Peri-Carotid Adipose Tissue and Atherosclerosis at Carotid Bifurcation

Author:

Ferreira Joana1234ORCID,Longatto-Filho Adhemar3456ORCID,Dionísio Ana7,Correia-Neves Margarida34,Cunha Pedro3489,Mansilha Armando110

Affiliation:

1. Vascular Surgery Department, Physiology and Surgery, University Hospital Centre of São João, 4200-319 Porto, Portugal

2. Academic Centre of Hospital Senhora da Oliveira, 4835-044 Guimarães, Portugal

3. Life and Health Science Research Institute (ICVS), School of Medicine, University of Minho, 4710-057 Braga, Portugal

4. ICVS/3B’s-PT Government Associate Laboratory, 4710-057 Braga, Portugal

5. Department of Pathology (LIM-14), Faculty of Medicine of the University of São Paulo, São Paulo 01246 903, Brazil

6. Molecular Oncology Research Centre, Barretos Cancer Hospital, São Paulo 14784-400, Brazil

7. Porto Vascular Conference Scientific Advising, 4050-430 Porto, Portugal

8. Medicine Department of Hospital Senhora da Oliveira, 4835-044 Guimarães, Portugal

9. Centre for the Research and Treatment of Arterial Hypertension and Cardiovascular Risk, Internal Medicine, 4835-044 Guimarães, Portugal

10. Faculty of Medicine of the University of Porto, 4200-319 Porto, Portugal

Abstract

Vulnerable carotid plaques are responsible for 20% of the ischemic strokes. The identification of these asymptomatic carotid plaques that will become symptomatic is essential but remains unclear. Our main goal was to investigate whether the amount of the peri-carotid adipose tissue, estimated by the extra-media thickness (EMT), is associated with the atherosclerotic characteristics at the carotid bifurcation in patients with PAD. An observational, prospective, single-center, longitudinal study was conducted. Overall, 177 patients were subjected to carotid Doppler ultrasound at the study admission. The following data were collected: EMT, intima-media thickness (IMT), the presence of carotid plaques, the area of the highest plaque, the presence of “acute culprit” carotid stenosis, and the grade of internal carotid stenosis. “Acute culprit” carotid stenosis was defined as a significant atherosclerotic plaque that leads to a neurologic event within 15 days. From each carotid bifurcation, a right and a left EMT were determined. We analyzed both the mean EMTs (calculated as the mean between the right and the left EMT) and the EMT ipsilateral to the carotid bifurcation. The presence of carotid plaques was associated with a higher mean EMT [Median = 1.14; IQR = 0.66 versus Median = 0.97; IQR = 0.40; p = 0.001]. A positive correlation was found between the mean EMT and IMT (right: ρ = 0.20; p = 0.010; left: ρ = 0.21; p = 0.007) and between the mean EMT and the area of the largest carotid plaque (right: ρ = 0.17; p = 0.036; left: ρ = 0.22; p = 0.004). Left carotid stenosis ≥ 70% was associated with higher ipsilateral EMT [Median = 1.56; IQR = 0.70 versus Median = 0.94; IQR = 0.42; p = 0.009]. Patients with “acute culprit” carotid stenosis had a higher ipsilateral EMT [left ipsilateral EMT: Median = 1.46; IQR = 0.63; “non-acute”: Median = 0.94; IQR = 0.43; p = 0.009; right ipsilateral EMT: Median = 2.25; IQR = 0.62; “non-acute”: Median = 1.00; IQR = 0.51; p = 0.015]. This difference was not found in the contra-lateral EMT. Six months after the neurologic event, EMT ipsilateral to an “acute culprit” carotid stenosis decreased (p = 0.036). The amount of peri-carotid adipose tissue, estimated with EMT, was associated with atherosclerosis at the carotid arteries. The mean EMT was associated with the features of chronic atherosclerosis lesions: the presence of carotid plaques, IMT, and the area of the highest plaque. Ipsilateral EMT was linked with “acute culprit” atherosclerotic plaque.

Funder

Portuguese Society of Vascular Surgery

Northern Portugal Regional Operational Programme

Foundation for Science and Technology

Publisher

MDPI AG

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