Lipoprotein(a) Is an Independent Risk Factor for Cardiovascular Disease in Heterozygous Familial Hypercholesterolemia

Holmes, Daniel T.; Schick, Brian A.; Humphries, Karin H.; Fröhlich, Jiří

doi:10.1373/clinchem.2005.055228

Cited by 63 publications

(38 citation statements)

References 26 publications

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“…22 The elevated lipoprotein(a) levels at baseline in the present study were reduced by 11.7% and 18.6% with every-4-week and every-2-week dosing of AMG 145, respectively. Interestingly, patients with LDL receptor-negative function appeared to experience a reduction in lipoprotein(a); however, because it was based on only 2 patients, this finding needs to be validated.…”

mentioning

confidence: 43%

Effect of the Proprotein Convertase Subtilisin/Kexin 9 Monoclonal Antibody, AMG 145, in Homozygous Familial Hypercholesterolemia

et al. 2013

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More than 95% of HoFH patients have a mutation in the LDL receptor, <4% in have a mutation in apolipoprotein B, and <0.5% have a mutation in proprotein convertase subtilisin/kexin 9 (PCSK9). 2,3 Although true genetic HoFH is not uncommon, the majority of patients are compound heterozygotes. 4 The residual LDL receptor activity, either negative (<2% function) or defective (2%-25% function), is associated with severity of LDL cholesterol elevation and the propensity for early cardiovascular disease. 1 Clinical Perspective on p 2120Conventional therapies such as statins 5,6 and ezetimibe 7 are the most commonly used drugs for HoFH and result in LDL cholesterol reductions of 15% to 25%. Patients usually also require LDL apheresis when available. 8 These improvements in LDL cholesterol, particularly with statins, appear to reduce cardiovascular disease morbidity and mortality.

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confidence: 43%

Effect of the Proprotein Convertase Subtilisin/Kexin 9 Monoclonal Antibody, AMG 145, in Homozygous Familial Hypercholesterolemia

et al. 2013

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“…Diet management should also be performed for cardiovascular events increased 2.5-fold in those with lipoprotein (a) of 56 mg/dL or more 22) . Recently, Nenseter et al indicated that lipoprotein (a) of 35 mg/ dL or more was a significant risk factor for heterozygous FH 23) .…”

Section: Diet Therapymentioning

confidence: 99%

Guidelines for the Management of Familial Hypercholesterolemia

Harada‐Shiba

Arai

Oikawa

et al. 2012

JAT

167

164

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Familial hypercholesterolemia (FH) is a highly prevalent autosomal dominant hereditary disease, generally characterized by three major signs, hyper-low-density-lipoprotein (LDL) cholesterolemia, tendon/skin xanthomas and premature coronary artery disease (CAD). Because the risk of CAD is very high in these patients, they should be identified at an early stage of their lives and started on intensive treatment to control LDL-cholesterol. We here introduce a new guideline for the management of FH patients in Japan intending to achieve better control to prevent CAD. Diagnostic criteria for heterozygous FH are 2 or more of 1) LDL-cholesterol ≥ 180 mg/dL, 2) tendon/skin xanthoma(s), and 3) family history of FH or premature CAD within second degree relatives, for adults; and to have both 1) LDL-cholesterol ≥ 140 mg/dL and 2) family history of FH or premature CAD within second degree relatives, for children. For the treatment of adult heterozygous FH, intensive lipid control with statins and other drugs is necessary. Other risks of CAD, such as smoking, diabetes mellitus, hypertension etc., should also be controlled strictly. Atherosclerosis in coronary, carotid, or peripheral arteries, the aorta and aortic valve should be screened periodically. FH in children, pregnant women, and women who wish to bear a child should be referred to specialists. For homozygotes and severe heterozygotes resistant to drug therapies, LDL apheresis should be performed. The treatment cost of homozygous FH is authorized to be covered under the program of Research on Measures against Intractable Diseases by the Japanese Ministry of Health, Labour, and Welfare.

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“…The apo(a) size is inversely correlated with plasma Lp(a) levels: KIV repeat numbers below 23 are associated with elevated mean plasma Lp(a) levels [6]. Elevated plasma Lp(a) levels are considered a major risk factor for CVD in the general population [7,8] as well as in FH patients [9][10][11]. It has been suggested that Lp(a) mediates CVD via its effects on atherosclerotic stenosis, fibrinolysis and wound healing [12].…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein(a) levels are associated with aortic valve calcification in asymptomatic patients with familial hypercholesterolaemia

Vongpromek¹,

Bos²,

Kate

et al. 2015

J Intern Med

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Objectives. Lipoprotein(a) [Lp(a)] is an independent risk factor for aortic valve stenosis and aortic valve calcification (AVC) in the general population. In this study, we determined the association between AVC and both plasma Lp(a) levels and apolipoprotein(a) [apo(a)] kringle IV repeat polymorphisms in asymptomatic statin-treated patients with heterozygous familial hypercholesterolaemia (FH).Methods. A total of 129 asymptomatic heterozygous FH patients (age 40-69 years) were included in this study. AVC was detected using computed tomography scanning. Lp(a) concentration and apo(a) kringle IV repeat number were measured using immunoturbidimetry and immunoblotting, respectively. Univariate and multivariate logistic regression were used to assess the association between Lp(a) concentration and the presence of AVC.Results. Aortic valve calcification was present in 38.2% of patients, including three with extensive AVC (>400 Agatston units). Lp(a) concentration was significantly correlated with gender, number of apo(a) kringle IV repeats and the presence and severity of AVC, but not with coronary artery calcification (CAC). AVC was significantly associated with plasma Lp(a) level, age, body mass index, blood pressure, duration of statin use, cholesterolyear score and CAC score. After adjustment for all significant covariables, plasma Lp(a) concentration remained a significant predictor of AVC, with an odds ratio per 10-mg dL À1 increase in Lp(a) concentration of 1.11 (95% confidence interval 1.01-1.20, P = 0.03).Conclusion. In asymptomatic statin-treated FH patients, plasma Lp(a) concentration is an independent risk indicator for AVC.

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Lipoprotein(a) Is an Independent Risk Factor for Cardiovascular Disease in Heterozygous Familial Hypercholesterolemia

Cited by 63 publications

References 26 publications

Effect of the Proprotein Convertase Subtilisin/Kexin 9 Monoclonal Antibody, AMG 145, in Homozygous Familial Hypercholesterolemia

Effect of the Proprotein Convertase Subtilisin/Kexin 9 Monoclonal Antibody, AMG 145, in Homozygous Familial Hypercholesterolemia

Guidelines for the Management of Familial Hypercholesterolemia

Lipoprotein(a) levels are associated with aortic valve calcification in asymptomatic patients with familial hypercholesterolaemia

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