Abstract
BackgroundCholesterol deposition in arterial wall drives atherosclerosis. The key goal of this study was to examine the relationship between plaque cholesterol content and patient characteristics that typically associate with disease state and lesion vulnerability. Quantitative assays for free cholesterol, cholesteryl ester, triglyceride, and protein markers in atherosclerotic plaque were established and applied to plaque samples from multiple patients and arterial beds (Carotid and peripheral arteries; 98 lesions in total).ResultsWe observed a lower cholesterol level in restenotic than primary peripheral plaque. We observed a trend toward a higher level in symptomatic than asymptomatic carotid plaque. Peripheral plaque from a group of well-managed diabetic patients displayed a weak trend of more free cholesterol deposition than plaque from non-diabetic patients. Plaque triglyceride content exhibited less difference in the same comparisons. We also measured cholesterol in multiple segments within one carotid plaque sample, and found that cholesterol content positively correlated with markers of plaque vulnerability, and negatively correlated with stability markers.ConclusionsOur results offer important biological validation of cholesterol as a key lipid marker for plaque severity. Results also suggest cholesterol is a more sensitive plaque marker than routine histological staining for neutral lipids.
Highlights
Cholesterol deposition in arterial wall drives atherosclerosis
Since it is known that restenotic plaque has proteoglycan-enriched extracellular matrix[16], we were curious about a small soluble proteoglycan, Lumican, in this study
Our analysis revealed Lumican was highly abundant in plaque samples, with its SDS-PAGE migration pattern similar to previously observed[17] (Fig. 1G); restenotic lesions had significantly more Lumican than primary lesions (Fig. 1H), suggesting that Lumican may be involved in the smooth muscle cell proliferation process underlying restenosis
Summary
Cholesterol deposition in arterial wall drives atherosclerosis. The key goal of this study was to examine the relationship between plaque cholesterol content and patient characteristics that typically associate with disease state and lesion vulnerability. Atherosclerosis is a chronic disease characterized by lipid deposition and inflammation in the arterial wall[1]. A large body of evidence supporting cholesterol's central role in atherosclerosis was generated using histochemical analysis with lipid-soluble Sudan dyes such as Oil Red O (ORO). These dyes stain neutral lipids including cholesteryl ester and triglyceride, but they do not stain free cholesterol[6]. Such stains in human plaque have demonstrated that lipid enrichment is usually associated with higher degrees of inflammation and characteristics of plaque vulnerability[7]
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