Case-control analysis of risk factors for presence of aortic stenosis in adults (age 50 years or older)

Hoagland, P.; Cook, E. Francis; Flatley, Margaret; Walker, C H; Goldman, Lee

doi:10.1016/0002-9149(85)90149-3

Cited by 60 publications

(28 citation statements)

References 10 publications

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“…9,10 Epidemiological studies have demonstrated an association between hypercholesterolemia and AS. [11][12][13][14][15][16] Furthermore, retrospective studies have shown that statin use was associated with slower progression of AS, although this finding has not been supported by recent trials. [17][18][19][20][21][22] It is possible that AS in patients in these trials may be too advanced and the aortic valves too calcified to benefit from lipid-lowering therapy.…”

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confidence: 99%

Effect of Lipid Lowering With Rosuvastatin on Progression of Aortic Stenosis

et al. 2010

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Background-Aortic stenosis (AS) is an active process with similarities to atherosclerosis. The objective of this study was to assess the effect of cholesterol lowering with rosuvastatin on the progression of AS. Methods and Results-This was a randomized, double-blind, placebo-controlled trial in asymptomatic patients with mild to moderate AS and no clinical indications for cholesterol lowering. The patients were randomized to receive either placebo or rosuvastatin 40 mg daily. A total of 269 patients were randomized: 134 patients to rosuvastatin 40 mg daily and 135 patients to placebo. Annual echocardiograms were performed to assess AS progression, which was the primary outcome; the median follow-up was 3.5 years. The peak AS gradient increased in patients receiving rosuvastatin from a baseline of 40.8Ϯ11.1 to 57.8Ϯ22.7 mm Hg at the end of follow-up and in patients with placebo from 41.6Ϯ10.9 mm Hg at baseline to 54.8Ϯ19.8 mm Hg at the end of follow-up. The annualized increase in the peak AS gradient was 6.3Ϯ6.9 mm Hg in the rosuvastatin group and 6.1Ϯ8.2 mm Hg in the placebo group (Pϭ0.83). Treatment with rosuvastatin was not associated with a reduction in AS progression in any of the predefined subgroups. Conclusion-Cholesterol lowering with rosuvastatin 40 mg did not reduce the progression of AS in patients with mild to moderate AS; thus, statins should not be used for the sole purpose of reducing the progression of AS. Clinical Trial Registration Information-URL: http://www.controlled-trials.com/.

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confidence: 99%

Effect of Lipid Lowering With Rosuvastatin on Progression of Aortic Stenosis

et al. 2010

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“…Epidemiological studies have revealed no major risk factors for the disease, with the exception of the presence of bicuspid valves. 3,4 The latter observation has been taken as an indication of an involvement of mechanical stress in the disease process. This notion is also supported by the finding that valvular fibrosis and calcification initially occurs at the base of the cusps.…”

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confidence: 99%

Presence of Oxidized Low Density Lipoprotein in Nonrheumatic Stenotic Aortic Valves

Olsson

Thyberg

Nilsson

1999

ATVB

351

216

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Abstract-The aim of the present study was to analyze if LDL particles trapped in stenotic aortic valve tissue undergo oxidative modification. Degenerative aortic stenosis affects Ͼ3% of the population Ͼ75 years of age in the Western world. Recent studies have revealed the presence of a chronic inflammatory process similar to what has been described in other degenerative diseases such as atherosclerosis. However, the underlying disease mechanisms of degenerative aortic stenosis still remain largely unknown. Six tricuspid stenotic valves, obtained at valve replacement, were compared with 3 control valves collected from hearts taken out during transplantation. The stenotic valves and the control valves were examined by immunohistochemistry, using antibodies against apoB, 4-hydroxynonenal-modified LDL, leukocytes, and HLA-DR. All valves were also stained with oil red O for neutral lipids. Extracellular neutral lipids were found in all stenotic valves, extending from the bases along the fibrosa layer. This lipid colocalized with apoB-and 4-hydroxynonenal-modified LDL immunoreactivity. 4-Hydroxynonenal-modified LDLs were present around calcium deposits, subendothelially, and in the deeper layer of the fibrosa. There was also a colocalization with macrophages,

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“…8 There was no statistically significant association with age, gender, hypertension or diabetes mellitus with aortic stenosis in the study similar to the findings by Hoagland and colleagues. 9 Mean body mass index of patient in this study was only 22.74. Studies by Mautner GC, and Gottdiener JS et al, had shown that BMI of >29 is an independent predictor of aortic stenosis.…”

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confidence: 63%