High plasma immunoreactive endothelin levels in patients with Chagas’ cardiomyopathy

Abstract

Chagas’disease is a major cause of morbidity and death in South America,1 where a great proportion of seropositive patients with chronic infection by Trypanosoma cruzi (T. cruzi) develop dilated cardiomyopathy, whose pathophysiology remains elusive. Because T. cruzi is seldom isolated from blood or tissue of chronically infected patients, several pathophysiologic mechanisms other than direct myocardial aggression by the parasite have been proposed.2,3 One of these focuses on the frequent coronary microvascular alterations found in patients with Chagas’ cardiomyopathy, which may lead to myocardial damage and dysfunction through different mechanisms, including myocardial ischemia. This “microvascular hypothesis” has received strong support from experimental4,5 and clinical observations.6,7 Plasma endothelin-1, a powerful vasoconstrictor peptide, has been found to be elevated in a number of cardiac conditions associated with endothelial injury and dysfunction.8,9 Wittner et al10 recently reported that human endothelial cells infected with T. cruzi release endothelin-1, suggesting a role for endothelins in the genesis of microvascular dysfunction as observed in patients with Chagas’cardiomyopathy. In the present study, we sought to assess the relation between plasma endothelin-1 levels and Chagas’cardiomyopathy in a group of patients with positive serology for chronic T. cruzi infection.