Thoracic Aortic 18F-Sodium Fluoride Activity and Ischemic Stroke in Patients with Established Cardiovascular Disease

Alexander J Fletcher , Yong Yong Tew, Evangelos Tzolos, Shruti Joshi, Jakub Kaczynski, Jennifer Nash, Samuel Debono, Maria Lembo, Jacek Kwiecinski, Rong Bing, Maaz B J Syed, Mhairi Doris, Edwin J R van Beek, Alistair J Moss, William Jenkins, Niki L Walker, Nikhil V Joshi, Tania A Pawade, Philip D Adamson, William N WhiteleyJoanna M. Wardlaw, Piotr J Slomka, Michelle C Williams, David E Newby, Marc R Dweck*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Objective:
To investigate whether thoracic 18F-sodium fluoride positron emission tomography (PET) could improve the identification of patients at the highest risk of ischemic stroke.

Background:
Aortic atherosclerosis represents an important contributor to ischemic stroke risk. Identifying patients with high-risk aortic atheroma could improve preventative treatment strategies for future ischemic stroke.

Methods:
In a post-hoc observational cohort study, we quantified thoracic aortic and coronary 18F-sodium fluoride activity in 461 patients with stable cardiovascular disease undergoing PET combined with computed tomography (CT). Progression of atherosclerosis was assessed by change in aortic and coronary CT calcium volume. Clinical outcomes were determined by the occurrence of ischemic stroke and myocardial infarction. We compared the prognostic utility of 18F-sodium fluoride activity for predicting stroke to clinical risk scores and CT calcium quantification using survival analysis and multivariable logistic regression.

Results:
After 12·7±2·7 months, progression of thoracic aortic calcium volume correlated with baseline thoracic aortic 18F-sodium fluoride activity (n=140, r=0·31, p=0·00016). In 461 patients, 23 (5%) patients experienced an ischemic stroke and 32 (7%) a myocardial infarction after 6·1±2·3 years of follow up. High thoracic aortic 18F-sodium fluoride activity was strongly associated with ischemic stroke (HR 10·3 [3·1 to 34·8], p=0·0017), but not myocardial infarction (p=0·40). Conversely, high coronary 18F-sodium fluoride activity was associated with myocardial infarction (HR 4·8 [1·9 to 12·2], p=0·00095) but not ischemic stroke (p=0·39). In a multivariable logistic regression model including imaging and clinical risk factors, thoracic aortic 18F-sodium fluoride activity was the only variable associated with ischemic stroke (OR 1·76 [1·12 to 2·78], p=0·0014).

Conclusion:
In patients with established cardiovascular disease, thoracic aortic 18F-sodium fluoride activity is associated with the progression of atherosclerosis and future ischemic stroke. Arterial 18F-sodium fluoride activity identifies localised areas of atherosclerotic disease activity that are directly linked to disease progression and downstream regional clinical atherothrombotic events.

Original languageEnglish
JournalJACC: Cardiovascular Imaging
DOIs
Publication statusPublished - 16 Feb 2022

Keywords

  • Stroke
  • Calcification
  • Computed tomography
  • Positron emission tomography
  • Sodium fluoride
  • Thoracic aorta

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