden cardiac death. Cardiac resynchronisation therapy can be given to patients on optimal medical therapy and with lengthened QRS complex. Heart transplantation is the treatment of choice for patients with end-stage Chagas heart failure.

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

Abstract: Background: Little is known about the outcome of patients with Chagas cardiomyopathy in comparison to that of patients with Idiopathic Dilated Cardiomyopathy in the contemporary era.

Cited by 43 publications

References 30 publications

Myocardial Chemokine Expression and Intensity of Myocarditis in Chagas Cardiomyopathy Are Controlled by Polymorphisms in CXCL9 and CXCL10

Myocardial Chemokine Expression and Intensity of Myocarditis in Chagas Cardiomyopathy Are Controlled by Polymorphisms in CXCL9 and CXCL10

Genetic susceptibility to Chagas disease cardiomyopathy: involvement of several genes of the innate immunity and chemokine-dependent migration pathways

Chagas Heart Failure in Patients from Latin America

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