Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, Brazil.
Department of Nuclear Medicine, Hannover Medical School, Hannover, Germany.
J Nucl Med. 2018 Sep;59(9):1430-1436. doi: 10.2967/jnumed.117.205450. Epub 2018 Apr 26.
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 resting Tc-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.
慢性恰加斯心肌病（CCC）患者常存在心肌灌注异常，但具体的组织学变化尚未阐明。我们在仓鼠 CCC 实验模型中研究了心肌灌注缺陷（MPD）的发生及其与组织学的相关性。 雌性叙利亚仓鼠（n=34）感染 3.5×10 至 10 个 Y 株的锥虫体，6-10 个月后行静息 Tc- sestamibi SPECT 检查、二维超声心动图评估节段和整体左心室功能，以及 F-FDG PET 评估心肌活力。组织学分析包括纤维化、炎症浸润、心肌微循环直径和密度的定量。 在 17 只（50%）感染动物中存在 MPD。组织学分析显示，MPD 节段无穿透性瘢痕，且 F-FDG 摄取正常或轻度减少，提示存活心肌。与无 MPD 的感染动物和对照动物相比，存在 MPD 的感染动物的左心室射血分数较低（=0.012），壁运动评分指数较高（=0.004），炎症浸润程度较高（=0.018），但纤维化程度相似（=0.15），微血管直径和密度相似（>0.05）。与同一动物中正常灌注区域（n=156）相比，存在 MPD 的节段壁运动评分指数较高（=0.005），但炎症浸润程度、纤维化程度和微血管直径和密度相似。 实验性 CCC 中常存在静息 MPD，与心肌炎症相关，但不代表瘢痕组织，与代谢存活心肌的区域相对应。
