Lipoprotein(a) as a risk factor for calcific aortic valvulopathy in heterozygous familial hypercholesterolemia

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http://hdl.handle.net/10138/313761

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Vuorio , A , Watts , G F & Kovanen , P T 2019 , ' Lipoprotein(a) as a risk factor for calcific aortic valvulopathy in heterozygous familial hypercholesterolemia ' , Atherosclerosis , vol. 281 , pp. 25-30 . https://doi.org/10.1016/j.atherosclerosis.2018.11.040

Title: Lipoprotein(a) as a risk factor for calcific aortic valvulopathy in heterozygous familial hypercholesterolemia
Author: Vuorio, Alpo; Watts, Gerald F.; Kovanen, Petri T.
Contributor: University of Helsinki, Department of Forensic Medicine
University of Helsinki, Wihuri Research Institute
Date: 2019-02
Language: eng
Number of pages: 6
Belongs to series: Atherosclerosis
ISSN: 0021-9150
URI: http://hdl.handle.net/10138/313761
Abstract: A large number of epidemiological studies in ethnically diverse populations show that lipoprotein(a) [Lp(a)] levels above 30-50 mg/dL are significantly associated with calcific aortic valve stenosis, although less so in African Americans. Patients with heterozygous familial hypercholesterolemia (he-FH) have a marked lifelong elevation of serum low-density lipoprotein cholesterol (LDL-C) level, and the prevalence of aortic valve calcification (AVC) is at least two-fold higher among adult he-FH patients compared with healthy controls. Additionally, Lp(a) levels above 50 mg/dL were recently found to be an independent risk factor for AVC among asymptomatic statin-treated he-FH patients. Given that worldwide an estimated 1.4 billion people have an Lp(a) level over 50 mg/dL, and that one out of 250 individuals has he-FH, then globally about 5 million he-FH patients should have an Lp(a) level higher than 50 mg/dL. However, because Lp(a) levels are, on average, significantly higher in he-FH patients than the general population, the actual number of he-FH patients with such high Lp(a) levels must be even higher. We proposed recently that Lp(a) life-years is a useful metric of cumulative burden of risk for atherosclerotic cardiovascular disease (ASCVD), and now posit that this metric may be extended to the development of AVC. The Lp(a) life-years illustrates the age-dependent exposure to a given Lp(a) level (years x mg/dL). Effective novel pharmacotherapies using apo(a) antisense oligonucleotides (ASOs) or small interfering RNA (siRNA)-based therapies targeting the hepatic expression of apo(a) offer unprecedented potential for significant reduction in the cumulative exposure of the aortic valves to Lp(a), and need to be tested in controlled clinical trials on the progression of AVC.
Subject: Familial hypercholesterolemia
lipoprotein(a)
Atherosclerosis
Valvulopathy
Aortic calcification
Aortic stenosis
VALVE STENOSIS
OXIDIZED PHOSPHOLIPIDS
CARDIOVASCULAR-DISEASE
TARGETING APOLIPOPROTEIN(A)
DENSITY-LIPOPROTEINS
HEART-DISEASE
DOUBLE-BLIND
DIAGNOSIS
ATHEROSCLEROSIS
MANAGEMENT
3121 General medicine, internal medicine and other clinical medicine
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