scholarly journals Research on the correlation between activating transcription factor 3 expression in the human coronary artery and atherosclerotic plaque stability

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
J. Peng ◽  
C. Y. Le ◽  
B. Xia ◽  
J. W. Wang ◽  
J. J. Liu ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Necrotic Core ◽  
Inflammatory Factors ◽  
Lesion Group ◽  
Control Group ◽  
Atherosclerotic Plaques ◽  
Activating Transcription Factor 3 ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness ◽  
Activating Transcription Factor

Abstract Background Activating transcription factor 3 (ATF3) is an early response gene that is activated in response to atherosclerotic stimulation and may be an important factor in inhibiting the progression of atherosclerosis. In this study, we directly measured the expression of ATF3 and inflammatory factors in human coronary atherosclerotic plaques to examine the relationship between ATF3 expression, inflammation and structural stability in human coronary atherosclerotic plaques. Methods A total of 68 coronary artery specimens were collected from the autopsy group, including 36 cases of sudden death from coronary heart disease (SCD group) and 32 cases of acute death caused by mechanical injury with coronary atherosclerosis (CHD group). Twenty-two patients who had no coronary heart disease were collected as the control group (Con group). The histological structure of the coronary artery was observed under a light microscope after routine HE staining, and the intimal and lesion thicknesses, thickness of the fibrous cap, thickness of necrosis core, degree of lumen stenosis were assessed by image analysis software. Western blotting and immunohistochemistry were used to measure the expression and distribution of ATF3, inflammatory factors (CD45, IL-1β, TNF-α) and matrix metalloproteinase-9 (MMP-9) and vascular cell adhesion molecule 1 (VCAM1) in the coronary artery. The Pearson correlation coefficient was used to analyse the correlation between ATF3 protein expression and inflammatory factors and between ATF3 protein expression and structure-related indexes in the lesion group. Results Compared with those in the control group, the intima and necrotic core in the coronary artery were thickened, the fibrous cap became thin and the degree of vascular stenosis was increased in the lesion group, while the intima and necrotic core became thicker and the fibrous cap became thinner in the SCD group than in the CHD group (P < 0.05). There was no or low expression of ATF3, inflammatory factors, VCAM1 and MMP-9 in the control group, and the expression of inflammatory factors, VCAM1 and MMP-9 in the SCD group was higher than that in CHD group, while the expression of ATF3 in the SCD group was significantly lower than that in CHD group (P < 0.05). In the lesion group, the expression of ATF3 was negatively correlated with intimal and necrotic focus thickness, positively correlated with fibrous cap thickness (P < 0.01), and negatively correlated with inflammatory factors, VCAM1 and MMP-9 (P < 0.01). Conclusions The expression of ATF3 may be related to the progression and stability of atherosclerotic plaques, and may affect the structural stability of atherosclerotic plaques by regulating the inflammatory response, thus participating in the regulation of atherosclerotic progression.

scholarly journals Research on the Correlation Between Activating Transcription Factor 3 Expression in the Human Coronary Artery and Atherosclerotic Plaque Stability

2021 ◽  
Author(s):  
J. Peng ◽  
C. Y. Le ◽  
B. Xia ◽  
J. W. Wang ◽  
J. J. Liu ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Coronary Artery ◽  
Necrotic Core ◽  
Inflammatory Factors ◽  
Lesion Group ◽  
Control Group ◽  
Atherosclerotic Plaques ◽  
Activating Transcription Factor 3 ◽  
Fibrous Cap ◽  
Activating Transcription Factor

Abstract Background: Activating transcription factor 3 (ATF3) is an early response gene that is activated in response to atherosclerotic stimulation and may be an important factor in inhibiting the progression of atherosclerosis. In this study, we directly measured the expression of ATF3 and inflammatory factors in human coronary atherosclerotic plaques to examine the relationship between ATF3 expression, inflammation and structural stability in human coronary atherosclerotic plaques. Methods: A total of 68 coronary artery specimens were collected from the autopsy group, including 36 cases of sudden death from coronary heart disease (SCD group) and 32 cases of acute death caused by mechanical injury with coronary atherosclerosis (CHD group). Twenty-two patients who had no coronary heart disease were collected as the control group (CON group). Haematoxylin-eosin staining was used to observe changes in arterial structure. Western blotting and immunohistochemistry were used to measure the expression and distribution of ATF3, Full list of author information is available at the end of the article-2-inflammatory factors and matrix metalloproteinase-9 (MMP-9) and vascular cell adhesion molecule 1 (VCAM1) in the coronary artery. The Pearson correlation coefficient was used to analyse the correlation between ATF3 protein expression and inflammatory factors and between ATF3 protein expression and structure-related indexes in the lesion group. Results: Compared with those in the control group, the intima and necrotic core in the coronary artery were thickened, the fibrous cap became thin and the degree of vascular stenosis was increased in the lesion group, while the intima and necrotic core became thicker and the fibrous cap became thinner in the SCD group than in the CHD group (P < 0.05). There was no or low expression of ATF3, inflammatory factors, VCAM1 and MMP-9 in the control group, and the expression of inflammatory factors, VCAM1 and MMP-9 in the SCD group was higher than that in CHD group, while the expression of ATF3 in the SCD group was significantly lower than that in CHD group (P < 0.05). In the lesion group, the expression of ATF3 was negatively correlated with intimal and necrotic focus thickness, positively correlated with fibrous cap thickness (P < 0.01), and negatively correlated with inflammatory factors, VCAM1 and MMP-9 (P < 0.01). Conclusions: The expression of ATF3 may be related to the progression and stability of atherosclerotic plaques, and may affect the structural stability of atherosclerotic plaques by regulating the inflammatory response, thus participating in the regulation of atherosclerotic progression.

scholarly journals The impact of vildagliptin on the daily glucose profile and coronary plaque stability in impaired glucose tolerance patients with coronary artery disease: VOGUE—A multicenter randomized controlled trial

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hiroyuki Yamamoto ◽  
Akihide Konishi ◽  
Toshiro Shinke ◽  
Hiromasa Otake ◽  
Masaru Kuroda ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Controlled Trial ◽  
Control Group ◽  
Randomized Controlled ◽  
Fibrous Cap ◽  
Multicenter Randomized Controlled Trial ◽  
The Mean ◽  
Artery Disease ◽  
Fibrous Cap Thickness ◽  
The Impact

Abstract Background The impact of reduction in glycemic excursion on coronary plaques remains unknown. This study aimed to elucidate whether a dipeptidyl peptidase 4 inhibitor could reduce the glycemic excursion and stabilize the coronary plaques compared with conventional management in coronary artery disease (CAD) patients with impaired glucose tolerance (IGT). Methods This was a multicenter, randomized controlled trial including CAD patients with IGT under lipid-lowering therapy receiving either vildagliptin (50 mg once a day) or no medication (control group) regarding glycemic treatment. The primary endpoint was changes in the minimum fibrous cap thickness and lipid arc in non-significant native coronary plaques detected by optical coherence tomography at 6 months after intervention. Glycemic variability expressed as the mean amplitude of glycemic excursion (MAGE) measured with a continuous glucose monitoring system was evaluated before and 6 months after intervention. Results A total of 20 participants with 47 lesions were allocated to either the vildagliptin group (10 participants, 22 lesions) or the control group (10 participants, 25 lesions). The adjusted difference of mean changes between the groups was − 18.8 mg/dl (95% confidence interval, − 30.8 to − 6.8) (p = 0.0064) for the MAGE (vildagliptin, − 20.1 ± 18.0 mg/dl vs. control, 2.6 ± 12.7 mg/dl), − 22.8° (− 40.6° to − 5.1°) (p = 0.0012) for the mean lipid arc (vildagliptin, − 9.0° ± 25.5° vs. control, 15.8° ± 16.8°), and 42.7 μm (15.3 to 70.1 μm) (p = 0.0022) for the minimum fibrous cap thickness (vildagliptin, 35.7 ± 50.8 μm vs. control, − 15.1 ± 25.2 μm). Conclusions Vildagliptin could reduce the MAGE at 6 months and may be associated with the decreased lipid arc and increased minimum FCT of the coronary plaques in CAD patients with IGT as compared with the control group. These findings may represent its potential stabilization effect on coronary plaques, which are characteristic in this patient subset. Trial registration Registered in the UMIN clinical trial registry (UMIN000008620), Name of the registry: VOGUE trial, Date of registration: Aug 6, 2012, URL: https://upload.umin.ac.jp/cgi-open-bin/ctr/ctr_view.cgi?recptno=R000010058

Utility of high-resolution MR imaging to assess fibrous cap thickness, lipid-rich necrotic core and haemorrhage of carotid atheroma

2009 ◽  
Vol 96 (S1) ◽  
pp. 1-1
Author(s):  
U. Sadat ◽  
V. E. Young ◽  
M. J. Graves ◽  
M. E. Gaunt ◽  
K. Varty ◽  
...  
Keyword(s):  
High Resolution ◽  
Mr Imaging ◽  
Necrotic Core ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness

scholarly journals Measurement of fibrous cap thickness in atherosclerotic plaques by spatiotemporal analysis of laser speckle images

2006 ◽  
Vol 11 (2) ◽  
pp. 021006 ◽  
Author(s):  
Seemantini K. Nadkarni ◽  
Alberto Bilenca ◽  
Brett E. Bouma ◽  
Guillermo J. Tearney
Keyword(s):  
Spatiotemporal Analysis ◽  
Laser Speckle ◽  
Atherosclerotic Plaques ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness

scholarly journals Reactive oxygen species scavenging and inflammation mitigation enabled by biomimetic prussian blue analogues boycott atherosclerosis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yan Zhang ◽  
Yifei Yin ◽  
Wei Zhang ◽  
Hongyan Li ◽  
Taixia Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prussian Blue ◽  
Foam Cell ◽  
Atherosclerotic Plaques ◽  
Fibrous Cap ◽  
Theranostic Agent ◽  
Fibrous Cap Thickness ◽  
Anti Inflammation

Abstract Background As one typical cardiovascular disease, atherosclerosis severely endanger people’ life and cause burden to people health and mentality. It has been extensively accepted that oxidative stress and inflammation closely correlate with the evolution of atherosclerotic plaques, and they directly participate in all stages of atherosclerosis. Regarding this, anti-oxidation or anti-inflammation drugs were developed to enable anti-oxidative therapy and anti-inflammation therapy against atherosclerosis. However, current drugs failed to meet clinical demands. Methods Nanomedicine and nanotechnology hold great potential in addressing the issue. In this report, we engineered a simvastatin (Sim)-loaded theranostic agent based on porous manganese-substituted prussian blue (PMPB) analogues. The biomimetic PMPB carrier could scavenge ROS and mitigate inflammation in vitro and in vivo. Especially after combining with Sim, the composite Sim@PMPB NC was expected to regulate the processes of atherosclerosis. As well, Mn2+ release from PMPB was expected to enhance MRI. Results The composite Sim@PMPB NC performed the best in regulating the hallmarks of atherosclerosis with above twofold decreases, typically such as oxidative stress, macrophage infiltration, plaque density, LDL internalization, fibrous cap thickness and foam cell birth, etc. Moreover, H2O2-induced Mn2+ release from PMPB NC in atherosclerotic inflammation could enhance MRI for visualizing plaques. Moreover, Sim@PMPB exhibited high biocompatibility according to references and experimental results. Conclusions The biomimetic Sim@PMPB theranostic agent successfully stabilized atherosclerotic plaques and alleviated atherosclerosis, and also localized and magnified atherosclerosis, which enabled the monitoring of H2O2-associated atherosclerosis evolution after treatment. As well, Sim@PMPB was biocompatible, thus holding great potential in clinical translation for treating atherosclerosis. Graphic abstract

scholarly journals 1082-186 Reduced inflammation and neovascularization and increased fibrous cap thickness in advanced aortic atherosclerotic plaques from cigarette smokers

2004 ◽  
Vol 43 (5) ◽  
pp. A477 ◽  
Author(s):  
K.Raman Purushothaman ◽  
Dario Echeverri ◽  
William N O'Connor ◽  
Juan J Badimon ◽  
Samin K Sharma ◽  
...  
Keyword(s):  
Atherosclerotic Plaques ◽  
Cigarette Smokers ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness

scholarly journals Tianeptine Reduces Mechanical Allodynia in Spinal Nerve-ligated and Chemotherapyinduced Neuropathic Mice

2017 ◽  
Vol 4 (20;4) ◽  
pp. E593-E600
Author(s):  
Hue Jung Park
Keyword(s):  
Transcription Factor ◽  
Mechanical Allodynia ◽  
Tricyclic Antidepressants ◽  
Spinal Nerve ◽  
Control Group ◽  
Activating Transcription Factor 3 ◽  
Mechanical Stimuli ◽  
Activating Transcription Factor ◽  
Trial Setting ◽  
Transcription Factor 3

Background: Spinal nerve-ligated neuropathy and chemotherapy-induced neuropathy produce a persistent tactile allodynia in mice. Tianeptine is an antidepressant that exhibits structural similarities to tricyclic antidepressants but has distinct neurochemical properties. Objective: Here we examined the effects of intraperitoneal (i.p.) tianeptine on allodynia in spinal nerve-ligated and chemotherapy-induced neuropathic mice. Study Design: A randomized, experimental trial. Setting: Laboratory animal study. Methods: Spinal nerve-ligated neuropathy was induced in a Chung model made by ligating the L5 spinal nerve. Chemotherapy-induced neuropathy was induced by injecting vincristine (0.1 mg/kg/day; i.p.) on the following schedule: 5 days on, 2 days off, for14 days. Tianeptine (10, 30, and 50 mg/kg) and saline were administered, respectively, to both groups of neuropathic mice (n = 5 for each group). We evaluated mechanical allodynia using von Frey hairs prior to drug injections and at 30, 60, 90, 120, 180, and 240 minutes, and 24 hours after injections. We also measured the changes in activate transcription factor 3 (ATF3) level in the dorsal root ganglion (DRG) in each group in order to understand the analgesic mechanism of tianeptine. Results: Both spinal nerve-ligated and chemotherapy-induced neuropathic mice showed prominent allodynia. The control group showed no differences in mechanically induced allodynia compared to the experimental groups. For the tianeptine groups, paw-withdrawal thresholds in response to mechanical stimuli were significantly lower than the pre-administration values and values from the control group (P < 0.05). The increase in DRG ATF3 in neuropathic mice was reduced by tianeptine (P < 0.05). Limitations: Less is known about the transcription factors that affect inflammation signaling. Conclusions: Tianeptine administered i.p. reduces mechanical allodynia in spinal nerveligated and chemotherapy-induced neuropathic mice models. These effects were confirmed by attenuation of previously increased DRG ATF3. Key words: Tianeptine, spinal-nerve ligation, chemotherapy-induced neuropathic, activating transcription factor 3

Myocardial bridge analysis by multidetector computed tomography and its association with coronary atherosclerosis

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Mohamed Ismail Ahmed Abd El Ati Mousa ◽  
Yasser Gomaa Mohamed ◽  
Ahmed Mohamed Onsy
Keyword(s):  
Coronary Artery ◽  
Coronary Angiography ◽  
Atherosclerotic Plaque ◽  
Significant Risk ◽  
Atherosclerotic Lesion ◽  
Lesion Group ◽  
Atherosclerotic Plaques ◽  
Myocardial Bridge ◽  
Group A ◽  
Group B

Abstract Background Myocardial Bridging an inborn coronary abnormality, is defined as a segment of a major epicardial coronary artery, the tunneled artery, that goes intramurally through the myocardium beneath the muscle bridge. Objective To evaluate noninvasively the presence and distribution of atherosclerotic plaques in relation to myocardial bridge coronary segments and to determine the prevalence of myocardial bridges and their location and morphology by using MDCT. Patients and Methods The study population consisted of 55 patients presented with chest pain, referred for MDCT coronary angiography and found to have myocardial bridge at during the period from April 2018 and August 2019. 23 patients was found having Myocardial Bridge and coronary artery atherosclerotic plaques included in Group (A), 29 persons found having Myocardial Bridge without CAD included in Group (B). All patients were subjected to detailed history taking, clinical evaluation, ECG analysis and MSCT coronary angiography. Results In the present study, patients with atherosclerotic plaque (group A) (n = 29), mean age was 52.41 ± 10.55 years ranged from 35.0 to 73.0 years, 41.4% were males, while in Myocardial bridge without atherosclerotic lesion group (group B) (n = 26), mean age was 51.65 ± 7.58 ranged from 38.0 to 65.0 years., 30.8% were males. Conclusion Our study showed that diabetes mellitus and dyslipidemia are a significant risk factor for developing atherosclerotic plaque in the segment proximal to myocardial bridge. Myocardial bridge were usually located over the Mid segment of the left anterior descending coronary artery

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