用氟-18氟脱氧葡萄糖正电子发射断层扫描/CT评价左心所致肺动脉高压和肺动脉高压患者肺糖摄取

Hiroshi Ohira, Robert deKemp, Yoshito Kadoya, Jennifer Renaud, Duncan J Stewart, Ross A Davies, George Chandy, Vladimir Contreras-Dominguez, Carolyn Pugliese, Rosemary Dunne, Rob Beanlands, Lisa Mielniczuk
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摘要

目的:先前的研究表明,在动物模型或小肺动脉高压(PAH)队列中,18f -氟脱氧葡萄糖正电子发射断层扫描(FDG-PET)在肺组织中增加了葡萄糖摄取。然而,目前尚不清楚肺中FDG摄取增加是否是PAH的独特现象,或者肺动脉压升高是否会诱导FDG摄取。方法与结果:纳入19例PAH患者,8例左心肺动脉高压(PH-LHD)患者,14例年龄匹配的对照组。所有PH患者均行右心导管和FDG-PET检查。计算各肺中FDG的平均标准摄取值(SUV g/mL),并计算两肺的平均值作为平均肺FDG SUV。还分析了PH患者血流动力学与肺平均FDG SUV的相关性。平均PAP (mPAP)在PAH和PH-LHD之间无显著差异(45±11 vs 43±5 mmHg, p=0.51)。与PH-LHD和对照组相比,PAH患者的平均肺FDG SUV显著增加(PAH: 0.76±0.26 vs PH-LHD: 0.51±0.12 vs对照组:0.53±0.16,p=0.0025)。PAH和PH-LHD患者肺平均FDG SUV与mPAP均无相关性。结论:多环芳烃与肺部FDG摄取增加有关,表明肺部葡萄糖利用增加。这可能代表代谢转变为糖酵解和/或重塑肺血管的活动性炎症,并且在PAH中观察到的程度大于继发于LHD的PH患者和没有PH的对照组。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Evaluation of Lung Glucose Uptake with Fluorine-18 Fluorodeoxyglucose Positron Emission Tomography/CT in Patients with Pulmonary Arterial Hypertension and Pulmonary Hypertension Due to Left Heart Disease.

Aim: Previous studies have demonstrated increased glucose uptake by 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) in lung parenchyma in animal models or small pulmonary arterial hypertension (PAH) cohorts. However, it is not well known whether increased FDG uptake in the lung is a unique phenomenon in PAH or whether elevated pulmonary artery pressure (PAP) induces FDG uptake. Methods and results: Nineteen patients with PAH, 8 patients with pulmonary hypertension due to left heart disease (PH-LHD), and 14 age matched control subjects were included. All PH patients underwent right heart catheterization and FDG-PET. The mean standard uptake value (SUV g/mL) of FDG in each lung was obtained and average values of both lungs were calculated as mean lung FDG SUV. The correlation between hemodynamics and mean lung FDG SUV was also analyzed in PH patients. Mean PAP (mPAP) was not significantly different between PAH and PH-LHD (45±11 vs 43±5 mmHg, p=0.51). PAH patients demonstrated significantly increased mean lung FDG SUV compared with PH-LHD and controls (PAH: 0.76±0.26 vs PH-LHD: 0.51±0.12 vs controls: 0.53±0.16, p=0.0025). The mean lung FDG SUV did not correlate with mPAP either in PAH or PH-LHD. Conclusion: PAH is associated with increased lung FDG uptake indicating increased glucose utilization in the lung. This may represent metabolic shift to glycolysis and/or active inflammation in the remodeled pulmonary vasculature, and is observed to a greater extent in PAH than in patients with PH secondary to LHD and control subjects without PH.

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