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Journal ArticleDOI

Effect of cholesterol crystals on plaques and intima in arteries of patients with acute coronary and cerebrovascular syndromes.

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TLDR
By avoiding ethanol in tissue preparation, CCs perforating the intima were shown to be associated with PD, and crystal content was significantly associated with clinical events, suggesting that cholesterol crystallization may have a role in PD.
Abstract
Plaque disruption (PD) causes most acute cardiovascular events. Although cholesterol crystals (CCs) have been observed in plaques, their role in PD was unknown. However, cholesterol expands with crystallization tearing and perforating fibrous tissues. This study tested the hypothesis that CCs can damage plaques and intima, triggering PD, as observed in tissues prepared without ethanol solvents that dissolve CCs. Coronary arteries of patients who died of acute coronary syndrome (n = 19) and non–acute coronary syndrome causes (n = 12) and carotid plaques from patients with (n = 51) and without (n = 19) neurologic symptoms were studied. Samples were examined for CCs perforating the intima using light and scanning electron microscopy (SEM) with ethanol or vacuum dehydration. In addition, fresh unfixed carotid plaques were examined at 37°C using confocal microscopy. Crystal content using SEM was scored from 0 to +3. SEM using vacuum dehydration had significantly higher crystal content compared with SEM using ethanol dehydration (+2.5 ± 0.53 vs +0.25 ± 0.46; p

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Citations
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Journal ArticleDOI

Cholesterol Crystals Activate the NLRP3 Inflammasome in Human Macrophages: A Novel Link between Cholesterol Metabolism and Inflammation

TL;DR: It is shown that human macrophages avidly phagocytose cholesterol crystals and store the ingested cholesterol as cholesteryl esters, and cholesterol crystals induced dose-dependent secretion of mature IL-1β from human monocytes and macrophage.
Journal ArticleDOI

Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel

TL;DR: In this paper, the authors proposed a method to solve the problem of the problem: this paper ] of "uniformity" of the distribution of data points in the data set.
Journal ArticleDOI

The vascular smooth muscle cell in arterial pathology: a cell that can take on multiple roles.

TL;DR: The medial VSMC is the organizer of the inwardly directed angiogenic response arising from the adventitia by overexpressing vascular endothelial growth factor in response to lipid-stimulated peroxisome proliferator-activated receptor-γ, and probably also the organizers of the adventitial immune response by secreting chemokines.
Journal ArticleDOI

NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis.

TL;DR: The mechanisms of NLRP3 inflammasome activation and proinflammatory IL-1 family cytokine production in the context of atherosclerosis are reviewed and treatment possibilities are discussed in light of the positive outcomes of the CANTOS trial.
References
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Plaque fissuring--the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina.

M J Davies, +1 more
- 01 Apr 1985 - 
TL;DR: This controversy was concerned with whether coronary artery thrombi were or were not directly responsible for all three clinical pictures of acute ischaemia.
Journal ArticleDOI

Identification and isolation of endothelial cells based on their increased uptake of acetylated-low density lipoprotein.

TL;DR: Capillary and aortic endothelial cells were brilliantly fluorescent whereas the fluorescent intensity of retinal pericytes and smooth muscle cells was only slightly above background levels, and Dil-Ac-LDL at the concentration used for labeling cells had no effect on endothelial cell growth rate.
Journal ArticleDOI

Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content.

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Trending Questions (1)
When does cholesterol clog arteries?

The provided paper does not specifically mention when cholesterol clogs arteries. The paper focuses on the role of cholesterol crystals in plaque disruption and does not provide information on the timing of cholesterol clogging arteries.