The higher frequency of appropriate ICD therapy and the shorter event-free survival in ChD patients are consistent with the presence of an arrhythmogenic substrate that characterizes this cardiomyopathy.

Sudden death is one of the most characteristic phenomena of Chagas disease, and approximately one-third of infected patients develop life-threatening heart disease, including malignant ventricular arrhythmias. Fibrotic lesions secondary to chronic cardiomyopathy produce arrhythmogenic substrates that lead to the appearance and maintenance of ventricular arrhythmias. The objective of this study is to discuss the main clinical and epidemiological aspects of ventricular arrhythmias in Chagas disease, the specifi c workups and treatments for these abnormalities, and the breakthroughs needed to determine a more effective approach to these arrhythmias. A literature review was performed via a search of the PubMed database from 1965 to May 31, 2014 for studies of patients with Chagas disease. Clinical management of patients with chronic Chagas disease begins with proper clinical stratifi cation and the identifi cation of individuals at a higher risk of sudden cardiac death. Once a patient develops malignant ventricular arrhythmia, the therapeutic approach aims to prevent the recurrence of arrhythmias and sudden cardiac death by the use of implantable cardioverter defi brillators, antiarrhythmic drugs, or both. In select cases, invasive ablation of the reentrant circuit causing tachycardia may be useful. Ventricular arrhythmias are important manifestations of Chagas cardiomyopathy. This review highlights the absence of high-quality evidence regarding the treatment of ventricular arrhythmias in Chagas disease. Recognizing high-risk patients who require specifi c therapies, especially invasive procedures such as the implantation of cardioverter defi brillators and ablative approaches, is a major challenge in clinical practice.

The vasodilator effects of Ouratea semiserrata stem hydroethanolic extract (OSE) and its ethyl acetate fraction (OSR) were evaluated in endothelium-intact aortic rings. OSR produced a more potent vasodilatation (IC(50) = 3.5 +/- 0.8 microg/ml) than OSE (IC(50) > 30 microg/ml). OSR also presented a higher content of total proanthocyanidins (21.8 +/- 1.5 %) in comparison to OSE (6.5 +/- 0.4 %), suggesting that compounds of this class play a role in the vasorelaxing activity. The vasodilatation mechanism of OSR was further investigated. In endothelium-intact aortic rings, its vasorelaxing effect was completely abolished by L-NAME (300 microM), a nitric oxide (NO) synthase inhibitor, but not by a muscarinic antagonist (atropine, 1 microM) nor by a cyclo-oxygenase inhibitor (indomethacin, 10 microM). The OSR vasodilator effect was completely abolished in endothelium-denuded vessels. Furthermore, OSR did not change the vasodilatation produced by SIN-1, an NO donor, in endothelium-denuded vessels. These findings led us to conclude that OSR, a proanthocyanidin rich fraction of O. semiserrata, induces vasodilatation by a mechanism dependent on endothelium-derived factors, likely NO.

HighlightsCoronary artery disease (CAD) is one of the main causes of death.The stress test is indispensable before cardiac rehabilitation.The 6MWT is a simple, low-cost, valid, and reliable method.The 6MWT can be used safely in the hospital after an AMI.