Cardiac resynchronization therapy for patients with chronic systolic heart failure secondary to Chagas cardiomyopathy in the 21st century

In the 21st century, Chagas disease continues to be a major health problem in South America because it affects 10 million people, and other 20 million are at risk of acquiring the disease [1]. It must be emphasized, however, that the disease is no longer confined to South America due to international immigration. In fact, Chagas disease has persistently been identified in non-endemic countries such United States, Spain, Canada, and Australia [1]. As a result, the global economic burden of the disease is impressive, reaching the figure of US 8 billion annually [2]. Chagas disease is caused by the protozoan Trypanosoma cruzi, which is transmitted to humans when the feces of a sucking bug contaminate a skin lesion or eye mucosae [1]. However, chronic Chagas disease appears many years after initial infection (in general, up two decades). Chagas cardiomyopathy is the protean clinical manifestation of the chronic disease, manifesting by ventricular dysrhythmias [3], sudden cardiac death [4], thromboembolism [5], and chronic heart failure (CHF) [6]. In Chagas disease patients, CHF is associated with reduced systolic function, as no case of CHF with preserved left ventricular function has been described in patients with this condition. The disease can affect up to 5% of patients of a population-based and about 50% of a referral center-based cohort [6]. Chagas disease heart failure has a higher annual mortality [7], and its prognosis is worse than that observed in non-Chagas disease heart failure [8]. Irreversible left ventricular systolic dysfunction is the most frequent mode of death in patients with this condition in the contemporary era [9]. The pathogenesis of Chagas disease heart failure is similar to that seen in non-Chagas disease heart failure, with the neurohormonal activation playing a pivotal role. In addition, an intracardiac autonomic imbalance [10] can expose the myocardium to the toxic effects of catecholamine [11]. Some studies suggest a benefit effect for angiotensin converting enzyme inhibitor as well as for beta-blocker therapy both experimentally [12] and in patients with this condition [8,13,14]. Obviously, other types of treatment modality are necessary, mainly in patients in the advanced stages of CHF.