• Journal of Yeungnam Medical Science
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• 제21권2호
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• pp.143-150
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• 2004

A thromboembolic stroke is believed to be precipitated by a rupture of vulnerable atheromatous plaques. Until recently the assessment of a further risk of stroke in high-risk patients in whom atherosclerosis has presented with a transient ischaemic attack (TIA), has been confined to a quantitative assessment of the luminal patency of the internal carotid artery. These traditional stratification parameters are no longer believed to be the most accurate predictors of a thrombo-embolism. This is because the process of vessel wall remodeling can maintain a luminal patency, and consequently, quite large friable plaques may remain unidentified. Accordingly, there is a need for an improved risk assessment. The fibrous cap of a vulnerable plaque is thinner, and an intraplaque hemorrhage and inflammation can occur during the development of atherosclerotic plaque. Several imaging methods for identifying vulnerable plaques have been developed. Recently, high resolution magnetic resonance (MR) imaging has emerged as an accurate non-invasive tool that can characterize the carotid plaque components in vivo. A High resolution carotid magnetic resonance is capable of distinguishing an intact, thick fibrous cap from a thin and ruptured cap in carotid plaque. In addition, a plaque MR can identify the active inflammation and detect a hemorrhage. High resolution carotid MR imaging is a valuable noninvasive method for quantifying the plaque components and identifying vulnerable plaque.

• IMMUNE NETWORK
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• 제4권2호
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• pp.116-122
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• 2004

Background: LIGHT (TNFSF14) is a member of tumor necrosis factor superfamily and is the ligand for TR2 (TNFRSF14/HVEM). LIGHT is known to have proinflammatory roles in atherosclerosis. Methods: To find out the expression pattern of LIGHT in atherosclerotic plaques, immunohistochemical analysis was performed on human carotid atherosclerotic plaque specimens. LIGHT induced atherogenic events using human monocytic cell line THP-1 were also investigated. Results: Immunohistochemical analysis revealed expression of LIGHT and TR2 in foam cell rich regions in the atherosclerotic plaques. Double immunohistochemical analysis further confirmed the expression of LIGHT in foam cells. Stimulation of THP-1 cells, which express TR2, with either recombinant LIGHT or immobilized anti-TR2 monoclonal antibody induced interleukin-8 and matrix metalloproteinase(MMP)-9. Electrophoretic mobility shift assay demonstrated that LIGHT induces nuclear localization of transcription factor, nuclear factor $(NF)-{\kappa}B$. LIGHT induced activation of MMP-9 is mediated by $NF-{\kappa}B$, since treatment of THP-1 cells with the $NF-{\kappa}B$ inhibitor PDTC (pyrrolidine dithiocarbamate) completely blocked the activation of MMP-9. Conclusion: These data indicate that LIGHT is expressed in foam cells in atherosclerotic plaques and is involved in atherogenesis through activation of pro-atherogenic cytokine IL-8 and destabilization of plaque by inducing matrix degrading enzyme.

• 한국방사선학회논문지
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• 제17권3호
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• pp.465-472
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• 2023

본 연구는 혈관질환을 예측하는 데 있어서 일차 선별검사로서 경동맥 초음파 검사와 혈액학적 검사를 실시한 환자를 대상으로 경동맥 내중막 두께의 변화를 확인하고 죽상경화반의 발현에 위험인자들이 미치는 영향을 알아보고자 하였다. 일개 병원에서 건강검진을 목적으로 내원하여 경동맥 초음파 검사를 실시한 건강한 성인 469명을 대상으로 후향적으로 분석하였다. 그 결과 경동맥 내중막 두께, 연령, 체질량지수, 허리둘레, 수축기 혈압, 총콜레스테롤, 고비중지단백 콜레스테롤, 저비중지단백 콜레스테롤, 공복혈당이 죽상경화반의 유의한 예측인자로 분석되었다(p<0.001). ROC curve 분석을 통해 결정된 죽상경화반 위험인자들의 Cut off value를 기준으로 위험비를 산출하였으며 경동맥 내중막 두께는 8.06배, 연령은 7.53배, 허리둘레는 3.97배, 공복혈당은 2.02배 순으로 높게 나타났다. 따라서 본 연구에서는 죽상경화반의 유무에 영향을 주는 임상학적 위험요인들의 한국인 기준치를 마련할 수 있었으며, 초음파를 이용한 경동맥의 관찰은 심뇌혈관 질환을 조기에 진단하거나 예측하는데 도움이 될 것으로 생각된다.

• Nutrition Research and Practice
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• 제18권5호
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• pp.617-632
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• 2024

BACKGROUND/OBJECTIVES: Atherosclerosis particularly due to high circulating level of low-density lipoprotein is a major cause of cardiovascular diseases. Ellagic acid is a natural polyphenolic compound rich in pomegranates and berries. Our previous study showed that ellagic acid improved functionality of reverse cholesterol transport in murine model of atherosclerosis. The aim of this study is to investigate whether ellagic acid inhibited inflammation-associated atherosclerotic plaque formation in cholesterol-fed apolipoprotein E (apoE)-knockout (KO) mice. MATERIALS/METHODS: Wild type mice and apoE-KO mice were fed a cholesterol-rich Paigen diet for 10 weeks to induce severe atherosclerosis. Concurrently, 10 mg/kg ellagic acid was orally administered to the apoE-KO mice. Plaque lesion formation and lipid deposition were examined by staining with hematoxylin and eosin, Sudan IV and oil red O. RESULTS: The plasma leukocyte profile of cholesterol-fed mice was not altered by apoE deficiency. Oral administration of ellagic acid attenuated plaque lesion formation and lipid deposition in the aorta tree of apoE-KO mice. Ellagic acid substantially reduced plasma levels of soluble vascular cell adhesion molecule and interferon-γ in Paigen diet-fed apoE-KO mice. When 10 mg/kg ellagic acid was administered to cholesterol-fed apoE-KO mice, the levels of CD68 and MCP-1 were strongly reduced in aorta vessels. The protein expression level of nitric oxide synthase-2 (NOS2) in the aorta was highly enhanced by supplementation of ellagic acid to apoE-KO mice, but the expression level of heme oxygenase-1 (HO-1) in the aorta was reduced. Furthermore, ellagic acid diminished the increased aorta expression of the inflammatory adhesion molecules in cholesterol-fed apoE-KO mice. The treatment of ellagic acid inhibited the scavenger receptor-B1 expression in the aorta of apoE-KO mice, while the cholesterol efflux-related transporters were not significantly changed. CONCLUSION: These results suggest that ellagic acid may be an atheroprotective compound by attenuating apoE deficiency-induced vascular inflammation and reducing atherosclerotic plaque lesion formation.

• 대한핵의학회:학술대회논문집
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• 대한핵의학회 2000년도 2nd Korea-China Congress of Nuclear Medicine and 39th Annual Spring Meeting if the Korea SOciety Nuclear Medicine
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• pp.72.1-72.1
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• 2000

• Investigative Magnetic Resonance Imaging
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• 제16권2호
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• pp.97-102
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• 2012

고해상도 경동맥 자기공명영상(MRI)을 이용하여 경화판 특성을 파악할 수 있다. MRI는 경화판의 활동성 염증이나 경화판내 출혈을 비침습적으로 진단할 수 있는 능력이 있다. 3T MRI는 1.5T MRI에 비해 신호 대 잡음비와 대조도 대 잡음비가 높다. 동맥벽의 면적이나 표준화된 동맥벽 면적을 MRI로 측정하면 약물 치료 후 반응을 평가할 수 있다. 결론적으로 고행상도 MRI는 일과성 허혈이나 뇌졸중을 발생하기 쉬운 경화판의 진단과 치료 후 평가에 유용하다.

• Journal of Yeungnam Medical Science
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• 제35권1호
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• pp.121-126
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• 2018

Coronary spasm generally occurs in patients with minimal atherosclerotic plaque lesion, and it has a rather favorable prognosis. However, in some cases, coronary spasm may induce myocardial infarction and even sudden cardiac death (SCD). Here, we report a case in which multi-vessel intractable coronary vasospasm suddenly occurred in a diffuse atherosclerotic lesion after percutaneous coronary intervention (PCI) in a patient with aborted SCD. We identified the characteristics of the spasm portion in intravascular ultrasound (IVUS) images and conducted percutaneous cardiopulmonary bypass support-PCI with stenting as treatment. Intima and media thickening and a large attenuated plaque burden with rupture were identified in IVUS images at the obstructive spasm portion.

• 대한방사성의약품학회지
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• 제4권1호
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• pp.26-31
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• 2018

Macrophages play a key role in atherosclerotic plaque formation, but their participation has been discerned largely via ex vivo analyses of atherosclerotic lesions. Therefore, we aimed to identify atherosclerosis on noninvasive in vivo imaging using reporter gene system. This study demonstrated that recruitment of macrophages could be detected in atherosclerotic plaques of Apolipoprotein E knockout (ApoE-/-) mice with a sodium iodide symporter (NIS) gene imaging system using $^{99m}Tc-SPECT$. This novel approach to tracking macrophages to atherosclerotic plaques in vivo could have applications in studies of arteriosclerotic vascular disease.

• Korean Journal of Radiology
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• 제24권4호
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• pp.338-348
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• 2023

Objective: Patients with a history of ischemic stroke are at risk for a second ischemic stroke. This study aimed to investigate the relationship between carotid plaque enhancement on perfluorobutane microbubble contrast-enhanced ultrasonography (CEUS) and future recurrent stroke, and to determine whether plaque enhancement can contribute to risk assessment for recurrent stroke compared with the Essen Stroke Risk Score (ESRS). Materials and Methods: This prospective study screened 151 patients with recent ischemic stroke and carotid atherosclerotic plaques at our hospital between August 2020 and December 2020. A total of 149 eligible patients underwent carotid CEUS, and 130 patients who were followed up for 15-27 months or until stroke recurrence were analyzed. Plaque enhancement on CEUS was investigated as a possible risk factor for stroke recurrence and as a possible adjunct to ESRS. Results: During follow-up, 25 patients (19.2%) experienced recurrent stroke. Patients with plaque enhancement on CEUS had an increased risk of stroke recurrence events (22/73, 30.1%) compared to those without plaque enhancement (3/57, 5.3%), with an adjusted hazard ratio (HR) of 38.264 (95% confidence interval [CI]:14.975-97.767; P < 0.001) according to a multivariable Cox proportional hazards model analysis, indicating that the presence of carotid plaque enhancement was a significant independent predictor of recurrent stroke. When plaque enhancement was added to the ESRS, the HR for stroke recurrence in the high-risk group compared to that in the low-risk group (2.188; 95% CI, 0.025-3.388) was greater than that of the ESRS alone (1.706; 95% CI, 0.810-9.014). A net of 32.0% of the recurrence group was reclassified upward appropriately by the addition of plaque enhancement to the ESRS. Conclusion: Carotid plaque enhancement was a significant and independent predictor of stroke recurrence in patients with ischemic stroke. Furthermore, the addition of plaque enhancement improved the risk stratification capability of the ESRS.

• Animal cells and systems
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• 제15권4호
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• pp.259-267
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• 2011

This study was undertaken to produce a $F_{ab}$ fragment of a human monoclonal antibody reactive to oxidized and carbamylated low-density lipoprotein (oxLDL and cLDL) using phage display technology. An analysis of DNA sequences of this $F_{ab}$, termed plaque 15,16-46 $F_{ab}$, revealed that the rearranged $V_H$ was highly mutated. Complementarity-determining regions of the $V_H$ showed a very high R/S ratio and contained many positively charged amino acids. In direct binding and competitive ELISA, the $F_{ab}$ reacted strongly with both MDA-LDL and Cu-oxLDL forms of oxLDL, and also showed high affinity for cLDL. Immunofluorescence and immunohistochemical analyses showed that this $F_{ab}$ positively stained atherosclerotic aortic plaques in $ApoE^{-/-}$ mice as well as those in patients with atherosclerosis. The $F_{ab}$ also showed positive staining in placental decidua from patients with preeclampsia. It is suggested that the plaque 15,16-46 $F_{ab}$ against oxLDL and cLDL might possibly be applicable for developing a diagnostic reagent for both human and rodent animal research to detect and characterize atherosclerotic disease progression in atherosclerotic lesions as well as exploring the pathogenesis of atherogenic diseases such as preeclampsia.