Thoracic aortic atherosclerosis in patients with aortic regurgitation

Shimoni, Sara; Zilberman, Liaz; Edri, Orly; Bar, Iris; Goland, Sorel; Gendelman, Gera; Swissa, Moshe; Livshitz, Shay; Paz, Ofir; Ayzenberg, Oded; George, Jacob

doi:10.1016/j.atherosclerosis.2011.05.026

Cited by 10 publications

(9 citation statements)

References 16 publications

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“…This observation is confirmed clinically. Studies by Shimoni et al showed more severe atherosclerosis of descending aorta in patients with aortic regurgitation (regardless of etiology and risk profile) in comparison to a control group similar with regard to age and presence of risk factors [21]. These observations corroborate contribution of hemodynamics and reversal flow to development of aortic calcifications.…”

Section: Topography Of Atherosclerotic Lesions In Thoracic Aortasupporting

confidence: 56%

Not at random location of atherosclerotic lesions in thoracic aorta and their prognostic significance in relation to the risk of cardiovascular events

2013

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SummaryThoracic aortic calcium deposits are frequently detected on tomography of the chest, and in other imaging modalities. Numerous studies indicated the correlation of hemodynamic parameters such as wall shear stress in relation to distribution aortic calcifications. This publication discusses similarities and differences of two distinct pathomechanisms of arterial calcifications: intimal associated with atherosclerosis and medial knows as Mönckeberg’s arteriosclerosis. This review also analyzes the frequent coexistence of aortic calcification and coronary artery disease in terms of risk of cardiovascular events.

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Section: Topography Of Atherosclerotic Lesions In Thoracic Aortasupporting

confidence: 56%

Not at random location of atherosclerotic lesions in thoracic aorta and their prognostic significance in relation to the risk of cardiovascular events

2013

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“…However, no strain differences in the asymmetrical flow pattern at either location were observed. Additionally, both experimental and clinical data show that the oscillatory flow pattern associated with aortic regurgitation (AR) increases atherosclerosis in the descending aorta (20,23,24). Interestingly, the AR severity, measured by early diastolic TVI, correlated positively with plaques in the descending aorta, while it was negatively correlated with the presence of plaques in the aortic arch in low-density lipoprotein receptor-null mice (20).…”

Section: Discussionmentioning

confidence: 99%

Relationship between hemodynamics and atherosclerosis in aortic arches of apolipoprotein E-null mice on 129S6/SvEvTac and C57BL/6J genetic backgrounds

et al. 2012

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Objective We investigated the relationships between hemodynamics and differential plaque development at the aortic arch of apolipoprotein E (apoE)-null mice on 129S6/SvEvTac (129) and C57BL/6J (B6) genetic backgrounds. Methods Mean flow velocities at the ascending and descending aorta (mVAA and mVDA) were measured by Doppler ultrasound in wild type and apoE-null male mice at 3 and 9 months of age. Following dissection of the aortic arches, anatomical parameters and plaque areas were evaluated. Results Arch plaques were five times bigger in 129-apoE than in B6-apoE mice at 3 months, and twice as large at 9 months. The geometric differences, namely larger vessel diameter in the B6 strain and broader inner curvature of the aortic arch in the 129 strain, were exaggerated in 9-month-old apoE-null mice. Cardiac output and heart rate under anesthesia were significantly higher in the B6 strain than in the 129 strain. The values of mVAA were similar in the two strains, while mVDA was lower in the 129 strain. However, there was a 129-apoE-specific reduction of flow velocities with age, and both mVAA and mVDA were significantly lower in 129-apoE than in B6-apoE mice at 9 months. The mean relative wall shear stress (rWSS) over the aortic arch in 129-apoE and B6-apoE mice were not different, but animals with lower mean rWSS had larger arch plaques within each strain. Conclusions The plaque formation in the arch of apoE-null mice is accompanied by strain-dependent changes in both arch geometry and hemodynamics. While arch plaque sizes negatively correlate with mean rWSS, additional factors are necessary to account for the strain differences in arch plaque development.

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“…Most animal models of volume overload have used arteriovenous fistulae (aortocaval shunts) (8,9) which, however, rarely occur in humans (10). Moreover, arteriovenous fistulae result in mixing of arterial and venous blood and do not recapitulate the increases in diastolic blood flow in the ventricles observed with valve disorders, thereby potentially limiting the relevance and applicability of these animal models (11,12). Taking these issues into consideration, we have previously established an AR model to induce volume overload in mice, by disrupting the aortic valve cusps.…”

Section: Introductionmentioning

confidence: 99%

Left ventricular response in the transition from hypertrophy to failure recapitulates distinct roles of Akt, β-arrestin-2, and CaMKII in mice with aortic regurgitation

You

Wang

et al. 2020

Ann Transl Med

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Background: Although aortic regurgitation (AR) is a clinically important condition that is becoming increasingly common, few relevant murine models and mechanistic studies exist for this condition. In this study, we attempted to delineate the pathological and molecular changes and address the roles of some potentially relevant molecules in an animal model of surgically induced AR.Methods: AR was induced by puncturing the aortic valve leaflets in C57BL/6J mice under echocardiographic guidance.Results: As early as 1 week following AR, the left ventricles (LV) displayed marked impairments in diastolic function and coronary flow reserve (CFR), as well as cardiac hypertrophy and chamber dilatation at both end-systole and end-diastole. LV free wall thickening and cardiomyocyte hypertrophy in LV were observed 2 weeks following of AR while a decline in ejection fraction was not seen until after 4 weeks. Nppa (natriuretic peptide A) and Nppb (natriuretic peptide B) increased over time, in conjunction with prominent Akt activation as well as slight CaMKII (Ca 2+ /calmodulin-dependent protein kinase II) activation and biphasic changes in β-arrestin-2 expression. Treatment of AR mice with Akt inhibition exacerbated the eccentric hypertrophy, while neither inhibition of CaMKII nor β-arrestin-2 overexpression influenced the response to AR.Conclusions: Our structural, functional, molecular and therapeutic analyses reveal that Akt, but not CaMKII or β-arrestin-2, plays a regulatory role in the development of LV remodeling after AR in Mice.These results may shed important light on therapeutic targets for volume overloaded cardiomyopathy.

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Thoracic aortic atherosclerosis in patients with aortic regurgitation

Cited by 10 publications

References 16 publications

Not at random location of atherosclerotic lesions in thoracic aorta and their prognostic significance in relation to the risk of cardiovascular events

Not at random location of atherosclerotic lesions in thoracic aorta and their prognostic significance in relation to the risk of cardiovascular events

Relationship between hemodynamics and atherosclerosis in aortic arches of apolipoprotein E-null mice on 129S6/SvEvTac and C57BL/6J genetic backgrounds

Left ventricular response in the transition from hypertrophy to failure recapitulates distinct roles of Akt, β-arrestin-2, and CaMKII in mice with aortic regurgitation

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