Role of inflammation in nonrheumatic, regurgitant heart valve disease. A comparative, descriptive study regarding apolipoproteins and inflammatory cells in nonrheumatic heart valve disease

Wallby, Lars; Steffensen, Thora S.; Broqvist, Mats

doi:10.1016/j.carpath.2006.10.004

Cited by 16 publications

(7 citation statements)

References 31 publications

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“…On the other hand, we found a much lesser involvement of inflammatory cells than reported in aortic valves [22]. Although some degree of lymphocytes and macrophages infiltration in non-rheumatic regurgitant mitral valves has been described, it is significantly lower than in calcific aortic stenosis [30,31], suggesting differential pathophysiological mechanisms with a more prominent role of VICs and VECs in mitral valve disease than in calcific aortic degeneration -which presents features more similar to the atherosclerotic process. The prevalence in our patients of coronary artery disease, defined as coronary stenosis ≥50% of the lumen, was 21%, mostly subclinical, since only 6% had previously had myocardial infarction.…”

Section: Discussioncontrasting

confidence: 55%

Activation of the Interleukin-33/ST2 Pathway Exerts Deleterious Effects in Myxomatous Mitral Valve Disease

García-Peña

Ibarrola

Navarro

et al. 2021

IJMS

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Mitral valve disease (MVD) is a frequent cause of heart failure and death worldwide, but its etiopathogenesis is not fully understood. Interleukin (IL)-33 regulates inflammation and thrombosis in the vascular endothelium and may play a role in the atherosclerotic process, but its role in mitral valve has not been investigated. We aim to explore IL-33 as a possible inductor of myxomatous degeneration in human mitral valves. We enrolled 103 patients suffering from severe mitral regurgitation due to myxomatous degeneration undergoing mitral valve replacement. Immunohistochemistry of the resected leaflets showed IL-33 and ST2 expression in both valve interstitial cells (VICs) and valve endothelial cells (VECs). Positive correlations were found between the levels of IL-33 and molecules implicated in the development of myxomatous MVD, such as proteoglycans, extracellular matrix remodeling enzymes (matrix metalloproteinases and their tissue inhibitors), inflammatory and fibrotic markers. Stimulation of single cell cultures of VICs and VECs with recombinant human IL-33 induced the expression of activated VIC markers, endothelial–mesenchymal transition of VECs, proteoglycan synthesis, inflammatory molecules and extracellular matrix turnover. Our findings suggest that the IL-33/ST2 system may be involved in the development of myxomatous MVD by enhancing extracellular matrix remodeling.

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Section: Discussioncontrasting

confidence: 55%

Activation of the Interleukin-33/ST2 Pathway Exerts Deleterious Effects in Myxomatous Mitral Valve Disease

García-Peña

Ibarrola

Navarro

et al. 2021

IJMS

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“…The prevalence of oxidized lipids in RFH leaflets also supports the conclusion that these valves are undergoing early CAVD processes, rather than myxomatous degeneration, a condition that is also characterized by GAG enrichment and collagen disruption. In addition to aortic valve myxomatous degeneration being rare in humans who do not also have congenital abnormalities or inflammation-related disease, 53 nonrheumatic myxomatous human aortic valves tend to not be highly enriched in oxidized lipids, 54 nor is hypercholesterolemia believed to be a risk factor for myxomatous aortic valve disease.…”

Section: Insights Into Early Cavd Provided By Adult Rfh Swinementioning

confidence: 99%

Development of Aortic Valve Disease in Familial Hypercholesterolemic Swine: Implications for Elucidating Disease Etiology

Porras

Shanmuganayagam

Meudt

et al. 2015

JAHA

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BackgroundFamilial hypercholesterolemia (FH) is a prevalent hereditary disease associated with increased atherosclerosis and calcific aortic valve disease (CAVD). However, in both FH and non‐FH individuals, the role of hypercholesterolemia in the development of CAVD is poorly understood. This study used Rapacz FH (RFH) swine, an established model of human FH, to investigate the role of hypercholesterolemia alone in the initiation and progression of CAVD. The valves of RFH swine have not previously been examined.Methods and ResultsAortic valve leaflets were isolated from wild‐type (0.25‐ and 1‐year‐old) and RFH (0.25‐, 1‐, 2‐, and 3‐year‐old) swine. Adult RFH animals exhibited numerous hallmarks of early CAVD. Significant leaflet thickening was found in adult RFH swine, accompanied by extensive extracellular matrix remodeling, including proteoglycan enrichment, collagen disorganization, and elastin fragmentation. Increased lipid oxidation and infiltration of macrophages were also evident in adult RFH swine. Intracardiac echocardiography revealed mild aortic valve sclerosis in some of the adult RFH animals, but unimpaired valve function. Microarray analysis of valves from adult versus juvenile RFH animals revealed significant upregulation of inflammation‐related genes, as well as several commonalities with atherosclerosis and overlap with human CAVD.ConclusionsAdult RFH swine exhibited several hallmarks of early human CAVD, suggesting potential for these animals to help elucidate CAVD etiology in both FH and non‐FH individuals. The development of advanced atherosclerotic lesions, but only early‐stage CAVD, in RFH swine supports the hypothesis of an initial shared disease process, with additional stimulation necessary for further progression of CAVD.

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“…32,91,98 In canine valves, mast cells were slightly increased in the perimeter of pathologic areas of diseased valves suggesting a potential role of mast cells in this disease. Interestingly, the human myxomatous valve is prone to develop bacterial endocarditis.…”

Section: Inflammatory Cellsmentioning

confidence: 96%

“…7A and B). 98 Several researchers believe that myofibroblasts or a-actin positive VIC may be a major phenotype that mediates degeneration. A study on human myxomatous valve disease suggested that a-actin positive VIC might be an activated VIC phenotype which play a role in producing catabolic enzymes and ECM.…”

Section: Valve Interstitial Cellsmentioning

confidence: 99%

Pathology, protein expression and signaling in myxomatous mitral valve degeneration: Comparison of dogs and humans

Aupperle

Disatian

2012

Journal of Veterinary Cardiology

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Role of inflammation in nonrheumatic, regurgitant heart valve disease. A comparative, descriptive study regarding apolipoproteins and inflammatory cells in nonrheumatic heart valve disease

Cited by 16 publications

References 31 publications

Activation of the Interleukin-33/ST2 Pathway Exerts Deleterious Effects in Myxomatous Mitral Valve Disease

Activation of the Interleukin-33/ST2 Pathway Exerts Deleterious Effects in Myxomatous Mitral Valve Disease

Development of Aortic Valve Disease in Familial Hypercholesterolemic Swine: Implications for Elucidating Disease Etiology

Pathology, protein expression and signaling in myxomatous mitral valve degeneration: Comparison of dogs and humans

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