Abstract
Recent advances in atherosclerotic plaque detection have shown that not only does lipid core size and depth play important roles in plaque rupture and thrombi formation, but lipid composition, especially cholesterol deposition, is equally important in determining lesion vulnerability. Here, we demonstrate a spectral analysis assisted photoacoustic imaging approach to differentiate and map lipid compositions within an artery wall. The approach is based on the classification of spectral curves obtained from the sliding windows along time-of-flight photoacoustic signals via a numerical k-means clustering method. The evaluation result on a vessel-mimicking phantom containing cholesterol and olive oil shows accuracy and efficiency of this method, suggesting the potential to apply this approach in assessment of atherosclerotic plaques.
Highlights
Cardiovascular disease has been the leading cause of death over the past century in developed countries [1]
Discussion method used in virtual histology IVUS and differentiated tissue types based on the distribution patterns of spectral parameters, such as slope, y-intercept and mid-band fit, within regions of interest
We demonstrated a spectral analysis assisted Intravascular photoacoustic (IVPA) approach for lipid composition differentiation, which can be potentially applied in atherosclerotic plaque detection and identification
Summary
Cardiovascular disease has been the leading cause of death over the past century in developed countries [1]. Atherosclerosis is recognized as the pathologic basis of cardiovascular disease, in which lipids accumulate in an artery wall leading to plaque growth and subsequent obstructive lumen narrowing or rupture [2]. The vulnerable, or rupture-prone plaque is typically characterized by a thin fibrous cap, a large lipid-rich necrotic core, and inflammatory infiltrate [3,4]. Of these hallmarks, lipid accumulation has been shown to be the most frequently observed precondition of a plaque rupture [5]. Cholesterol found in early atherosclerotic lesions participates the formation of macrophage foam cells, while crystalline cholesterol is thought to induce plaque rupture by physical disruption of the fibrous cap [7]. Cholesteryl esters mainly accumulate in cytoplasmic droplets [2] and constitute a major fraction of lipid-rich necrotic core [10]
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