scholarly journals Calculation of the Correct Angle of Bifurcation Predicts the Atherosclerotic Lesion Severity More Accurately

2021 ◽  
Vol 33 (2) ◽  
pp. 147-148
Author(s):  
Mehmet Ozgeyik ◽  
Onur Kaypakli ◽  
Mufide Okay Ozgeyik
Keyword(s):  
Atherosclerotic Lesion ◽  
Correct Angle ◽  
Lesion Severity

scholarly journals Alirocumab, evinacumab, and atorvastatin triple therapy regresses plaque lesions and improves lesion composition in mice

2019 ◽  
Vol 61 (3) ◽  
pp. 365-375 ◽  
Author(s):  
Marianne G. Pouwer ◽  
Elsbet J. Pieterman ◽  
Nicole Worms ◽  
Nanda Keijzer ◽  
J. Wouter Jukema ◽  
...  
Keyword(s):  
Triple Therapy ◽  
Atherosclerotic Lesion ◽  
Lesion Size ◽  
Lipid Lowering ◽  
Atherosclerosis Progression ◽  
Cholesterol Levels ◽  
Baseline Group ◽  
Current Therapies ◽  
Triple Treatment ◽  
Lesion Severity

Atherosclerosis-related CVD causes nearly 20 million deaths annually. Most patients are treated after plaques develop, so therapies must regress existing lesions. Current therapies reduce plaque volume, but targeting all apoB-containing lipoproteins with intensive combinations that include alirocumab or evinacumab, monoclonal antibodies against cholesterol-regulating proprotein convertase subtilisin/kexin type 9 and angiopoietin-like protein 3, may provide more benefit. We investigated the effect of such lipid-lowering interventions on atherosclerosis in APOE*3-Leiden.CETP mice, a well-established model for hyperlipidemia. Mice were fed a Western-type diet for 13 weeks and thereafter matched into a baseline group (euthanized at 13 weeks) and five groups that received diet alone (control) or with treatment [atorvastatin; atorvastatin and alirocumab; atorvastatin and evinacumab; or atorvastatin, alirocumab, and evinacumab (triple therapy)] for 25 weeks. We measured effects on cholesterol levels, plaque composition and morphology, monocyte adherence, and macrophage proliferation. All interventions reduced plasma total cholesterol (37% with atorvastatin to 80% with triple treatment; all P < 0.001). Triple treatment decreased non-HDL-C to 1.0 mmol/l (91% difference from control; P < 0.001). Atorvastatin reduced atherosclerosis progression by 28% versus control (P < 0.001); double treatment completely blocked progression and diminished lesion severity. Triple treatment regressed lesion size versus baseline in the thoracic aorta by 50% and the aortic root by 36% (both P < 0.05 vs. baseline), decreased macrophage accumulation through reduced proliferation, and abated lesion severity. Thus, high-intensive cholesterol-lowering triple treatment targeting all apoB-containing lipoproteins regresses atherosclerotic lesion area and improves lesion composition in mice, making it a promising potential approach for treating atherosclerosis.

scholarly journals Discriminating Carotid Atherosclerotic Lesion Severity by Luminal Stenosis and Plaque Burden

Stroke ◽  
2011 ◽  
Vol 42 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Xihai Zhao ◽  
Hunter R. Underhill ◽  
Qian Zhao ◽  
Jianming Cai ◽  
Feiyu Li ◽  
...  
Keyword(s):  
Atherosclerotic Lesion ◽  
Plaque Burden ◽  
Luminal Stenosis ◽  
Lesion Severity

scholarly journals Oxidised plant sterols as well as oxycholesterol increase the proportion of severe atherosclerotic lesions in female LDL receptor+/ − mice

2013 ◽  
Vol 111 (1) ◽  
pp. 64-70 ◽  
Author(s):  
Jogchum Plat ◽  
Elke Theuwissen ◽  
Constanze Husche ◽  
Dieter Lütjohann ◽  
Marion J. J. Gijbels ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Control Diet ◽  
Ldl Receptor ◽  
Atherosclerotic Lesion ◽  
Serum Levels ◽  
Plant Sterols ◽  
Atherosclerotic Lesions ◽  
Human Situation ◽  
Diet Control ◽  
Lesion Severity

Oxysterols (oxidised cholesterol) may play a role in the pathogenesis of CVD. Similar to cholesterol, plant sterols are susceptible to oxidation. However, less is known about the potential atherogenicity of oxidised plant sterols (oxyphytosterols). In the present study, the atherogenicity of a mixture of oxyphytosterols was examined by feeding female LDL receptor-deficient (LDLR+/ −) mice for 35 weeks a control diet (atherogenic high-fat diet; n 9), an oxysterol diet (control diet+0·025 % (w/w) oxysterols; n 12) or an oxyphytosterol diet (control diet+0·025 % (w/w) oxyphytosterols; n 12). In the LDLR+/ − mice, serum levels of cholesterol, lipoprotein profiles, cholesterol exposure and inflammatory markers at the end of the experiment were comparable between the three diet groups. Nevertheless, the proportion of severe atherosclerotic lesions was significantly higher after oxysterol (41 %; P= 0·004) and oxyphytosterol (34 %; P= 0·011) diet consumption than after control diet consumption (26 %). Oxyphytosterol levels in the lesions were the highest in the oxyphytosterol group. Here, we show that not only dietary oxysterols but also dietary oxyphytosterols increase the proportion of severe atherosclerotic lesions. This suggests that plant sterols when oxidised may increase atherosclerotic lesion severity instead of lowering the size and severity of lesions when fed in their non-oxidised form. Therefore, this finding might give an indication as to where to find the answer in the current hot debate about the potential atherogenicity of plant sterols. However, to what extent these results can be extrapolated to the human situation warrants further investigation.

scholarly journals Western Versus Heart Healthy Dietary Pattern Alters Genes Expression Associated with Lipid Metabolism, Interferon Signaling and Inflammation in Jejunum of Ossabaw Pigs

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 577-577
Author(s):  
Shumao Ye ◽  
Nirupa Matthan ◽  
Stefania Lamon-Fava ◽  
Gloria Solano-Aguilar ◽  
Jerrold Turner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lipid Metabolism ◽  
Statin Therapy ◽  
Critical Role ◽  
Atherosclerotic Lesion ◽  
Jejunal Mucosa ◽  
Interferon Signaling ◽  
Expression Of Genes ◽  
Tnf Α ◽  
Lesion Severity

Abstract Objectives A gastrointestinal tract (GI) that allows for bacterial translocation has been associated with enhanced systemic inflammation and may play a critical role in the development of coronary artery disease (CAD). Diet quality and statin therapy are established modulators of CAD, but their effect in GI health is relatively unexplored. Jejunal mucosa gene expression was compared in Ossabaw pigs fed a heart healthy-type diet (HHD) and Western-type diet (WD), with and without statin therapy. Methods Pigs (N = 32) were randomized into 4 groups and fed isocalorically for 6 months: WD (high in saturated fat, refined carbohydrate, cholesterol, and low in fiber) or HHD (high in unsaturated fat, whole grains, fruits and vegetables, fiber, supplemented with fish oil, and low in cholesterol), with or without statin therapy. RNA sequencing was conducted in isolated jejunal mucosa at the end of the study. Principal component analysis, hierarchical clustering and xCell analysis were used to cross-check and ensure consistent sampling. Two-factor edgeR analysis and Ingenuity Pathway Analysis were used to identify genes, pathways, and biological functions altered by diet and/or statin. Independent of groups, Spearman's correlation coefficients were calculated to identify associations between genes of interest and atherosclerotic lesion severity in the coronary arteries or cardiometabolic risk factors (serum triglyceride, LDL, HDL, TNF-α, hsCRP). Results HHD and WD resulted in differential expression of genes related to lipid metabolism (SCD, FADS1, SQLE) in the jejunal mucosa. The expression of these genes was associated with atherosclerotic lesion severity and serum lipoprotein concentrations. Higher interferon signaling and inflammation were observed in pigs fed WD versus HHD. In the jejunal mucosa, 7 genes related to inflammation were significantly associated with serum TNF-α and/or hsCRP concentrations. There was no significant effect of statin on gene expression, nor diet x statin interaction. Expression of genes related to jejunum permeability was unaffected by diet or statin. Conclusions Gene expression in the jejunum of Ossabaw pigs was altered by dietary patterns, but not statin, and linked to atherosclerotic lesion severity associated with lipid metabolism and inflammatory markers. Funding Sources USDA-ARS-NEA, JM-USDA-HNRCA, and Tufts University.

Observation of Atherosclerotic Lesion with a Photosensitizer

1992 ◽  
Vol 13 (Supplement) ◽  
pp. 141-144
Author(s):  
K. AIZAWA ◽  
J. HAYASHI ◽  
H. SATO ◽  
H. KAWABE ◽  
U. KUROIWA ◽  
...  
Keyword(s):  
Atherosclerotic Lesion

Do mitochondrial DNA mutations play the key role in chronification of sterile inflammation? Special focus on atherosclerosis

2020 ◽  
Vol 26 ◽  
Author(s):  
Alexander N. Orekhov ◽  
Elena V. Gerasimova ◽  
Vasily N. Sukhorukov ◽  
Anastasia V. Poznyak ◽  
Nikita G. Nikiforov
Keyword(s):  
Innate Immunity ◽  
Mitochondrial Dna ◽  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Sterile Inflammation ◽  
Special Focus ◽  
Mitochondrial Dysfunctions ◽  
Mtdna Mutations ◽  
Dna Mutations

Background: The elucidation of mechanisms implicated in the chronification of inflammation is able to shed the light on the pathogenesis of disorders that are responsible for the majority of the incidence of disease and deaths, and also causes of ageing. Atherosclerosis is an example of the most significant inflammatory pathology. The inflammatory response of innate immunity is implicated in the development of atherosclerosis arising locally or focally. Modified low-density lipoprotein (LDL) was regarded as the trigger for this response. No atherosclerotic changes in the arterial wall occur due to the quick decrease in inflammation rate. Nonetheless, the atherosclerotic lesion formation can be a result of the chronification of local inflammation, which, in turn, is caused by alteration of the response of innate immunity. Objective: In this review, we discussed potential mechanisms of the altered response of the immunity in atherosclerosis with a particular emphasis on mitochondrial dysfunctions. Conclusion: A few mitochondrial dysfunctions can be caused by the mitochondrial DNA (mtDNA) mutations. Moreover, mtDNA mutations were found to affect the development of defective mitophagy. Modern investigations have demonstrated the controlling mitophagy function in the response of the immune system. Therefore, we hypothesized that impaired mitophagy, as a consequence of mutations in mtDNA, can raise a disturbed innate immunity response resulting in the chronification of inflammation in atherosclerosis.

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