Artery Research (Dec 2017)

4.1 PILOT STUDY ON THE PRECLINICAL VASCULAR DAMAGE IN BOLIVIAN PATIENTS WITH CHAGAS INDETERMINATE CHRONIC PHASE

  • Filippo Valbusa,
  • Andrea Angheben,
  • Verena Zerbato,
  • Andrea Chiampan,
  • Davide Agnoletti,
  • Cristiano Fava,
  • Zeno Bisoffi,
  • Guido Arcaro

DOI
https://doi.org/10.1016/j.artres.2017.10.039
Journal volume & issue
Vol. 20

Abstract

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Background: In Italy, the prevalence of seropositivity for Trypanosoma cruzi in immigrants from endemic countries is about 11.3% (30.7% for Bolivian immigrants). The disease acute phase is usually asymptomatic, often leading to chronic infection that may remain silent for life (chronic indeterminate phase). Chagas heart disease is the most severe and frequent (20–30%) form of chronic phase; its pathophysiology shares similar mechanisms with the arterial impairment associated to other diseases (diabetes, hypertension, aging), leading to chronic inflammation and stiffening. In literature there are no data about the possible elastic arteries deterioration in Chagas disease. Our hypothesis was that early arterial compliance modifications might be found in the chronic indeterminate phase of Chagas disease. Methods: 35 consecutive Bolivian subjects (21 with indeterminate Chagas disease, mean age [SD] 44.2 [8.2], 5 women, and 14 controls, mean age 40.2 [8.2], 5 women) accessing the service of Tropical Medicine were enrolled. Staging of the disease, laboratory assay, and hemodynamics (central and peripheral blood pressure [BP], aortic pulse wave velocity [PWV], carotid intima media thickness, cardiac ultrasound) were assessed. Results: No clinical nor laboratory differences were found between the cases and controls. Peripheral and central BPs components were similar. Chagas patients presented higher PWV than controls (7.87 ± 1.29 vs 6.43 ± 1.12 m/s, p = 0.002), even when adjusting for age, mean BP, heart rate, body mass index, smoking status (p = 0.001). Conclusion: Patients with Chagas indeterminate chronic phase presented higher arterial stiffness than controls, pointing out an early arterial involvement as the possible etiological mechanism underlying the increased cardiovascular risk in these patients.