Prevalence of aortic valve abnormalities in the elderly: An echocardiographic study of a random population sample

Lindroos, Magnus; Kupari, Markku; Heikkilä, J; Tilvis, Reijo S.

doi:10.1016/0735-1097(93)90249-z

Cited by 983 publications

(558 citation statements)

References 18 publications

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“…The prevalence of aortic sclerosis increases with age and is present in 37% of adults aged > 75 years. 1 In a populationbased echocardiographic study, in patients aged > 65 years, 29% exhibited age-related aortic valve sclerosis. 2 Independent clinical factors associated with aortic sclerosis include age (two-fold increased risk for each 10-year increase in age), male gender (two-fold excess risk), present smoking (35% risk increase), and a history of hypertension (20% risk increase).…”

Section: Introductionmentioning

confidence: 99%

Aortic sclerosis—a marker of coronary atherosclerosis

Prasad

Bhalodkar

2004

Clinical Cardiology

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Summary: Aortic valve sclerosis is defined as calcification and thickening of a trileaflet aortic valve in the absence of obstruction of ventricular outflow. Its frequency increases with age, making it a major geriatric problem. Of adults aged > 65 years, 21-29% exhibit aortic valve sclerosis. Incidence of aortic sclerosis increases with age, male gender, smoking, hypertension, high lipoprotein (Lp) (a), high low-density lipoprotein (LDL), and diabetes mellitus. Aortic valves affected by aortic sclerosis contain a higher amount of oxidized LDL cholesterol and show increased expression of metalloproteinases. Clinically, it can be suspected in the presence of soft ejection systolic murmur at the aortic area, normal split of the second heart sound, and normal volume carotid pulse, but it can be best detected by echocardiography. Aortic sclerosis may be accompanied by mitral annulus calcification up to 50% of cases. It is associated with an increase of approximately 50% in the risk of death from cardiovascular causes and the risk of myocardial infarction. The mechanism by which aortic sclerosis contributes to or is associated with increased cardiovascular risk is not known. Aortic sclerosis is associated with systemic endothelial dysfunction, and a small percentage of cases may progress to aortic stenosis. Lowering of LDL cholesterol by 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have been shown to decrease progression of aortic valve calcification. Aortic sclerosis is not a mere benign finding. Once diagnosis of aortic sclerosis has been made, it should be considered a potential marker of coexisting coronary disease. Aggressive management of modifiable risk factors, especially LDL cholesterol lowering, may slow progression of the disease.

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Section: Introductionmentioning

confidence: 99%

Aortic sclerosis—a marker of coronary atherosclerosis

Prasad

Bhalodkar

2004

Clinical Cardiology

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“…Aortic valve disease, or FAVD, is a leading cause of adult heart disease (Thom et al ., 2006; Lloyd‐Jones et al ., 2010) and is the most common form of acquired valvular disease in the USA (Lindroos et al ., 1993; Baumgartner, 2005; Freeman & Otto, 2005). Unfortunately, due to its unknown etiology, there is currently no cure.…”

Section: Discussionmentioning

confidence: 99%

“…Our study provides the first experimental evidence that Klotho deficiency is a pathological factor for AVF, which is an important remodeling process that causes aortic valve stiffening, eventually leading to aortic valve calcification and aortic stenosis. It is known that serum levels of Klotho decrease after age 40 (Xiao et al ., 2004), while the prevalence of aortic stenosis increases with age (Lindroos et al ., 1993). In this study, we found that the serum level of Klotho was reduced by 50% in KL +/− mice (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…The findings from the current study suggest that pharmacological activation of AMPKα should be tested for treating FAVD. Aortic valve stenosis, which is the most common valvular disease in the elderly population (Lindroos et al ., 1993), is associated with a decline in serum levels of Klotho (Xiao et al ., 2004; Xu & Sun, 2015). Thus, an additional study is warranted for assessing the effect of administration of recombinant Klotho protein on aging‐related aortic stenosis.…”

Section: Discussionmentioning

confidence: 99%

“…By age 80, the serum level of Klotho is about a half of what it was at age 40 (Xiao et al ., 2004). By contrast, the prevalence of AVD and aortic stenosis increases with age (Lindroos et al ., 1993). However, whether a reduction in Klotho contributes to AVF has never been investigated.…”

Section: Introductionmentioning

confidence: 99%

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Deficiency in the anti‐aging gene Klotho promotes aortic valve fibrosis through AMPK α‐mediated activation of RUNX 2

2016

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SummaryFibrotic aortic valve disease (FAVD) is an important cause of aortic stenosis, yet currently there is no effective treatment for FAVD due to its unknown etiology. The purpose of this study was to investigate whether deficiency in the anti‐aging Klotho gene (KL) promotes high‐fat‐diet‐induced FAVD and to explore the underlying molecular mechanism. Heterozygous Klotho‐deficient (KL +/−) mice and WT littermates were fed with a high‐fat diet (HFD) or normal diet for 13 weeks, followed by treatment with the AMPKα activator (AICAR) for an additional 2 weeks. A HFD caused a greater increase in collagen levels in the aortic valves of KL +/− mice than of WT mice, indicating that Klotho deficiency promotes HFD‐induced aortic valve fibrosis (AVF). AMPKα activity (pAMPKα) was decreased, while protein expression of collagen I and RUNX2 was increased in the aortic valves of KL +/− mice fed with a HFD. Treatment with AICAR markedly attenuated HFD‐induced AVF in KL +/− mice. AICAR not only abolished the downregulation of pAMPKα but also eliminated the upregulation of collagen I and RUNX2 in the aortic valves of KL +/− mice fed with HFD. In cultured porcine aortic valve interstitial cells, Klotho‐deficient serum plus cholesterol increased RUNX2 and collagen I protein expression, which were attenuated by activation of AMPKα by AICAR. Interestingly, silencing of RUNX2 abolished the stimulatory effect of Klotho deficiency on cholesterol‐induced upregulation of matrix proteins, including collagen I and osteocalcin. In conclusion, Klotho gene deficiency promotes HFD‐induced fibrosis in aortic valves, likely through the AMPKα–RUNX2 pathway.

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The Risk of the Development of Aortic Stenosis in Patients With "Benign" Aortic Valve Thickening

Cosmi¹,

Kort²,

Tunick³

et al. 2002

Arch Intern Med

170

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Prevalence of aortic valve abnormalities in the elderly: An echocardiographic study of a random population sample

Abstract: Calcific aortic valve stenosis constitutes a significant health problem in the elderly. Only a minority of those with potentially operable aortic valve stenosis undergo surgery.

Cited by 983 publications

References 18 publications

Aortic sclerosis—a marker of coronary atherosclerosis

Aortic sclerosis—a marker of coronary atherosclerosis

Deficiency in the anti‐aging gene Klotho promotes aortic valve fibrosis through AMPK α‐mediated activation of RUNX 2

The Risk of the Development of Aortic Stenosis in Patients With "Benign" Aortic Valve Thickening

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