Calcific degeneration of the aortic valve in old age: is the development of flow obstruction predictable

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

doi:10.1046/j.1365-2796.1996.454000.x

Cited by 10 publications

(7 citation statements)

References 22 publications

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“…Some reports shown an association of hyperlipidemia and diabetes with AVC [4,11], whereas others have failed to find this association [2,10]. In our study, we also failed to identify clinical variables associated with advanced AVC except age.…”

Section: Discussioncontrasting

confidence: 82%

Aortic valve calcification in hypertensive patients: prevalence, risk factors and association with transvalvular flow velocity

Tenenbaum

Fisman

Schwammenthal

et al. 2004

International Journal of Cardiology

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Section: Discussioncontrasting

confidence: 82%

Aortic valve calcification in hypertensive patients: prevalence, risk factors and association with transvalvular flow velocity

Tenenbaum

Fisman

Schwammenthal

et al. 2004

International Journal of Cardiology

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“…Although investigations are underway to determine whether statin therapy may prevent or delay disease progression, at present, the mainstay of treatment for severe calcific AS is valve replacement surgery (5). AS is already the most common indication for valve replacement surgery in the US (5), and, given the aging US population, calcific AS is predicted to become an increasing health burden (1,21,22,45). Although several risk factors have been associated with increased prevalence and/or progression of AS, growing evidence suggests that genetic factors also modify susceptibility to congenital and calcific valvular disease (11,16,17,26,27,36,41,42).…”

mentioning

confidence: 99%

Reduced EGFR causes abnormal valvular differentiation leading to calcific aortic stenosis and left ventricular hypertrophy in C57BL/6J but not 129S1/SvImJ mice

Barrick

Roberts²,

Rojas³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Epidermal growth factor receptor (EGFR) signaling contributes to aortic valve development in mice. Because developmental phenotypes in Egfr-null mice are dependent on genetic background, the hypomorphic Egfr(wa2) allele was made congenic on C57BL/6J (B6) and 129S1/SvImJ (129) backgrounds and used to identify the underlying cellular cause of EGFR-related aortic valve abnormalities. Egfr(wa2/wa2) mice on both genetic backgrounds develop aortic valve hyperplasia. Many B6-Egfr(wa2/wa2) mice die before weaning, and those surviving to 3 mo of age or older develop severe left ventricular hypertrophy and heart failure. The cardiac phenotype was accompanied by significantly thicker aortic cusps and larger transvalvular gradients in B6-Egfr(wa2/wa2) mice compared with heterozygous controls and age-matched Egfr(wa2) homozygous mice on either 129 or B6129F1 backgrounds. Histological analysis revealed cellular changes in B6-Egfr(wa2/wa2) aortic valves underlying elevated pressure gradients and progression to heart failure, including increased cellular proliferation, ectopic cartilage formation, extensive calcification, and inflammatory infiltrate, mimicking changes seen in human calcific aortic stenosis. Despite having congenitally enlarged valves, 129 and B6129F1-Egfr(wa2/wa2) mice have normal lifespans, absence of left ventricular hypertrophy, and normal systolic function. These results show the requirement of EGFR activity for normal valvulogenesis and demonstrate that dominantly acting genetic modifiers curtail pathological changes in congenitally deformed valves. These studies provide a novel model of aortic sclerosis and stenosis and suggest that long-term inhibition of EGFR signaling for cancer therapy may have unexpected consequences on aortic valves in susceptible individuals.

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“…2,3 The disease shows a progressive course, especially after the threshold to mild aortic stenosis has been crossed. 2,4 Common pathomechanisms of aortic valve stenosis and atherosclerosis have been discussed, and several studies have demonstrated an influence of cardiovascular risk factors on the progression and outcome of aortic valve stenosis, but results have been inhomogeneous as to the relative importance of specific risk factors. [5][6][7][8][9] Several studies have identified the degree of aortic valve calcification as a strong predictor both for the progression and outcome of aortic stenosis.…”

mentioning

confidence: 99%

Progression of Aortic Valve Calcification

et al. 2001

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Background-Recent studies demonstrated an influence of atherosclerotic risk factors on the progression of aortic valve stenosis. The extent of aortic valve calcification (AVC) was also found to be a strong predictor of stenosis progression. We investigated the influence of the LDL cholesterol level (LDL), other standard cardiovascular risk factors, and the extent of coronary calcification (CC) on the progression of AVC quantified by electron beam tomography (EBT). Methods and Results-In 104 patients (64.7Ϯ8 years, 89 male) with an EBT scan positive for AVC, CC and AVC were quantified using a volumetric score. EBT was repeated at a mean interval of 15 months (10 to 36 months), and the progression of AVC and CC was determined. Patients were divided into 2 groups according to LDL: group 1, LDLՅ3.36 mmol/L (130 mg/dL), 57 patients; group 2, LDLϾ3.36 mmol/L (130 mg/dL), 47 patients. Mean values for CC were 546Ϯ932 mm 3 in scan 1 and 665Ϯ1085 mm 3 in scan 2 for AVC 324Ϯ796 mm 3 and 404Ϯ1076 mm 3 , respectively. The mean progression of CC was 27Ϯ37% (group 1, 16Ϯ22%; group 2, 39Ϯ46%, PՅ0.001) and of AVC was 25Ϯ38% (group 1, 9Ϯ22%; group 2, 43Ϯ44%, PՅ0.001). Conclusions-Quantification of AVC by EBT permits new insights into the progression of aortic valve sclerosis. We observed a strong influence of LDL cholesterol level on the progression of AVC and CC, suggesting that lipid-lowering therapy may decrease the progression of aortic valve calcification.

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Calcific degeneration of the aortic valve in old age: is the development of flow obstruction predictable

Cited by 10 publications

References 22 publications

Aortic valve calcification in hypertensive patients: prevalence, risk factors and association with transvalvular flow velocity

Aortic valve calcification in hypertensive patients: prevalence, risk factors and association with transvalvular flow velocity

Reduced EGFR causes abnormal valvular differentiation leading to calcific aortic stenosis and left ventricular hypertrophy in C57BL/6J but not 129S1/SvImJ mice

Progression of Aortic Valve Calcification

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