scholarly journals Attenuation of inflammation and expansive remodeling by Valsartan alone or in combination with Simvastatin in high-risk coronary atherosclerotic plaques

2009 ◽  
Vol 203 (2) ◽  
pp. 387-394 ◽  
Author(s):  
Yiannis S. Chatzizisis ◽  
Michael Jonas ◽  
Roy Beigel ◽  
Ahmet U. Coskun ◽  
Aaron B. Baker ◽  
...  
Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Xihai Zhao ◽  
Huilin Zhao ◽  
Feiyu Li ◽  
Jie Sun ◽  
Ye Cao ◽  
...  

Introduction Rupture of vulnerable atherosclerotic plaques in the intracranial and extracranial carotid arteries could trigger ischemic stroke. However, the incidence of high risk atherosclerotic lesions in these vascular beds is not well known. This study sought to investigate the incidence of high risk atherosclerotic lesions in intracranial and extracranial carotid arteries in stroke patients using magnetic resonance (MR) imaging. Methods Seventy-five patients (mean age 62.7 years, 56 males) with acute ischemic stroke underwent MR imaging for index carotid arteries, assigned as the same side as the brain lesions, with a Philips 3.0T MR scanner. Intracranial carotid MR angiography was performed using 3D TOF sequence with FOV of 23 × 23 cm 2 , matrix of 256 × 256, and a slice thickness of 1mm. The multi-contrast vessel wall images (3D TOF, T1W, T2W, and MP-RAGE) were acquired for extracranial carotid arteries with FOV of 14 × 14 cm 2 , matrix of 256 × 256, and slice thickness of 2 mm. The intracranial artery includes middle cerebral artery (MCA), anterior cerebral artery (ACA), and posterior cerebral artery (PCA). The extracranial carotid artery was divided into internal carotid artery (ICA), bulb, and common carotid artery (CCA). Luminal stenosis for each intracranial and extracranial carotid segment was measured and graded (normal or mild = 0-29%, moderate =30-69%, severe=70-99%). Normalized wall index (NWI = wall area/total vessel area × 100%), and presence/absence of calcification, lipid-rich necrotic core (LRNC), and intraplaque hemorrhage (IPH) and/or fibrous cap rupture in each extracranial carotid segment were determined. Results MCAs developed more severe stenotic lesions (24.6%), followed by extracranial carotids (16.5%), PCAs (5.4%), and ACAs (4.1%) in stroke patients ( Figure 1 A). For extracranial carotid arteries, ICAs showed the largest plaque burden as measured by NWI (44.3%±13.1%), followed by bulbs (39.4%±13%), and CCAs (37%±6.8%). Compared to CCAs, ICAs and bulb regions had more LRNCs (38.4% and 49.3% for ICA and bulb respectively) and IPH and/or rupture (11% and 9.6% for ICA and bulb respectively) ( Figure 1 B). Conclusions In patients with acute ischemic stroke, high risk atherosclerotic plaques can be found in both intracranial and extracranial carotid arteries, particularly in the MCA, ICA and bulb regions. Compared to extracranial carotid arteries, intracranial arteries develop more high risk lesions. The findings of this study suggest the necessity for early screening to detect high risk atherosclerotic lesions in these carotid vascular beds prior to cerebravascular events.


2017 ◽  
Vol 11 (6) ◽  
pp. 455-461 ◽  
Author(s):  
Daniel R. Obaid ◽  
Patrick A. Calvert ◽  
Adam Brown ◽  
Deepa Gopalan ◽  
Nick E.J. West ◽  
...  

2020 ◽  
Vol 28 (3) ◽  
pp. 346-352
Author(s):  
George C Drosos ◽  
George Konstantonis ◽  
Petros P Sfikakis ◽  
Maria G Tektonidou

Abstract Aims The aim of this study was to assess the performance of eight clinical risk prediction scores to identify individuals with systemic lupus erythematosus (SLE) at high cardiovascular disease (CVD) risk, as defined by the presence of atherosclerotic plaques. Methods CVD risk was estimated in 210 eligible SLE patients without prior CVD or diabetes mellitus (female: 93.3%, mean age: 44.8 ± 12 years) using five generic (Systematic Coronary Risk Evaluation (SCORE), Framingham Risk Score (FRS), Pooled Cohort Risk Equations (ASCVD), Globorisk, Prospective Cardiovascular Münster Study risk calculator (PROCAM)) and three ‘SLE-adapted’ (modified-SCORE, modified-FRS, QRESEARCH risk estimator, version 3 (QRISK3)) CVD risk scores, as well as ultrasound examination of the carotid and femoral arteries. Calibration, discrimination and classification measures to identify high CVD risk based on the presence of atherosclerotic plaques were assessed for all risk models. CVD risk reclassification was applied for all scores by incorporating ultrasound results. Results Moderate calibration (p-value range from 0.38 to 0.63) and discrimination (area under the curve 0.73–0.84), and low-to-moderate sensitivity (8.3–71.4%) and classification ability (Matthews correlation coefficient (MCC) 0.25–0.47) were observed for all risk models to identify patients with plaques at any arterial site as high-risk. MCC was improved for modified-FRS versus FRS (0.43 vs 0.36), but not for modified-SCORE versus SCORE (0.25 vs 0.25). Based on plaque presence, CVD risk was upgraded to high-risk in 10%, 16.1%, 20.5%, 21.5%, 24%, 28.2% and 28.6% of cases classified as non-high-risk by QRISK3, modified-FRS, Globorisk, FRS/PROCAM, ASCVD, modified-SCORE and SCORE, respectively. Conclusions Most of the five generic and three ‘SLE-adapted’ clinical risk scores underestimated high CVD risk defined by atherosclerotic plaque presence in patients with SLE.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
R I Hodas ◽  
D Opincariu ◽  
N Rat ◽  
I Rodean ◽  
M Chitu ◽  
...  

Abstract Funding Acknowledgements PlaqueImage.- research grant no. 103544/2016, contract number 26/01.09.2016 - Background Previous studies demonstrated that plaque morphology has a crucial role in the development of an acute coronary syndrome (ACS). However, not all vulnerable coronary plaques produce an ACS and the prediction power of various vulnerability features to predict an acute coronary event in a close future, has not been elucidated so far. Objective We aimed to use multi-slice computed tomography angiography (CTA) for assessment of morphological characteristics of culprit lesions producing an ACS in the next several months after CT assessment, in comparison with morphological characteristics of unstable coronary atherosclerotic plaques which did not trigger an ACS. Material and methods We analyzed 40 patients in whom CTA revealed presence of unstable coronary lesions, exhibiting at least one marker of vulnerability: napkin ring sign (NRS), spotty calcium (SC), positive remodeling (PR) or presence of low attenuation plaque (LAP), divided in 2 groups: group 1 - 20 patients who developed an ACS in the next 6 months following CTA examination, and group 2 – 20 patients matched for age, gender and risk factors, who did not present any cardiovascular event 6 month after CTA assessment. Post-processing of multi-slice CTA images was performed in order to assess morphological characteristics and CT-derived markers of atherosclerotic plaque instability. Results Similar mean values of plaque length (17.1 +/- 5.9 mm vs 16.9 +/- 3.4 mm; p = 0.6) and total atheroma volume (188.1 +/- 104.7 mm3vs 186.4 +/- 90.7 mm3; p = 0.8) were obtained for both groups. The mean number of vulnerability markers was 1.6 in group 1 vs 1.2 in group 2 (p = 0.07). However, atherosclerotic lesions in patients from group 1 presented significantly higher values of lipid-rich atheroma (9.8 +/- 10.8 mm3vs 2.6 +/- 1.0 mm3; p = 0.01) and remodeling index (1.14 +/- 0.3 in group 1 vs 0.89 +/- 0.19 in group 2, p = 0.04). At the same time, atheromatous plaques in patients who developed an ACS during the 6-months follow-up showed in a significantly higher proportion LAP (45% in group vs 10% in group 2, p = 0.03) and PR (15%in group 1 versus 5% in group 2, p = 0.04), but not NRS (30% vs 25%, p = ns) or SC (65% vs 40%, p = 0.2). Conclusions Atherosclerotic plaques producing an ACS exhibit a different phenotype than unstable plaques that remain silent. The CTA profile of atheromatous plaques producing an ACS includes the presence of low attenuation, positive remodeling, higher RI and lipid-rich atheroma. Presence of these features in high-risk coronary plaques identifies very high risk patients, who can benefit from adapted therapeutic strategy in order to prevent the development of an ACS.


Circulation ◽  
2008 ◽  
Vol 117 (8) ◽  
pp. 993-1002 ◽  
Author(s):  
Yiannis S. Chatzizisis ◽  
Michael Jonas ◽  
Ahmet U. Coskun ◽  
Roy Beigel ◽  
Benjamin V. Stone ◽  
...  

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Nay Min Htun ◽  
Yung Chih Chen ◽  
Bock Lim ◽  
Tara Schiller ◽  
Ghassan J. Maghzal ◽  
...  

Nano Research ◽  
2019 ◽  
Vol 12 (4) ◽  
pp. 863-868 ◽  
Author(s):  
Tao Wang ◽  
Jiuyang He ◽  
Demin Duan ◽  
Bing Jiang ◽  
Peixia Wang ◽  
...  

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