TY - JOUR T1 - Comparative analysis of multi-modality cardiac imaging for prediction of postoperative myocardial infarction JF - Journal of Nuclear Medicine JO - J Nucl Med SP - 1665 LP - 1665 VL - 62 IS - supplement 1 AU - Wanwan Wen AU - Mingxin Gao AU - Jingjing Meng AU - Yujie Bai AU - Xiang Li AU - Xiaoli Zhang Y1 - 2021/05/01 UR - http://jnm.snmjournals.org/content/62/supplement_1/1665.abstract N2 - 1665Background: Predicting postoperative myocardial infarction (PMI) is important after coronary artery bypass grafting (CABG) in patients with coronary artery disease (CAD). Objectives: To validate and compare the value of coronary microcalcification, macrocalcification, stenosis, and serum inflammatory biomarkers in PMI prediction. Methods: We prospectively recruited 81 CAD patients scheduled for CABG. Patients underwent cardiac 18F-NaF PET/CT, coronary angiography, and coronary artery calcium (CAC) scoring. The target-to-blood ratio (TBR) in each coronary territory was calculated separately. Maximum coronary microcalcification activity (CMimax) and global coronary microcalcification activity (CMiglobal) were represented as the highest and average coronary 18F-NaF uptake, respectively. Optimal threshold TBRs for predicting vulnerable plaques and PMI were determined. Results: Seventy-five CAD patients were enrolled. CMimax (odds ratio 1.53, P=0.014) and CMiglobal(odds ratio 1.98, P=0.023) were significantly correlated with PMI. CMimax≥3.04 presented a sensitivity 82.4%, specificity 55.4%, (P=0.019) or CMiglobal≥2.85 presented a sensitivity 64.7%, specificity 71.4%, (P=0.015) for predicting PMI. CMi in the left anterior descending (CMiLAD-max) and CMi in the right coronary artery (CMiRCA-max) were significantly correlated with PMI in the anterior wall (PMIanterior) (odds ratio 1.73, P=0.005) and PMI in the inferior wall (PMIinferior) (odds ratio 2.23, P=0.048), respectively. And CMiLAD-max≥5.10 (sensitivity 50.0%, specificity 91.8%) and CMiRCA-max≥2.33 (sensitivity 80.0%, specificity 55.8%) were independent predictors of PMIanterior and PMIinferior, respectively. A lesional threshold TBR of 1.30 was a significant predictor of histologically high-risk plaques. The CD68 expression was significantly higher in lesions presenting elevated 18F-NaF uptake (TBR≥1.50) than reduced 18F-NaF uptake (TBR<1.50) (P=0.028). The baseline coronary stenosis level (SYNTAX score), CAC score and blood biomarkers didn’t correlated with PMI occurrence. Conclusions: Coronary microcalcification activity quantified by 18F-NaF PET might show superior potential in the prediction of PMI after CABG compared to conventional coronary macrocalcification burden and stenosis severity. Figure 1. Multi-modality cardiac imaging in CAD patients with PMIinferior. Elevated 18F-NaF uptake at LM (white-dotted arrow) and LAD (white-solid arrow) on the fused PET/CT images (A). The intense calcium density of LM (white-dotted arrow) and LAD proximal stenosis (white-solid arrow) on CT (B) and stenosis at the corresponding lesion site on coronary angiography (C). Histology and immunohistochemistry of the excised coronary atherosclerotic plaque (inflamed lesion) (D). H&E pathological staining (E) and immunostaining (F): CD68 (146258 IOD) strong expression indicated significant macrophage infiltration in corresponding excised coronary atherosclerotic plaque (F upper-right). Microcalcification (black-dotted arrow) and macrocalcification (black-solid arrow) regions on H&E corresponding to high (black-dotted arrow) and low (black-solid arrow) inflammation on immunostaining, respectively. Figure 2. Multi-modality cardiac imaging in CAD patients without PMI. Elevated 18F-NaF uptake at proximal LAD (white-solid arrow) on the fused PET/CT images (A). Stenosis of proximal LAD with coronary stent (white-solid arrow) on coronary angiography (C) and intense calcium density at the corresponding lesion site on CT (B). Histology and immunohistochemistry of the excised coronary atherosclerotic plaque (non-inflamed lesion) (D). H&E pathological staining (E) and immunostaining (F): expression of CD68 (3487 IOD) indicated no significant macrophage infiltration in corresponding excised coronary atherosclerotic plaque (F upper-right). ER -