The pathogenesis of atherosclerosis of the mitral and aortic valves

Walton, K. W.; Williamson, N. B.; Johnson, Agnes

doi:10.1002/path.1711010302

Cited by 74 publications

(31 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, lipid deposition was not observed in the stromal fibroblasts or within the extracellular spaces. Lipid deposition has been considered indicative of valvular atherosclerosis [15]. The absence of lipid in the valves is contrary to observations of the aorta in this patient in which lipid was deposited within fibroblasts, smooth muscle cells, and macrophages [4], In addition, changes related to the aging process [12] were not observed in the valvular stroma of this patient.…”

Section: Discussioncontrasting

confidence: 50%

Human Valvular Disease in Coxsackie B<sub>4</sub> Virus Infection

Burch¹,

Harb²,

Hiramoto³

1974

Cardiology

View full text Add to dashboard Cite

Valvular tissue from a patient with possible Coxsackie B₄ virus infection was studied. Antigen to Coxsackie B₄ virus was detected in cells of the mitral valve by immunofluorescent staining. Histologic examination of the mitral valve revealed widespread increase in collagenous fibers, subendocardial edema and infiltration of basophilic cells, formation of verruca on the mitral valve surface, and fibrinoid degeneration of collagen fibers. Fragmented fibroblasts and numerous fibers of elastin were observed electron microscopically. The pathologic changes were similar to lesions of endocarditis in rheumatic fever. This case reveals the possible role of viruses in production of valvular heart disease in man usually attributed to rheumatic fever due to streptococcal infections.

show abstract

Section: Discussioncontrasting

confidence: 50%

Human Valvular Disease in Coxsackie B<sub>4</sub> Virus Infection

Burch¹,

Harb²,

Hiramoto³

1974

Cardiology

View full text Add to dashboard Cite

show abstract

“…8 Previous histopathologic research has demonstrated similarities between atherosclerosis in the vasculature and chronic degenerative changes in the aortic and mitral valves. 26,27 For example, the initiating event for valve disease is likely to be injury or dysfunction of the endothelium, 28 especially in areas of altered shear stress and blood rheology. 29 Furthermore, the calcified aortic valve lesion develops in the setting of inflammation 30 and displays hallmarks of atherosclerosis, including lipid accumulation, 31 matrix metalloproteinase activation, 32 and interaction with the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 99%

Mitral and Aortic Annular Calcification Are Highly Associated With Systemic Calcified Atherosclerosis

et al. 2006

View full text Add to dashboard Cite

Background-Atherosclerosis has been implicated as a cause of valvular calcification. The aim of this study was to determine whether atherosclerotic calcification in multiple vascular areas is significantly associated with aortic or mitral annular calcification independent of traditional risk factors. Methods and Results-A total of 1242 consecutive asymptomatic patients free of clinical coronary heart disease were studied by electron-beam computed tomography for the extent of calcium due to atherosclerosis in 5 distinct vascular beds and calcium in the aortic and mitral annuli. Nearly 24% had calcium in the aortic annulus, whereas 8% were found to have mitral annular calcification. Age and a history of hypertension were the only traditional cardiovascular risk factors that were independently associated with prevalent calcification in the aortic and mitral annuli. After adjustment for age, gender, and cardiovascular disease risk factors, subjects with calcium in the thoracic aorta had the highest odds for the presence of aortic annular calcium (ORϭ3.9, PϽ0.01), whereas those with calcium in the abdominal aorta had the highest odds for mitral annular calcification (ORϭ5.1, Pϭ0.01). Standardized increases in calcium in the abdominal aorta (ORϭ2.0, PϽ0.01) and iliacs (ORϭ1.8, Pϭ0.01) were significantly associated with calcium in the aortic annulus after adjustment for the extent of calcium in the other vascular beds, whereas the thoracic aorta was significantly associated (ORϭ1.4, Pϭ0.02) with calcium in the mitral annulus. Conclusions-This

show abstract

“…In murine models of atherosclerosis, atherogenesis preferentially starts at the aortic root, 15 and lesions indicative of atherosclerosis have been described for human aortic and mitral valves. 19 This could be due to mechanical stresses from turbulent blood flow patterns at this site, 20 at which lipid is first deposited. In accord, areas within the vicinity of aortic valve commissures of 3-week-old apoE Ϫ/Ϫ mice were the first sites to express both hsps.…”

Section: Discussionmentioning

confidence: 99%

Temporal Expression of Heat Shock Proteins 60 and 70 at Lesion-Prone Sites During Atherogenesis in ApoE-Deficient Mice

Kanwar

Wang

et al. 2001

ATVB

View full text Add to dashboard Cite

Abstract-In the study, we investigate whether the expressions of heat shock protein (hsp)60 (a potential autoantigen) and the stress-inducible form of cytoprotector hsp70 are correlated with the development of atherosclerotic lesions in the aortic tree of apolipoprotein E-deficient (apoE Ϫ/Ϫ ) mice. The apoE Ϫ/Ϫ mouse model is advantageous because the stress-inducible form of hsp70 is not constitutively expressed in mice, unlike primates; hence, tissues under stress can be clearly defined. Both mammalian hsps were detected newly expressed (before mononuclear cell infiltration) on aortic valves and endothelia at lesion-prone sites of 3-week-old apoE Ϫ/Ϫ mice. In 8-and 20-week-old mice, they were strongly and heterogeneously expressed in early to advanced fibrofatty plaques, with levels correlating with lesion severity. Expression was markedly downregulated in advanced collagenous, acellular, calcified plaques of 40-and 69-week-old mice and was absent in control aortas of normocholesterolemic wild-type (apoE ϩ/ϩ ) mice. Western blot analysis of tissue homogenates confirmed the temporal expression of the hsps. Double immunostaining revealed that both hsps were expressed by lesional endothelial cells, macrophages, smooth muscle cells, and CD3ϩ T lymphocytes. This study provides evidence that hsp60 and hsp70 are temporally expressed on all major cell types in lesion-prone sites during atherogenesis, suggesting that few cells escape the toxic environment of the atherosclerotic plaque.

show abstract

The pathogenesis of atherosclerosis of the mitral and aortic valves

Cited by 74 publications

References 30 publications

Human Valvular Disease in Coxsackie B<sub>4</sub> Virus Infection

Human Valvular Disease in Coxsackie B<sub>4</sub> Virus Infection

Mitral and Aortic Annular Calcification Are Highly Associated With Systemic Calcified Atherosclerosis

Temporal Expression of Heat Shock Proteins 60 and 70 at Lesion-Prone Sites During Atherogenesis in ApoE-Deficient Mice

Contact Info

Product

Resources

About