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Myocardial perfusion disturbance precedes LV systolic dysfunction in experimental model of chronic Chagas cardiomyopathy

Session Poster session 1 - Basic Science

Speaker Associate Professor Marcus Vinicius Simoes

Event : Heart Failure 2018

  • Topic : heart failure
  • Sub-topic : Chronic Heart Failure – Diagnostic Methods: Imaging
  • Session type : Poster Session

Authors : L F L Oliveira (Ribeirao Preto,BR), J T Thackeray (Hannover,DE), D M Tanaka (Ribeirao Preto,BR), J A Marin-Neto (Ribeirao Preto,BR), M M D Romano (Ribeirao Preto,BR), C D Lopes (Ribeirao Preto,BR), A C L Barros-Filho (Ribeirao Preto,BR), F F F Ribeiro (Ribeirao Preto,BR), J Mejia (Sao Paulo,BR), C Malamut (Belo Horizonte,BR), F M Bengel (Hannover,DE), E Cunha-Neto (Sao Paulo,BR), M L Higuchi (Sao Paulo,BR), S G Nekolla (Munich,DE), M V Simoes (Ribeirao Preto,BR)

Authors:
L F L Oliveira1 , J T Thackeray2 , D M Tanaka1 , J A Marin-Neto1 , M M D Romano1 , C D Lopes1 , A C L Barros-Filho1 , F F F Ribeiro1 , J Mejia3 , C Malamut4 , F M Bengel2 , E Cunha-Neto5 , M L Higuchi5 , S G Nekolla6 , M V Simoes1 , 1Medical School of Ribeirao Preto - University of Sao Paulo - Ribeirao Preto - Brazil , 2Hannover Medical School, Department of Nuclear Medicine - Hannover - Germany , 3Hospital Israelita Albert Einstein - Sao Paulo - Brazil , 4Nuclear Technology Development Center (CDTN), Radiopharmaceutical Production and Development Unit - Belo Horizonte - Brazil , 5Heart Institute of the University of Sao Paulo (InCor) - Sao Paulo - Brazil , 6Technical University of Munich, Department of Nuclear Medicine - Munich - Germany ,

Citation:

Background: Myocardial perfusion defect (MPD) is a common finding in Chronic Chagas cardiomyopathy (CCC), but it is unclear if the perfusion derangement can precede the left ventricular (LV) systolic dysfunction. We investigated the time-course of myocardial perfusion changes and the correlation with the progression of LV systolic dysfunction in an experimental model of CCC.

Methods: Female Syrian hamsters (n=40) were infected with 3.5x104 trypomastigotes forms of T. cruzi Y-strain and the surviving animals (n= 22) were submitted to in vivo imaging 2, 4, 6, 8 and 10-months afterwards. Rest high-resolution SPECT imaging using 99mTc-sestamibi was used to assess MPD extension that was analyzed by using polar maps and compared to matched control animal database. The left ventricular (LV) systolic function was assessed by using 2D-echocardiogram. The animals underwent PET imaging for assessment of myocardial inflammation using 18F-FDG under myocardial uptake suppression conditions at 10-months after infection and co-registered with SPECT images. Histological analysis included quantification of myocardial fibrosis.

Results:  Compared to control animals, 7 out of 22 (32%) infected animals showed significant LV ejection fraction (LVEF) deterioration after 8-months (69±2% and 61±11%, respectively, p=0.03), and after 10-months (70±2% vs 54±10%, respectively, p=0.0002). Individual animals presented MPD at 2-months and progressive deterioration after 6-monts after infection. All animals that died during protocol, presented MPD in the last assessment. LVEF at 10m negatively correlated with MPD at 6m (r= -0.58, p=0.005), 8m (r= -0.62, p=0.002) and 10m (r= -0.7, p=0.0001). Animals with MPD showed higher 18F-FDG uptake topographically correlated with the LV regions with MPD. Segments with MPD in comparison to segments with normal perfusion displayed higher %ID/g (0.15±0.02 vs 0.13±0.03, p= 0.005), SUV (g/cc, 0.28±0.040 vs 0.23±0.05, p<0.0001) but similar extent of histological fibrosis (21±7.6% vs 22.9±7.1%, p=0.3). Compared to controls animals, infected animals presented higher interstitial fibrosis (%, 15±6 vs 9±1, p=0.002), however no transmural scar was revealed. Conclusions: Rest MPD precedes the development and correlates with the ulterior deterioration of LV systolic dysfunction in experimental CCC. The MPD was topographically associated with elevated 18F-FDG uptake, suggesting a correlation between inflammation and the myocardial perfusion derangement. Our findings suggest that MPD may be a surrogated marker of myocardial inflammation in CCC and raise the possibility of using perfusion imaging for risk stratification and monitoring the course of this myocardial disease.

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