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Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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A 37 years old Bolivian male was referred for cardiac evaluation after finding a right bundle branch block on an ECG performed in medical check-up exam at work (figure 1).
ChD is caused by infection with the protozoan parasite Trypanosoma cruzi. Historically, the disease occurred predominantly in rural areas of Latin America where poor housing conditions facilitates recurrent contact with infected vectors. However, given the new patterns of immigration and the introduction of successful programs to reduce transmission in endemic areas, the epidemiology of the disease is changing .The natural history of Chagas heart disease comprises an acute phase, an indeterminate form, and a cardiomyopathy form in the chronic phase. Approximately one-third to one-half of patients eventually develops chronic Chagas cardiomyopathy (CChC), which is characterized by biventricular dilatation. Clinical manifestations range from asymptomatic to heart failure, cardiac arrhythmias, thromboembolism (systemic and pulmonary), and chest pain. The most common ECG abnormalities are right bundle branch block often associated with left anterior fascicular block and diffuse ST-T changes. Abnormal Q waves, various degrees of AV block, QT interval prolongation, and variation in the QT interval (QT dispersion) can also be seen. Echocardiography may demonstrate one or more areas of hypokinesia or dyskinesia. Left ventricular apical aneurysm is also common in patients with moderate to severe cardiac impairment . Sudden cardiac death (SD) accounts for approximately 60% of deaths in patients with CChC. It is often precipitated by exercise and can be caused by ventricular tachycardia or fibrillation, asystole, or complete AV block . Another relevant pathophysiologic mechanism of ventricular arrhythmias and sudden death in CChC may be related to the extensive myocardial sympathetic denervation . Mortality rate for patients presenting with heart failure due to CChD is higher than that reported in other heart failure associated conditions .Major risk factors for mortality in patients with CChC are heart failure, evidence of left ventricular dilatation or systolic dysfunction, and non-sustained ventricular tachycardia (NSVT). A risk score (Rassi score) for mortality has been developed and validated. Six independent predictors have been proposed: NYHA class III/IV (5 points), cardiomegaly on chest X-ray (5 points), left ventricular systolic dysfunction on echocardiogram (3 points), NSVT on Holter monitoring (3 points), low QRS voltage (2 points) and male gender (2 points). According to the Rassi score, our patient would have been classified as low risk (5 points), providing that Holter monitoring was not performed in our patient. In this study, the combination of left ventricular systolic dysfunction and NSVT was associated with particularly high risk (15.1 fold increase risk of death) .Although data on treatment of chronic ChD are limited, most experts recommend antitrypanosomal therapy, using Benznidazole as first-line agent, to treat patients with chronic infection up to 50 years of age including those with evidence of early Chagas heart disease (eg, isolated ECG abnormalities) but not in those with advanced CChC [7,8]. The results from BENEFIT, a large multicenter randomized controlled trial of trypanocidal therapy in patients with Chagas heart disease is ongoing and will provide useful information.Appropriate measures to reduce SD risk in patients with CChC are uncertain due to paucity of data. No randomized clinical trials had evaluated primary prevention of SD in patients with ChD. The 2008 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) guidelines for device-based therapy of arrhythmias recommend ICD implantation for primary prevention in patients with non-ischaemic dilated cardiomyopathy with an LVEF ≤35 percent and NYHA functional class II or III. However, these guidelines include scant discussion of treatment of CChC. They note only that ICD implantation is reasonable for patients with ChD . According to the international guidelines at the moment of our evaluation our patient did not have a definite indication to ICD implantation.
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