Effects of pentoxifylline in patients with chronic Chagas cardiomyopathy: A randomized, double-blind, controlled pilot trial.

BACKGROUND

Chronic Chagas cardiomyopathy (CCC) is a major public health issue in endemic areas of Latin America, representing one of the leading causes of heart failure and sudden death. The hallmark histopathological lesion of CCC is low-intensity, persistent myocarditis associated with cytokine production. Long-term use of pentoxifylline (PTX) may serve as an effective pharmacological intervention for immunomodulation, reducing inflammation and, consequently, diminishing myocardial perfusion abnormalities and thus preserving left ventricular systolic function.

METHODS

We investigated 38 patients with CCC, randomly assigned to PTX (n = 19), 400 mg 3 times a day for 6 months, or placebo (PLC) (n = 19). At baseline and post-treatment, patients underwent cytokine measurements, quality of life assessment, 2D echocardiography, and myocardial perfusion scintigraphy. After treatment, TNF-α levels in the PTX group decreased from 10.14 ± 5.5 to 8.32 ± 3.6 and from 9.12 ± 4.4 to 10.32 ± 8.5 in the PLC group (p = 0.06). Additionally, IL-10 levels increased from 2.74 ± 0.7 to 5.61 ± 8.6 in the PTX group, while in the placebo group, they decreased from 6.96 ± 11.8 to 5.50 ± 8.3 (p = 0.09); neither of these findings reached statistical significance. Also, no significant changes were observed in the echocardiographic variables after treatment. LVEF showed a modest change from 46.2% ± 7.9 to 47.4% ± 7.0 in the PTX group and from 48.2% ± 6.6 to 48.0% ± 6.9 in the PLC group (p = 0.37). No significant positive effects on myocardial perfusion were noted. However, the quality-of-life assessment documented a significant improvement of functional capacity in the PTX group.

CONCLUSIONS

The results of this study suggest a potential positive effect of PTX in modulating the inflammatory profile of CCC patients. However, use of pentoxifylline in these patients did not attenuate the degree of ventricular dysfunction or reduce myocardial perfusion defects.