The prolonged use of DIPY in this experimental model of CCC has reduced the rest myocardial perfusion defects, supporting the notion that those areas correspond to viable hypoperfused myocardium.
Altered myocardial perfusion is a common finding in chronic Chagas cardiomyopathy (CCC), but its underlying histologic changes have not been elucidated. We investigated the occurrence of myocardial perfusion defects (MPDs) and the correlated regional changes to histology in an experimental model of CCC in hamsters. Female Syrian hamsters ( = 34) were infected with 3.5 × 10 to 10 trypomastigote forms of Y strain, and 6-10 mo afterward underwent in vivo imaging including restingTc-sestamibi SPECT, segmental and global left ventricular function assessment using 2-dimensional echocardiography, and F-FDG PET for evaluation of myocardial viability. Histologic analysis included quantification of fibrosis, inflammatory infiltration, and the diameter and density of myocardial microcirculation. MPDs were present in 17 (50%) of the infected animals. Histologic analysis revealed no transmural scar in segments with an MPD, and normal or mildly reduced F-FDG uptake, indicating viable myocardium. Infected animals with an MPD, in comparison to infected animals without an MPD and control animals, showed a lower left ventricular ejection fraction ( = 0.012), a higher wall motion score index ( = 0.004), and a higher extent of inflammatory infiltration ( = 0.018) but a similar extent of fibrosis ( = 0.15) and similar microvascular diameter and density ( > 0.05). Segments with an MPD ( = 65), as compared with normally perfused regions in the same animal ( = 156), showed a higher wall motion score index ( = 0.005) but a similar extent of inflammatory infiltration, a similar extent of fibrosis, and a similar microvascular diameter and density. Resting MPDs are frequent in experimental CCC and are associated with myocardial inflammation but do not designate scar tissue, corresponding to regions with metabolically viable myocardium.
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