Abstract
Objectives To evaluate the diagnostic performance of contrast-enhanced ultrasound (CEUS) for atherosclerotic carotid plaque neovascularization. Methods The electronic databases like PubMed, Embase, OVID, and Web of Science were used to search for the relevant studies, which are involved in the evaluation of the diagnostic parameters of QUS for atherosclerotic carotid plaque neovascularization. Review Manager 5.4 and Stata 14.0 were used to estimate the pooled diagnostic value of CEUS. Forest plots, sensitivity analysis, and Deeks' funnel plots were performed on the included studies. Results Ten studies eventually met the final inclusion criteria. For diagnostic performance, CUES showed that the pooled values of sensitivity, specificity, positive likelihood odds ratios, negative likelihood odds ratios, and diagnostic odds ratios were 0.83 (95% CI 0.78-0.86), 0.77 (95% CI 0.68-0.84), 3.61 (95% CI 2.59-5.03), 0.23 (95% CI 0.18-0.28), and 16.02 (95% CI 10.02-25.60), respectively. The estimate of the area under curve (AUC) was 0.85 (95% CI 0.82-0.88). Conclusion Our research supported that CEUS had high sensitivity and specificity in the diagnosis of atherosclerotic carotid plaque neovascularization. More high-quality prospective multicenter studies focusing on the accuracy of CEUS for carotid atherosclerotic plaque should be performed to verify our conclusions.
Highlights
Atherosclerotic disease is a systemic disease of the arterial wall, which may be a form of cardiovascular inflammatory disease [1]
There are many theories about its pathogenesis, but at present, the main theory is that the arterial wall is a chronic response to endothelial cell injury, which promotes the progress of the disease through the interaction of oxidized lipoproteins, macrophages, T cells, and normal cell components of the arterial wall [2–4]
Ritter et al performed ipsilateral intracranial microemboli signal detection in 41 patients with symptomatic carotid atherosclerosis and performed contrast-enhanced ultrasound 30 minutes later to evaluate the neovascularization in plaque [33]
Summary
Atherosclerotic disease is a systemic disease of the arterial wall, which may be a form of cardiovascular inflammatory disease [1]. There are many theories about its pathogenesis, but at present, the main theory is that the arterial wall is a chronic response to endothelial cell injury, which promotes the progress of the disease through the interaction of oxidized lipoproteins, macrophages, T cells, and normal cell components of the arterial wall [2–4]. With the development of atherosclerosis, various local and systemic factors will promote neovascularization. Neovascularization in plaque (IPN) is one of the important characteristics of vulnerable plaque formation [5, 6]. Fleiner et al.’s study have confirmed that the presence and degree of neovascularization in vulnerable plaques are related to plaque rupture and clinical cardiovascular and cerebrovascular events, which can increase the risk of sudden cardiovascular and cerebrovascular events, such as stroke, transient ischemic attack, and myocardial infarction [9]
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