医学
罪魁祸首
心肌梗塞
血栓
四分位间距
心脏病学
内科学
放射科
冠状动脉
冠状动脉疾病
动脉
作者
Evangelos Tzolos,Rong Bing,Jack Andrews,Mark G. MacAskill,A Tavares,Gillian Macnaught,Toni‐Kim Clarke,Michelle C. Williams,Edwin J.R. van Beek,Norman Koglin,Andrew Stephens,Marc R. Dweck,David E. Newby
标识
DOI:10.1093/eurheartj/ehab724.0261
摘要
Abstract Background Coronary artery thrombus is typically present in type 1 myocardial infarction, but small volumes in the setting of an uncertain culprit lesion may be beyond the detection limit of current imaging modalities. Purpose Using a novel glycoprotein IIb/IIIa-receptor radiotracer, 18F-GP1, we investigated whether positron emission tomography-computed tomography (PET-CT) could detect thrombus formation in coronary arteries. Methods In a single centre cross-sectional study, patients over 40 years of age with myocardial infarction were recruited after myocardial infarction and underwent underwent CT angiography and 18F-GP1 PET-CT. Stable patients with and without coronary artery disease formed a control cohort. Coronary artery 18F-GP1 uptake was visually assessed and quantified using maximum target-to-background ratios (TBRmax). Results Ninety-four (44 post-myocardial infarction and 50 control patients) were included in the cross-sectional analysis. The mean age of the post-myocardial infarction group was 61±9 years, three-quarters were male and two thirds had presented with ST elevation on electrocardiography. 34 (80%) patients post-myocardial infarction, but none of the control patients, demonstrated focal 18F-GP1 uptake in the coronary arteries. Of 42 vessels with an angiographic culprit lesion, 35 (83%) had 18F-GP1 uptake which was significantly higher than non-culprit vessels (p<0.0001) as well as control vessels (p<0.0001), while non-culprit vessel uptake was similar to control vessel uptake (p=0.567): culprit vessel median TBRmax 1.2 [interquartile range 0.96–1.44], non-culprit vessel TBRmax 0.96 [0.84–1.03] and control vessel TBRmax 0.9 [0.76 to 0.94]. Linear regression models demonstrated univariable associations between coronary 18F-GP1 TBRmax and time from myocardial infarction, male sex and presence of culprit vessel. On multivariable analysis, only culprit vessel status was associated with TBRmax (adjusted R2= 0.22, P<0.001). Based on the Youden's index of the ROC curves, the optimal cut-off of predicting the presence of a culprit vessel was 1.20 with a specificity of 97%, accuracy of 83%, sensitivity (60%) and c-statictic of 0.74. A patient with ectatic vessel and visual thrombus demonstrated the most intense 18F-GP1 uptake (TBRmax 2.0, highest in the cohort) in the region of heaviest thrombus burden (Figure 2). Extra-coronary uptake was seen in regions of left ventricular thrombus, left atrial appendage thrombus, pulmonary thromboembolism and intramyocardial microvascular obstruction. Conclusions 18F-GP1 PET-CT is able to detect coronary artery thrombus in culprit lesions following myocardial infarction, as well as extra-coronary thrombotic pathologies that may be important in guiding patient management. 18F-GP1 is highly specific in recognising a culprit lesion from a non-culprit lesion both visually as well as quantitatively. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): British Heart Foundation Figure 1Figure 2
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