Regression of valvular aortic stenosis due to homozygous familial hypercholesterolemia following plasmapheresis

Keller, C.; Schmitz, H.; Theisen, K.; Zöllner, N.

doi:10.1007/bf01711956

Cited by 23 publications

(5 citation statements)

References 6 publications

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“…Regression of coronary atherosclerosis has been reported with LDL apheresis in homozygotes15 16 and consequently one can speculate that a similar beneficial effect could be expected for the aortic valve and root involvement 17. In homozygotes the arrest or regression of aortic root involvement should be the main therapeutic aim, since early fatal coronary events are usually related to ostial occlusion secondary to lipid deposition in the sinuses of Valsalva.…”

Section: Discussionmentioning

confidence: 70%

Extent and severity of atherosclerotic involvement of the aortic valve and root in familial hypercholesterolaemia

Rallidis

Naoumova

Thompson

et al. 1998

Heart

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Conclusions-In patients with familial hypercholesterolaemia, aortic stenosis is common in homozygotes, and aortic root involvement is always present despite the lower CYS than in heterozygotes. It appears to be determined by short term exposure to high cholesterol concentrations in early life. Conversely, aortic root and valve involvement are rare in heterozygotes and occur only with severe, prolonged hypercholesterolaemia, possibly accelerating age related degenerative effects. (Heart 1998;80:583-590)

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Section: Discussionmentioning

confidence: 70%

Extent and severity of atherosclerotic involvement of the aortic valve and root in familial hypercholesterolaemia

Rallidis

Naoumova

Thompson

et al. 1998

Heart

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“…Furthermore, similar to the regression of atherosclerosis, calcific AS seen in association with severe homozygous familial hypercholesterolemia has been reported to regress with aggressive lipid lowering therapy with plasmapheresis [51]. Conditions affecting calcium metabolism, such as renal impairment with secondary hyperparathyroidism or Paget's disease may predispose individuals to the development of calcific AS [52].…”

Section: Similarities and Differences Between Calcific Aortic Stenosimentioning

confidence: 97%

Calcific Aortic Stenosis: Molecular and Cellular Mechanisms, Medical Treatment Alternatives

Yildirir¹

2005

CCR

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Calcific aortic stenosis (AS) is the most prevalent heart disease requiring valve replacement in the elderly. Mild to moderate stenosis is usually asymptomatic, however, when becomes severe it is associated with significant morbidity and mortality including left ventricular hypertrophy, left ventricular diastolic and systolic dysfunction, congestive heart failure, angina, arrhythmias, and syncope. Aortic sclerosis, described as focal areas of increased echogenecity and thickening of aortic valve leaflets without restricted motility, is also associated with increased risk of death from cardiovascular causes. Regular follow-up is important to monitor hemodynamic progression of the aortic valve disease and the development of symptoms. Progression of AS shares many histological and immunochemical similarities with the process of atherosclerosis. They both are based on a chronic inflammatory process with infiltration and activation of leukocytes and a rise in systemic inflammatory markers. Epidemiological studies identified several risk factors for calcific aortic valve disease such as male sex, hypertension, smoking, and raised serum creatinin, cholesterol and calcium concentrations. Many of these are also the risk factors for atherosclerosis. Thus, AS is not just an age related degenerative process; its development is highly complex and shares a number of risk factors common for atherosclerosis. Lipids play an important role in the development and progression of AS, and there is growing evidence that cholesterol lowering may retard or prevent its progression. New research suggests that medical therapies may retard the progression of AS and reduce the need for surgery. This article will review the molecular and cellular basis of calcific AS, and mainly will focus on the potential for medical treatment alternatives.

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“…In patients with homozygous familial hypercholesterolaemia there is commonly an ejection systolic flow murmur and the severity of the atheroma in the aortic arch can lead to significant postvalvular stenosis and sometimes valvular stenosis. In this group of patients lipid-lowering therapies, often allied with apheresis, have been successful in reducing aortic valve region disease progression [5,6].…”

Section: Epidemiology Of Aortic Stenosismentioning

confidence: 99%

Aortic stenosis and lipids: does intervention work?

Wierzbicki

Viljoen

Chambers

2010

Current Opinion in Cardiology

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Regression of valvular aortic stenosis due to homozygous familial hypercholesterolemia following plasmapheresis

Cited by 23 publications

References 6 publications

Extent and severity of atherosclerotic involvement of the aortic valve and root in familial hypercholesterolaemia

Extent and severity of atherosclerotic involvement of the aortic valve and root in familial hypercholesterolaemia

Calcific Aortic Stenosis: Molecular and Cellular Mechanisms, Medical Treatment Alternatives

Aortic stenosis and lipids: does intervention work?

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