[Endothelial function and high-sensitivity C-reactive protein levels in patients with Chagas disease living in a nonendemic area]

Introduction and objectives: The number of patients with Chagas disease in Spain has increased significantly. Chronic inflammation and endothelial dysfunction have been considered among the physiopathological mechanisms of Chagas heart disease. However, there have been conflicting data from clinical studies. Our purpose was to assess endothelial function and systemic levels of nitric oxide and high-sensitivity C-reactive protein in patients with the indeterminate form and with chronic Chagas cardiomyopathy living in a nonendemic area.

Methods: Flow-mediated endothelium-dependent vasodilatation and nitroglycerin-mediated vasodilatation were assessed with high-resolution ultrasound of the brachial artery in 98 subjects (32 with the indeterminate form, 22 with chronic Chagas cardiomyopathy and 44 controls). Nitric oxide and high-sensitivity C-reactive protein levels were measured in peripheral venous blood.

Results: Mean age was 37.6 ± 10.2 years and 60% were female. Nitroglycerin-mediated vasodilatation was significantly reduced in chronic Chagas cardiomyopathy compared to controls (median 16.8% vs 22.5%; P=.03). No significant differences were observed in flow-mediated vasodilatation and nitric oxide levels, although a trend towards lower flow-mediated vasodilatation after correction by baseline brachial artery diameter was observed in chronic Chagas cardiomyopathy. Levels of C-reactive protein were significantly higher in patients with the indeterminate form and with Chagas cardiomyopathy compared with controls (P<.05).

Conclusions: Reduced nitroglycerin-mediated vasodilatation suggesting dysfunction of vascular smooth muscle cells was found in patients with chronic Chagas cardiomyopathy living in a nonendemic area. Higher C-reactive protein levels were observed in the indeterminate form and early stages of chronic Chagas cardiomyopathy, which could be related to the inflammatory response to the infection or early cardiovascular involvement.