Projects per year
Abstract
Aims
Quantitative assessment of carotid artery plaque on computed tomography (CT) may identify high-risk phenotypes associated with culprit lesions and subsequent ischaemic stroke or transient ischaemic attack.
Methods and results
Carotid CT angiography was performed in 48 patients with acute ischaemic stroke or transient ischaemic attack within 21 days. Quantitative plaque assessment was performed in the proximal 6 cm of the internal and external carotid artery, distal 6 cm of the common carotid artery, and residual common carotid artery. Semi-automated quantification included assessment of non-calcified, calcified, low-attenuation, and total plaque, area and diameter stenosis, and peri-vascular adipose tissue attenuation. In 48 patients (mean age 71 ± 11 years, 67% male), 96 vessels were assessed with 30 (31%) identified as culprit vessels. Culprit internal carotid arteries had greater area [83 (65, 94) vs. 64 (55, 77)%] and diameter [56 (39, 74) vs. 32 (21, 48)%] stenosis and more non-calcified [563 (413, 965) vs. 428 (283 649) mm3, P = 0.04], low-attenuation [33.7 (6.9, 72.4) vs. 16.3 (3.35, 54.3) mm3, P = 0.01], and total [699 (455, 1057) vs. 492 (311, 809), P = 0.04] plaque. There was no difference in calcified plaque or peri-vascular adipose tissue attenuation between culprit and non-culprit internal carotid arteries. There were no differences in quantitative plaque or peri-vascular adipose tissue attenuation in the external carotid artery or common carotid artery.
Conclusion
Carotid atherosclerotic plaque characteristics are the principal features associated with culprit plaques with little or no demonstrable relationship with calcified plaque or increased peri-vascular adipose tissue attenuation.
Quantitative assessment of carotid artery plaque on computed tomography (CT) may identify high-risk phenotypes associated with culprit lesions and subsequent ischaemic stroke or transient ischaemic attack.
Methods and results
Carotid CT angiography was performed in 48 patients with acute ischaemic stroke or transient ischaemic attack within 21 days. Quantitative plaque assessment was performed in the proximal 6 cm of the internal and external carotid artery, distal 6 cm of the common carotid artery, and residual common carotid artery. Semi-automated quantification included assessment of non-calcified, calcified, low-attenuation, and total plaque, area and diameter stenosis, and peri-vascular adipose tissue attenuation. In 48 patients (mean age 71 ± 11 years, 67% male), 96 vessels were assessed with 30 (31%) identified as culprit vessels. Culprit internal carotid arteries had greater area [83 (65, 94) vs. 64 (55, 77)%] and diameter [56 (39, 74) vs. 32 (21, 48)%] stenosis and more non-calcified [563 (413, 965) vs. 428 (283 649) mm3, P = 0.04], low-attenuation [33.7 (6.9, 72.4) vs. 16.3 (3.35, 54.3) mm3, P = 0.01], and total [699 (455, 1057) vs. 492 (311, 809), P = 0.04] plaque. There was no difference in calcified plaque or peri-vascular adipose tissue attenuation between culprit and non-culprit internal carotid arteries. There were no differences in quantitative plaque or peri-vascular adipose tissue attenuation in the external carotid artery or common carotid artery.
Conclusion
Carotid atherosclerotic plaque characteristics are the principal features associated with culprit plaques with little or no demonstrable relationship with calcified plaque or increased peri-vascular adipose tissue attenuation.
| Original language | English |
|---|---|
| Journal | European Heart Journal - Imaging Methods and Practice |
| Volume | 3 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 8 Apr 2025 |
Fingerprint
Dive into the research topics of 'Quantification of carotid artery plaque and peri-vascular adipose tissue attenuation on computed tomography'. Together they form a unique fingerprint.-
Incidental coronary calcification on thoracic computed tomography
Williams, M. (Principal Investigator), Mills, N. (Co-investigator) & Newby, D. (Co-investigator)
1/02/21 → 31/01/26
Project: Research
-
Myocardial fibrosis and left ventricular decompensation in patients with aortic stenosis
Dweck, M. (Principal Investigator), Dweck, M. (Principal Investigator), Lewis, S. (Co-investigator), Lewis, S. (Co-investigator), Mills, N. (Co-investigator) & Newby, D. (Co-investigator)
Sir Jules Thorn Charitable Trust
1/06/16 → 31/01/33
Project: Research
-
Role and origin of thromboembolism in the pathogenesis of ischaemic stroke
Newby, D. (Principal Investigator)
1/08/21 → 28/07/25
Project: Research
Equipment
-
Edinburgh Imaging Facility
Grant, A. (Manager), van Beek, E. (Manager) & Semple, S. (Manager)
School of Neurological and Cardiovascular SciencesFacility/equipment: Facility