Key result
Trypanosoma cruzi infection links to systolic impairment in ~24% of cases without coronary microcirculation differences.
Why the study?
Does myocardial contrast echocardiography detect microvascular abnormalities associated with systolic function impairment in baboons with Chagas disease?
Observational (n=30)
Does myocardial contrast echocardiography detect microvascular abnormalities associated with systolic function impairment in baboons with Chagas disease?
MCE reveals preserved coronary microcirculation at rest despite myocardial contractility alterations in a baboon model of Chagas disease.
Systolic impairment without microcirculatory changes in this Chagas baboon model is hypothesis-generating; leaves open microvascular role in human progression.
OBJECTIVE: Microvascular abnormalities have been postulated in the pathogenesis of chagasic cardiomyopathy. The objective of this study was to evaluate the relationship between coronary microcirculation and systolic function impairment in baboons with Chagas disease using myocardial contrast echocardiography (MCE). METHODS: Seventeen seropositive (5 males, 12 females; mean age 20 years) and 13 age- and gender-matched seronegative baboons underwent MCE using intravenous octafluoropropane human albumin microspheres. Color-coding was used to enhance tissue contrast in assessing regional myocardium uniformity and texture. Dipyridamole (0.54 mg/kg) was given to a subset of 4 animals to challenge coronary flow reserve. Systolic indices included left ventricular fractional shortening, velocity of circumferential fiber shortening, and left and right ventricular ejection fractions. RESULTS: Four of the 17 (24%) seropositive primates had decreased fractional shortening (25 +/- 8% vs. 40 +/-5%, p <.005), velocity of circumferential fiber shortening (1.05 +/- 0.36 circ/s vs. 1.84 +/- 0.23 circ/s, p <.0001), and reduced right ventricular ejection fraction (44 +/- 9% vs. 54 +/- 4%, p <.05) compared to other seropositive animals. Seropositive and seronegative groups showed no significant differences on the coronary microcirculation pattern as evaluated by MCE, including the 4 baboons with systolic function impairment. Moreover, coronary flow vasoreactivity resulted in a significant increase in myocardial flow as detected by color-coding masking. CONCLUSIONS: Chagasic heart disease is present in 24% of seropositive baboons spontaneously infected with Trypanosoma cruzi. MCE reveals a discrepancy between coronary microcirculation at rest and alterations in myocardial contractility, suggesting preservation of the microvascular integrity in this unique animal model.
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Zabalgoitia et al. (2004) conducted an observational in Chagas disease (n=30). Trypanosoma cruzi infection vs. Seronegative controls was evaluated on Coronary microcirculation pattern. Trypanosoma cruzi infection in baboons was associated with systolic impairment in 24% of cases, but showed no significant differences in coronary microcirculation compared to seronegative controls.
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