scholarly journals Intensive statin versus low-dose statin + ezetimibe treatment for fibrous cap thickness of coronary vulnerable plaques

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Pei-Na Meng ◽  
De-Lu Yin ◽  
Wen-Qi Lu ◽  
Tian Xu ◽  
Wei You ◽  
...  
Keyword(s):  
Low Dose ◽  
Fibrous Cap ◽  
Vulnerable Plaques ◽  
Ezetimibe Treatment ◽  
Fibrous Cap Thickness

Optical coherence tomography detection of vulnerable plaques at high risk of developing acute coronary syndrome

2021 ◽  
Author(s):  
Takashi Kubo ◽  
Yasushi Ino ◽  
Gary S Mintz ◽  
Yasutsugu Shiono ◽  
Kunihiro Shimamura ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Acute Coronary Syndrome ◽  
High Risk ◽  
Optical Coherence ◽  
Coronary Syndrome ◽  
Fibrous Cap ◽  
Vulnerable Plaques ◽  
Increased Risk ◽  
Lesion Level ◽  
Fibrous Cap Thickness

Abstract Aims The ability of optical coherence tomography (OCT) to detect plaques at high risk of developing acute coronary syndrome (ACS) remains unclear. The aim of this study was to evaluate the association between non-culprit plaques characterized as both lipid-rich plaque (LRP) and thin-cap fibroatheroma (TCFA) by OCT and the risk of subsequent ACS events at the lesion level. Methods and results In 1378 patients who underwent OCT, 3533 non-culprit plaques were analysed for the presence of LRP (maximum lipid arc > 180°) and TCFA (minimum fibrous cap thickness < 65 μm). The median follow-up period was 6 years [interquartile range (IQR): 5–9 years]. Seventy-two ACS arose from non-culprit plaques imaged by baseline OCT. ACS was more often associated with lipidic plaques that were characterized as both LRP and TCFA vs. lipidic plaques that did not have these characteristics [33% vs. 2%, hazard ratio 19.14 (95% confidence interval: 11.74–31.20), P < 0.001]. The sensitivity and specificity of the presence of both LRP and TCFA for predicting ACS was 38% and 97%, respectively. A larger maximum lipid arc [1.01° (IQR: 1.01–1.01°)], thinner minimum fibrous cap thickness [0.99 μm (IQR: 0.98–0.99 μm)], and smaller minimum lumen area [0.78 mm2 (IQR: 0.67–0.90 mm2), P < 0.001] were independently associated with ACS. Conclusion Non-culprit plaques characterized by OCT as both LRP and TCFA were associated with an increased risk of subsequent ACS at the lesion level. Therefore, OCT might be able to detect vulnerable plaques.

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

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 Fusion of fibrous cap thickness and wall shear stress to assess plaque vulnerability in coronary arteries: a pilot study

2016 ◽  
Vol 11 (10) ◽  
pp. 1779-1790 ◽  
Author(s):  
Guillaume Zahnd ◽  
Jelle Schrauwen ◽  
Antonios Karanasos ◽  
Evelyn Regar ◽  
Wiro Niessen ◽  
...  
Keyword(s):  
Shear Stress ◽  
Pilot Study ◽  
Wall Shear Stress ◽  
Coronary Arteries ◽  
Plaque Vulnerability ◽  
Fibrous Cap ◽  
Wall Shear ◽  
Fibrous Cap Thickness

Atherosclerotic plaque disruption induced by stress and lipopolysaccharide in apolipoprotein E knockout mice

2009 ◽  
Vol 296 (5) ◽  
pp. H1598-H1606 ◽  
Author(s):  
Mei Ni ◽  
Yan Wang ◽  
Mei Zhang ◽  
Peng Fei Zhang ◽  
Shi Fang Ding ◽  
...  
Keyword(s):  
Apolipoprotein E ◽  
High Fat Diet ◽  
Morphological Analysis ◽  
Fibrous Cap ◽  
Atherosclerotic Lesions ◽  
Plaque Disruption ◽  
Apolipoprotein E Knockout Mice ◽  
Fibrous Cap Thickness ◽  
And Control ◽  
Disruption Rate

To establish an animal model with disruptions of atherosclerotic plaques, 96 male apolipoprotein E knockout (apoE−/−) mice were randomly divided into stress, lipopolysaccharide (LPS), stress+LPS, and control groups ( n = 24 each). All mice were fed a high-fat diet throughout the experiment, and carotid atherosclerotic lesions were induced by placement of a constrictive perivascular collar. Four weeks after surgery, mice in the LPS and stress+LPS groups were intraperitoneally injected with LPS (1 mg/kg twice per week for 8 wk). Eight weeks after surgery, mice in the stress and stress+LPS groups were treated with intermittent physical stress (electric foot shock and noise stimulation) for 4 wk. Morphological analysis revealed a plaque disruption rate of 16.7% in control, 34.8% in LPS, 54.2% in stress, and 60.9% in stress+LPS groups. The disruption rates in stress and stress+LPS groups were both significantly higher than those of controls ( P = 0.007 and P = 0.002, respectively). Luminal thrombosis secondary to plaque disruption was observed only in the stress+LPS group. Both stress and LPS stimulation significantly decreased fibrous cap thickness and increased macrophage and lipid contents in plaques. Moreover, the combination of stress and LPS stimulation further lowered cap thickness and enhanced accumulation of macrophages and expression of inflammatory cytokines and matrix metalloproteinases. Stress activated the sympathetic nervous system, as manifested by increased blood pressure and flow velocity. Plasma fibrinogen levels were remarkably elevated in the stress and stress+LPS groups. In conclusion, stress- and LPS-costimulated apoE−/− mice provide a useful model for studies of plaque vulnerability and interventions.

scholarly journals Reproducibility of In Vivo Measurements for Fibrous Cap Thickness and Lipid Arc by OCT

2012 ◽  
Vol 5 (10) ◽  
pp. 1072-1074 ◽  
Author(s):  
Soo-Joong Kim ◽  
Hang Lee ◽  
Koji Kato ◽  
Taishi Yonetsu ◽  
Lei Xing ◽  
...  
Keyword(s):  
In Vivo Measurements ◽  
Fibrous Cap ◽  
Fibrous Cap Thickness

scholarly journals Optical Coherence Tomography Predictors for a Favorable Vascular Response to Statin Therapy

2021 ◽  
Vol 10 (1) ◽  
Author(s):  
Akihiro Nakajima ◽  
Yoshiyasu Minami ◽  
Makoto Araki ◽  
Osamu Kurihara ◽  
Tsunenari Soeda ◽  
...  
Keyword(s):  
Optical Coherence Tomography ◽  
Statin Therapy ◽  
Optical Coherence ◽  
Vascular Response ◽  
Unique Identifier ◽  
Tomography Imaging ◽  
3 Dimensional ◽  
Fibrous Cap ◽  
Optical Coherence Tomography Imaging ◽  
Fibrous Cap Thickness

Background Specific plaque phenotypes that predict a favorable response to statin therapy have not been systematically studied. This study aimed to identify optical coherence tomography predictors for a favorable vascular response to statin therapy. Methods and Results Patients who had serial optical coherence tomography imaging at baseline and at 6 months were included. Thin‐cap area (defined as an area with fibrous cap thickness <200 μm) was measured using a 3‐dimensional computer‐aided algorithm, and changes in the thin‐cap area at 6 months were calculated. A favorable vascular response was defined as the highest tertile in the degree of reduction of the thin‐cap area. Macrophage index was defined as the product of the average macrophage arc and length of the lesion with macrophage infiltration. Layered plaque was defined as a plaque with 1 or more layers of different optical density. In 84 patients, 140 nonculprit lipid plaques were identified. In multivariable analysis, baseline thin‐cap area (odds ratio [OR] 1.442; 95% CI, 1.024–2.031, P =0.036), macrophage index (OR, 1.031; 95% CI, 1.002–1.061, P =0.036), and layered plaque (OR, 2.767; 95% CI, 1.024–7.479, P =0.045) were identified as the significant predictors for a favorable vascular response. Favorable vascular response was associated with a decrease in the macrophage index. Conclusions Three optical coherence tomography predictors for a favorable vascular response to statin therapy have been identified: large thin‐cap area, high macrophage index, and layered plaque. Favorable vascular response to statin was correlated with signs of decreased inflammation. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01110538.

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