Why the study?
Despite advances in understanding the mechanisms underlying high mortality in chronic Chagas cardiomyopathy, this knowledge has not been efficiently translated into specific diagnostic and therapeutic approaches.
This review outlines the three main pathophysiological mechanisms driving the high mortality in chronic Chagas cardiomyopathy: progressive heart failure, stroke, and ventricular arrhythmias.
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Identifies HF progression, stroke, and arrhythmias as mortality targets in Chagas cardiomyopathy; leaves open optimal strategies pending prospective trials.
Chagas disease is a neglected tropical disease caused by the parasite Trypanosoma cruzi. Chronic Chagas cardiomyopathy (CCC), the most severe form of target organ involvement in Chagas disease, is characterized by a complex pathophysiology and a unique phenotype that differentiates it from other cardiomyopathies, highlighting its worse prognosis compared to other aetiologies of heart failure. The three pathophysiological mechanisms with the largest impact on this differential mortality include rapidly progressive heart failure, a high incidence of stroke, and a high burden of ventricular arrhythmias. However, despite significant advances in understanding the unique molecular circuits underlying these mechanisms, the new knowledge acquired has not been efficiently translated into specific diagnostic and therapeutic approaches for this unique cardiomyopathy. The lack of dedicated clinical trials and the limited CCC-specific risk stratification tools available are evidence of this reality. This review aims to provide an updated perspective of the evidence and pathophysiological mechanisms associated with the higher mortality observed in CCC compared to other cardiomyopathies and highlight opportunities in the diagnostic and therapeutic approaches of the disease.
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Echeverría et al. (2024) studied this question.
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