Experimental aortic valve stenosis in rabbits

Drolet, Marie‐Claude; Arsenault, Marie; Couët, Jacques

doi:10.1016/s0735-1097(03)00090-1

Cited by 137 publications

(97 citation statements)

References 30 publications

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“…20,21 Furthermore, in experimental animal models, aortic valve stenosis seemed to develop in hypercholesterolemic rabbits only if supplemented with vitamin D(2). 22 Hence, although increasing age and atherosclerotic factors are important acknowledged risks, it seems that additional factors such as calcium handling and genetic predisposition could be needed to develop calcific AS. To that effect, despite our study's high prevalence of traditional cardiac risk factors and coronary artery disease, the apoE4 allele was still found to be a significant independent predictor of AS.…”

Section: Discussionmentioning

confidence: 99%

Association Between Apolipoprotein E Alleles and Calcific Valvular Heart Disease

et al. 2003

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Background-Studies on apolipoprotein E (apoE) alleles have reported an increased risk of coronary heart disease in patients with the apoE4 allele. Given the risk factor and histological similarities between coronary and calcific valvular heart disease (aortic stenosis [AS] and mitral annular calcification [MAC]), we postulated that apoE alleles might be associated with the development of these valvular lesions. Methods and Results-We evaluated the association between apoE alleles and calcific valvular lesions in 802 patients undergoing transthoracic echocardiography using logistic regression analyses. No difference was noted in genotype distribution (Pϭ0.59) or prevalence of apoE4 between those with or without MAC (30% versus 27%, respectively; Pϭ0.57). Compared with patients without AS, the genotype distribution of patients with AS differed significantly (Pϭ0.03), with increasing prevalences of the apoE 4 allele (27% in those without versus 40% in those with AS; Pϭ0.01). In multivariate analyses adjusting for age, gender, low-density lipoprotein cholesterol levels, and coronary artery disease, increasing age and the apoE4 allele were significant independent predictors of AS (odds ratio, 1.94; 95% confidence interval, 1.01 to 3.71; Pϭ0.046), whereas the apoE4 allele was not predictive of MAC. Conclusions-These findings support extension of the importance of the apoE4 allele beyond atherosclerosis and Alzheimer's disease to calcific AS.

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Section: Discussionmentioning

confidence: 99%

Association Between Apolipoprotein E Alleles and Calcific Valvular Heart Disease

et al. 2003

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“…Additionally, animal models of hypercholesterolemia develop AV lesions. 79,80 These findings have stimulated interest in the possibility that the statin drugs, which lower systemic cholesterol and decrease inflammation in atherosclerosis, may decrease the rate of aortic stenosis progression. [81][82][83] VICs with an osteoblastic phenotype (obVICs) are found in calcifying valves.…”

Section: Calcific Av Stenosismentioning

confidence: 99%

Evolving Concepts of Cardiac Valve Dynamics

2008

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Abstract-Considerable progress has been made in recent years toward elucidating a conceptual framework that integrates the dynamic functional structure, mechanical properties, and pathobiological behavior of the cardiac valves. This communication reviews the evolving paradigm of a continuum of heart valve structure, function, and pathobiology and explores its implications. Specifically, we discuss (1) the interactions of valve biology and biomechanics (eg, correlations of function with structure at the cell, tissue, and organ levels and mechanical considerations, development, endothelial cell and interstitial cell biology, extracellular matrix biology, homeostasis, and adaptation to environmental change); (2) Key Words: aortic valve Ⅲ mitral valve Ⅲ pathology Ⅲ prosthesis Ⅲ tissue engineering I mportant conceptual advances, new data, and evolution in our understanding and application of the principles underlying the dynamic functional, biological, and mechanical behavior of the cardiac valves have occurred in recent years. Research in heart valve biology and disease has been enabled by the availability of cultures of heart valve cells, computational methodology, the design and use of in vitro and in vivo experimental systems that model elements of valve biological and pathobiological activity, and targeted study of normally functioning and pathological native and substitute human valves. Collectively, these developments have facilitated a growing understanding of how shortand long-term biomechanical valve function at the organ level relates to tissue and cell structure and normal valve function, elucidated the pathological anatomy and mechanisms of valvular dysfunction, fostered improvements in tissue heart valve substitutes and surgical repairs, and informed innovative approaches to heart valve tissue engineering and regeneration. [1][2][3][4] In this communication, we highlight key recent insights into heart valve function and dysfunction and their implications for the prevention, diagnosis, and treatment of clinical heart valve disease, currently and in the future. The heart valves are tissue structures whose motions are driven by mechanical forces exerted by the surrounding blood and heart. The ability of the valves to permit unobstructed forward flow depends on the mobility, pliability, and structural integrity of their leaflets (in the TV and MV) and cusps (in the PV and AV).The individual AV cusps attach to the aortic wall in a crescentic (or semilunar) fashion, ascending to the commissures (where adjacent cusps come together at the aorta) and descending to the basal attachment of each cusp to the aortic wall. Behind the cusps are dilated pockets in the aortic root, called sinuses of Valsalva, which bulge with each ejection of blood. The AV cusps and their respective sinuses are named for their relationship to the coronary artery ostia that arise from them, normally a left, a right, and a noncoronary (cusp and associated sinus). In the middle of the free edge of each cusp on the ventricular surface is a ...

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“…6,7 In addition to a lipid-lowering effect, statins have other beneficial effects in vascular atherosclerosis, including modification of endothelial function, decreased inflammation via inhibition of macrophage activation, upregulation of endothelial nitric oxide synthase (eNOS), and inhibition of smooth muscle cell proliferation. 8 Experimental models suggest that statins might have similar effects in valve tissue, with demonstration of a decrease in atherosclerotic effects, a reduction in osteoblast gene markers, and inhibition of calcification via upregulation of eNOS.…”

Section: See P 1291mentioning

confidence: 99%