Rationale and approach to evaluation of the impact of medical therapies on progression of atherosclerosis with arterial wall imaging

2010 ◽  
Vol 26 (3) ◽  
pp. 737-744 ◽  
Author(s):  
Kiyoko Uno ◽  
Ozgur Bayturan ◽  
Andrea Lavoie ◽  
Stephen J. Nicholls
Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Srinivasa R Kalidindi ◽  
Amy Hsu ◽  
Keon-Woong Moon ◽  
E. Murat Tuzcu ◽  
Steven E Nissen ◽  
...  

Background: While the importance of coronary artery disease in females has become increasingly recognized, little is known regarding the impact of gender with regard to changes in arterial wall dimensions with progression and regression of atherosclerosis. This study investigated the remodeling response of the artery wall accompanying changes in atheroma burden in response to use of medical therapies, stratified according to gender. Methods: 1533 patients (27.5% female) underwent serial intravascular ultrasound evaluation of a single coronary artery in the context of clinical trials that assess the impact of medical therapies on plaque progression. The relationship between gender and remodeling of the arterial wall at baseline and its serial change in association with plaque progression and regression were studied. Results: Females were older (59 v 57 years, p<0.01), had a higher body mass index (31.5 v 29.5 kg/m 2 , p<0.01), were more likely to have hypertension (86 v 71.5%, p<0.01) and metabolic syndrome (57 v 49%, p<0.01) and less likely to have a history of smoking (57.5 v 73.5%, p=0.01) and myocardial infarction (27.5 v 35.5%, p<0.01). After adjusting for body surface area, females demonstrated a trend towards smaller external elastic membrane (EEM) (226.3 v 234.3 mm 3 , p=0.09) and larger lumen (143.7 v 137.7 mm 3 , p=0.01) volumes. The remodeling index at the most diseased site did not differ between genders (0.95 v 0.95, p=0.95). No differences were observed between genders with regard to changes in EEM (−5.6 v −6.2 mm 3 , p=0.29) and lumen (−4.9 v −4.5 mm 3 , p=0.82) volumes and remodeling index (−0.02 v −0.03, p=0.43) in response to use of medical therapies. Similarly, there were no differences between genders with regard to the percentage of patients undergoing expansion (34.7 v 35.5%, p=0.86) or contraction (20.4 v 21.8%, p=0.69) of lumen volume in association with regression of atherosclerotic plaque. Conclusion: A similar pattern of remodeling of the arterial wall was observed between genders in association with serial changes in atheroscle-rotic plaque. This further highlights our understanding of the pathological interactions between atherosclerosis and the arterial wall in females.


2010 ◽  
Vol 26 (3) ◽  
pp. 745-751 ◽  
Author(s):  
Andrea Lavoie ◽  
Kiyoko Uno ◽  
Ozgur Bayturan ◽  
Stephen J. Nicholls

2021 ◽  
Vol 22 (11) ◽  
pp. 5843
Author(s):  
Chloé Turpin ◽  
Aurélie Catan ◽  
Olivier Meilhac ◽  
Emmanuel Bourdon ◽  
François Canonne-Hergaux ◽  
...  

The development and progression of atherosclerosis (ATH) involves lipid accumulation, oxidative stress and both vascular and blood cell dysfunction. Erythrocytes, the main circulating cells in the body, exert determinant roles in the gas transport between tissues. Erythrocytes have long been considered as simple bystanders in cardiovascular diseases, including ATH. This review highlights recent knowledge concerning the role of erythrocytes being more than just passive gas carriers, as potent contributors to atherosclerotic plaque progression. Erythrocyte physiology and ATH pathology is first described. Then, a specific chapter delineates the numerous links between erythrocytes and atherogenesis. In particular, we discuss the impact of extravasated erythrocytes in plaque iron homeostasis with potential pathological consequences. Hyperglycaemia is recognised as a significant aggravating contributor to the development of ATH. Then, a special focus is made on glycoxidative modifications of erythrocytes and their role in ATH. This chapter includes recent data proposing glycoxidised erythrocytes as putative contributors to enhanced atherothrombosis in diabetic patients.


Kardiologiia ◽  
2019 ◽  
Vol 59 (5) ◽  
pp. 36-44 ◽  
Author(s):  
D. Yu. Sedykh ◽  
A. N. Kazantsev ◽  
R. S. Tarasov ◽  
V. V. Kashtalap ◽  
A. N. Volkov ◽  
...  

Purpose. Determination of clinical and instrumental predictors of progressive course of multifocal atherosclerosis (MFA) in patients one year after myocardial infarction (MI), initially having hemodynamically insignificant stenoses of carotid arteries.Materials and methods. From database of patients with acute coronary syndrome treated in the Kemerovo Regional Clinical Cardiac Dispensary in 2009–2010 we selected for this study 141 patients with verified diagnosis of MI and hemodynamically insignificant lesions in the internal carotid artery (ICA) (stenosis up ≤ 55 %). All patients had coronary atherosclerosis verified on coronary angiography at admission because of MI. A multivariate analysis of possible predictors of the progressive course of multifocal atherosclerosis was made based on assessment of the development of cardiovascular complications (CVC) (death, MI, stroke and transient cerebral circulatory attacks [TIA]), as well as revascularizations and negative dynamics of parameters of color duplex scanning (CDS) of ICA during one year after MI. Results. One year after MI the overall incidence of CVC was 16.3 % (n=23). Structure of registered events was as follows: death from MI 7.1 % (n=10), deaths from stroke 2.1 % (n=3) and other causes 2.1 % (n=3), non-fatal MI 5.0 % (n=7), non-fatal stroke / TIA 2.1 % (n=3), carotid revascularization 2.8 % (n=4), coronary revascularization 14.9 % (n=21). CDC of ICAs was repeated in 125 patients. There were 17 (13.6 %) cases of progression of carotid atherosclerosis in the form of de novo bilateral stenoses in 14 (11.2 %) patients, stenoses in the left and right ICA 1 patient and 2 patients, respectively. The following predictors of progression of atherosclerosis of cerebral arteries were identified: family history of cardiovascular diseases (CVD),ICA stenosis ≥45 %, baseline circular atherosclerotic plaque (ASP). Predictors of high risk of stroke were family history of CVD, history of stroke,ICA stenosis ≥45 %, heterogeneous hypoechoic ASP. As predictors of lethal outcome, we identified history of MI, high functional class of angina preceding the index MI, severe coronary vascular bed involvement (SYNTAX score >23), presence of any bilateral atherosclerotic lesion in ICAs, and heterogeneous hypoechoic ASP. Assessment of the contribution of adherence to therapy in the prognosis 1 year after hospital discharge was fulfilled in 125 alive patients. It allowed to conclude that patients with progression of atherosclerosis and nonfatal CVC were characterized by insufficient adherence to standard therapy.Conclusion. Predictors of the progressive course of multifocal atherosclerosis during one year after MI were identified in this study. It is necessary to strengthen therapeutic and preventive measures aimed at minimization of the impact of these factors in this category of patients.   


Stroke ◽  
2018 ◽  
Vol 49 (4) ◽  
pp. 891-898 ◽  
Author(s):  
Nomazulu Dlamini ◽  
Ivanna Yau ◽  
Prakash Muthusami ◽  
David J. Mikulis ◽  
Jorina Elbers ◽  
...  

Author(s):  
Gérald Devuyst ◽  
Bart5omiej Piechowski-Józ´wiak ◽  
Julien Bogousslavsky
Keyword(s):  

Toxins ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 742
Author(s):  
Bogusz Trojanowicz ◽  
Christof Ulrich ◽  
Matthias Girndt

Apelin peptides (APLN) serve as second substrates for angiotensin-converting enzyme 2 (ACE2) and, in contrast to angiotensin II (AngII), exert blood-pressure lowering and vasodilatation effects through binding to G-coupled APLN receptor (APLNR). ACE2-mediated cleavage of the APLN may reduce its vasodilatory effects, but decreased ACE2 may potentiate the hypotensive properties of APLN. The role of APLN in uremia is unclear. We investigated the correlations between serum-APLN, leucocytic APLNR, and ACE2 in 32 healthy controls (NP), 66 HD, and 24 CKD3–5 patients, and the impact of APLN peptides on monocytic behavior and ACE2 expression under uremic conditions in vitro. We observed that serum APLN and leucocytic APLNR or SLCO2B1 were significantly elevated in uremic patients and correlated with decreased ACE2 on uremic leucocytes. APLN-treated THP-1 monocytes revealed significantly increased APLNR and ACE2, and reduced TNFa, IL-6, and MCSF. Uremic toxins induced a dramatic increase of miR-421 followed by significant reduction of ACE2 transcripts, partially counteracted with APLN-13 and -36. APLN-36 triggered the most potent transmigration and reduction of endothelial adhesion. These results suggest that although APLN peptides may partly protect against the decay of monocytic ACE2 transcripts, uremic milieu is the most dominant modulator of local ACE2, and likely to contribute to the progression of atherosclerosis.


Author(s):  
Frank Gijsen ◽  
Hans Schuurbiers ◽  
Michiel Schaap ◽  
Anton van der Steen ◽  
Jolanda Wentzel

Atherosclerosis is characterized by lipid accumulation in the arterial wall, followed by an inflammatory response. Plaque formation is generally observed near bifurcations in coronary arteries. The composition of atherosclerotic plaques depends on the location, and it was hypothesized that blood flow induced shear stress influences plaque composition2. To study the impact of shear stress on atherosclerotic disease in human coronary arteries, we developed a technique that enables us to generate 3D lumen reconstruction based on multislice computer tomography (MSCT) and intravascular ultrasound (IVUS).We describe two approaches to generate 3D reconstructions of human coronary artery bifurcations and apply them to coronary segments with bifurcations. We will evaluate the effect on shear stress distribution and its relationship to wall thickness.


1987 ◽  
Vol 5 (1) ◽  
pp. 160-169 ◽  
Author(s):  
J.R. Durham ◽  
J.M. Malone ◽  
V.M. Bernhard
Keyword(s):  

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Roch Listz Maurice ◽  
Nagib Dahdah ◽  
Johanne Tremblay

Background. Investigating the mechanical properties of the arteries is essential in cardiovascular diseases. Recent imaging modalities allow mapping mechanical properties within the arterial wall.Aims. We report the potential ofimaging-based biomarker(ImBioMark) to investigate the effect of aging on the rat. We also present preliminary data with ImBioMark characterizing vascular sequelae of Kawasaki disease (KD) in young humans.Methods. We investigatedin vivothe effect of aging on male Brown Norway (BN) rats' (n=5) carotid stiffness. In a second experiment, the impact of KD on the ascending aorta (AA) was examined in KD children (n=2) aged 13 ± 1.41 years old compared to KD-free children (n=5) aged 13.13 ± 0.18 years old.Results. The stiffness of BN's carotid artery was three times stiffer in the old rats, with a turning point at 40 weeks old (P=0.001). KD had a very significant impact on the AA stiffness with strain estimates of 2.39 ± 0.51% versus 4.24 ± 0.65% in controls (P<0.001).Conclusion. ImBioMark phenotypes hypertension in rat models noninvasivelyin vivowithout resorting to euthanasia. Quantifying aortic wall remodeling is also feasible in humans. Future investigations target human cardiovascular disease.


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