Aortic valve histology and its relation with mechanics—Preliminary report

Sauren, Aahj Fons; Kuijpers, W.; Steenhoven, van Aa Anton; Veldpaus, FE Frans

doi:10.1016/0021-9290(80)90183-9

Cited by 77 publications

(27 citation statements)

References 14 publications

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“…These findings might be a possible explanation for the echocardiographic results that thickened aortic valve occurred more frequently at the noncoronary leaflet than at either right or left coronary leaflet. The findings of the simulated study were consistent with the mechanical stress theory that long-term mechanical stress may have resulted in injury that led to aortic valve degenerative changes, and eventually became stenosis [16][17][18]. The simulated study also supported the theory proposed by Gradman who claimed that the hemodynamic bwear and tearQ predisposed to the aortic valve degeneration [19].…”

Section: Pressure Loading Studysupporting

confidence: 83%

Age-related changes in aortic valve with emphasis on the relation between pressure loading and thickened leaflets of the aortic valves

Lin

Liu

Young

et al. 2005

International Journal of Cardiology

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Section: Pressure Loading Studysupporting

confidence: 83%

Age-related changes in aortic valve with emphasis on the relation between pressure loading and thickened leaflets of the aortic valves

Lin

Liu

Young

et al. 2005

International Journal of Cardiology

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“…Previous studies have shown the similarities between early lesions of aortic valve disease and atherosclerosis, including lipid deposition [21] and location of focal changes of sclerosis on the aortic side of the leaflets [22], which suggests endothelial injury from low shear stress and high tensile stress as possible initiating factors in the disease process [23, 24]. AVS is also associated with systemic endothelial dysfunction [25].…”

Section: Discussionmentioning

confidence: 99%

A High Association of Aortic Valve Sclerosis Detected by Transthoracic Echocardiography with Coronary Arteriosclerosis

Sui¹,

Ren²,

et al. 2007

Cardiology

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Objective: To examine whether aortic valve sclerosis (AVS) detected by transthoracic echocardiography (TTE) has a high association with coronary arteriosclerosis. Methods: Clinical and angiographic features and TTE findings were retrospectively analyzed in a blinded fashion for 138 consecutive patients, of whom 58 had AVS and 80 had non-AVS diseases. Both histological and immunohistochemical studies were performed on frozen aortic valve sections obtained at autopsy from 7 AVS and 3 non-AVS patients. Results: AVS and coronary artery disease (CAD) had similar clinical risk factors. The AVS group had a higher positive rate of coronary angiography and a higher incidence rate of multivessel CAD than the non-AVS group. The sensitivity, specificity, positive predictive value and negative predictive value of AVS in diagnosing CAD were 63.8, 71.3, 61.7 and 73.1%, respectively. Early lesions of AVS were characterized by accumulation of lipid and infiltration of macrophages and T lymphocytes as indicated by immunohistochemical staining. Late lesions were characterized by formation of calcific plaques, proliferation of fibrous connective tissue and immunohistochemical staining identifying a few macrophages or T lymphocytes and little lipid accumulation on the surface of aortic valve leaflets. Late lesions in the basement of aortic valve leaflets were characterized by hyperplastic granulation tissues. Three aortic valve leaflets from the non-AVS group were characterized by nonspecific thickened tips, increased collagen, no calcification, no lipid accumulation and no inflammatory cells. Conclusions: There were significant similarities in clinical risk factors, histopathological alterations of AVS and coronary atherosclerosis. AVS detected by TTE had a high association with coronary arteriosclerosis.

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“…Proximity of activated T cells suggests that they may play a role in this process, though as noted previously, it is unclear whether inflammatory cells promote or retard calcification. Progressive thickening of the valve leaflets, due to calcification and accumulation of fibroblast-produced extracellular matrix molecules, leads to turbulent flow across the valve, possibly causing further repetitive injury and inflammation through increased tensile stress and decreased shear stress [16,17]. Advancing disease reveals a prominent lipid-laden core, and more confluent calcium deposition with diminished leaflet pliability and the advent of more severe sclerotic changes [2].…”

Section: Pathophysiology Of Calcific Aortic Valve Diseasementioning

confidence: 98%

Aortic valve sclerosis as a marker of active atherosclerosis

2002

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Aortic sclerosis is a calcific disease of the aortic valvular leaflets defined as focal leaflet thickening without significant obstruction to left ventricular outflow. Several clinical factors are associated with calcific aortic valve disease, including male sex, smoking, hypertension, age, hypercholesterolemia, and diabetes. Histologic and biochemical studies suggest similarities between the mechanisms involved in the development of aortic sclerosis and atherosclerosis, suggesting these two diseases may share common pathophysiologic mechanisms. In a recent prospective trial, the presence of aortic sclerosis was associated with an approximately 50% increase in cardiovascular mortality and myocardial infarction, even after correction for age, gender, known coronary artery disease, and clinical factors associated with a aortic sclerosis.

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Aortic valve histology and its relation with mechanics—Preliminary report

Cited by 77 publications

References 14 publications

Age-related changes in aortic valve with emphasis on the relation between pressure loading and thickened leaflets of the aortic valves

Age-related changes in aortic valve with emphasis on the relation between pressure loading and thickened leaflets of the aortic valves

A High Association of Aortic Valve Sclerosis Detected by Transthoracic Echocardiography with Coronary Arteriosclerosis

Aortic valve sclerosis as a marker of active atherosclerosis

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