Use of somatostatin receptor PET to differentiate between high-risk and low-risk atherosclerotic lesions: a prospective clinical study

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• 作者：Jason M Tarkin ; MRCP^a ; Francis R Joshi ; MRCP^a ; Nicholas R Evans ; MRCP^a ; Prof Ashley M Groves ; MRCP^b ; Deepa Gopalan ; FRCR^c ; Roie Manavaki ; PhD^a ; Peter J Kirkpatrick ; FMedSci^c ; Patrick A Coughlin ; FRCS^c ; John R Buscombe ; FRCR^c ; Tim D Fryer ; PhD^a ; Prof Martin R Bennett ; FMedSci^a ; Anthony P Davenport ; PhD^a ; Elizabeth A Warburton^a ; Dr James H F Rudd ; FRCP^a ; ^{jhfr2@cam.ac.uk" class="auth_mail" title="E-mail the corresponding author}
• 刊名：The Lancet
• 出版年：2016
• 出版时间：25 February 2016
• 年：2016
• 卷：387
• 期：supp_S1
• 页码：S97
• 全文大小：61 K

文摘

Inflammation drives atherosclerotic plaque rupture that underlies most myocardial infarctions and strokes. Upregulation of somatostatin receptor subtype-2 (SST₂) occurs on the cell surface of activated macrophages, offering a potential imaging target for tracking vascular inflammation. We tested the hypothesis that SST₂ PET-CT imaging with ⁶⁸Ga-DOTATATE can detect high-risk carotid and coronary plaque inflammation. We then compared its efficacy with ¹⁸F-fludeoxyglucose (¹⁸F-FDG), which has limited use in coronary imaging.

Methods

ra20">Prospective sequential ⁶⁸Ga-DOTATATE PET and ¹⁸F-FDG PET imaging, plus CT angiography, were performed in 42 patients with either a recent cardiovascular event (within 3 months of imaging) or stable atherosclerosis, and at least 30% carotid or coronary artery stenosis. Images were analysed, with investigators masked to clinical details, to derive median (IQR) maximum arterial tissue-to-background ratio (TBR). Arterial TBRs were statistically evaluated against clinical and biochemical data, as well as CT-derived plaque morphology.

Findings

ra30">70 carotid arteries and 230 coronary segments were included. 24 patients (57%) had a recent cardiovascular event. ⁶⁸Ga-DOTATATE TBR (1·98 [1·67–2·14]) was higher in symptomatic carotid arteries than in contralateral arteries (1·77 [1·46–2·08], p=0·0031) and asymptomatic plaques (1·49 [1·36–1·66], p=0·0012). ¹⁸F-FDG TBR was also higher on the symptomatic side (1·68 [1·49–1·97] vs 1·51 [1·44–1·80], p=0·0081). The two PET tracers were moderately correlated (r=0·40, p=0·0007). Coronary SST₂ signals were visible in all patients, but high myocardial muscle ¹⁸F-FDG uptake was prohibitive in 27 patients (64%). Culprit coronary arteries had higher ⁶⁸Ga-DOTATATE TBR (2·91 [2·69–4·08]) than the highest non-culprit segment (2·61 [1·94–3·01], p=0·0078), stable stented (2·00 [1·51–2·70], p=0·0063), and calcified (1·64 [1·33–2·04], p<0·0001) plaques. SST₂ signal from culprit and high-risk coronary arteries was correlated with total cholesterol (r=0·44, p=0·042).

Interpretation

ra40">We have shown that measurement of vascular inflammation with SST₂ PET is feasible and differentiates high-risk and low-risk carotid and coronary lesions. High target specificity, low myocardial binding, and lower cost owing to generator-production give advantage to ⁶⁸Ga-DOTATATE over ¹⁸F-FDG for atherosclerosis imaging. Correlations with ¹⁸F-FDG TBR and serum cholesterol further support the vascular SST₂ signal as a potential prognostic biomarker to identify patients most at risk of future cardiovascular events.

Funding

ra50">Wellcome Trust.