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Published on: October 22, 2014
Arterial Adventitial Vasa Vasorum Density Reflects The Progression Of Unstable Plaques: A Retrospective Clinical
Jiemei Yang1, Penghao Gao2, Qiannan Li3
1Department of Cardiology, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, P.R. China; Cardiac Ultrasound Division, the First Affiliated Hospital, Cardiovascular Institute, Harbin Medical University, Harbin, P.R. China.
Insights
Arterial adventitial vasa vasorum (AVV) density in carotid arteries indicates atherosclerosis severity. Sonodynamic therapy (SDT) effectively reduces AVV hyperplasia and shrinks atherosclerotic plaques in human lesions.
Area of Science:
- Vascular Biology
- Cardiovascular Disease
- Medical Imaging
Background:
- Arterial adventitial vasa vasorum (AVV) is implicated in atherosclerosis (AS) development, but effective anti-AVV therapies are lacking.
- AS is a systemic vascular disease involving multiple sites, not just local plaque formation.
- Current understanding of AVV's role in carotid AS and potential therapeutic interventions requires further investigation.
Purpose of the Study:
- To determine if human carotid AVV density correlates with plaque neovascularization and intimal-media hyperplasia.
- To investigate the efficacy of sonodynamic therapy (SDT) in reducing human AVV density.
Main Methods:
- A retrospective study of 160 carotid atherosclerosis patients.
- Utilized duplex ultrasound scanning (DUS), contrast-enhanced ultrasound (CEUS), coronary angiography, and CT angiography (CTA).
- Employed Pearson correlation and ROC curve analysis to assess AVV/VV hyperplasia and intima-media thickness (IMT); developed SDT for treatment.
Main Results:
- Local AVV presence in carotid plaques correlated with plaque echogenicity, progression, and acute coronary syndrome (ACS) events.
- AVV hyperplasia in carotid plaques was associated with coronary artery stenosis.
- SDT demonstrated a reduction in local AVV hyperplasia and plaque size in femoral and carotid lesions.
Conclusions:
- AVV presence in human carotid arteries reflects the severity of both carotid and coronary artery AS.
- SDT is a potential therapeutic approach to reduce AVV hyperplasia and mitigate AS progression in human arteries.
Objective:
Arterial adventitial vasa vasorum (AVV) plays an important role in the occurrence and development of atherosclerotic (AS) disease. AS is a systemic disease, and plaque is not only a local vascular event, but also occurs at multiple sites throughout the vascular bed. Currently, effective anti-AVV therapies are lacking. Therefore, we posed the following scientific questions: "does human carotid adventitial vasa vasorum density reflect plaque neovascularization and intimal-media hyperplasia in carotid?"; and "is it possible to reduce human AVV density by sonodynamic therapy (SDT)?"
Methods:
A retrospective study was conducted on 160 patients with carotid atherosclerosis. Duplex ultrasound scanning (DUS), contrast-enhanced ultrasound (CEUS), coronary angiography, and coronary CT angiography (CTA) were used for diagnosis and screening. Pearson correlation tests and Receiver operating characteristic (ROC) curve were used to analyze the relationships between AVV hyperplasia, vasa vasorum (VV) hyperplasia and the intima-media thickness (IMT). SDT was developed for the treatment of arterial AVV hyperplasia and AS plaques.
Results:
The presence of local AVV in carotid unstable plaques correlated with the echogenic properties of the carotid plaque and the extent of plaque progression; Furthermore local AVV hyperplasia in patients with carotid atherosclerotic plaques was associated with acute coronary syndrome (ACS) events; Local AVV hyperplasia in patients with carotid atherosclerotic plaques was associated with coronary artery stenosis. Notably, SDT reduced local AVV hyperplasia and shrank the plaques in human femoral and carotid atherosclerotic lesions.
Conclusions:
The presence of AVV in human carotid arteries reflects the severity of carotid and coronary artery AS. Further, SDT can reduce the hyperplasia of local AVV in human femoral and carotid plaques.
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