Association of lipoprotein(a) levels and apolipoprotein(a) phenotypes with coronary heart disease in patients with essential hypertension

Gazzaruso, Carmine; Buscaglia, Paola; Garzaniti, Adriana; Falcone, Colomba; Mariotti, Stefania; Savino, Sandra; Bonetti, Graziella; Finardi, G; Geroldi, Diego

doi:10.1097/00004872-199715030-00003

Cited by 33 publications

(25 citation statements)

References 37 publications

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“…Japanese Circulation Journal Vol.63, September 1999 patients with end-stage renal disease, 20 hypertension (HT) 21 or diabetes mellitus (DM), 12 those undergoing coronary bypass surgery, 22 and hemodialysis patients with or without DM. 13 However, the relation between apo(a) isoform size polymorphism and MI has rarely been studied, 23 and it would be interesting to determine whether, and how much, apo(a) isoform size polymorphism contributes to the increased serum Lp(a) levels in MI, because an inverse relation does exist between plasma Lp(a) levels and apo(a) size.…”

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confidence: 99%

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

Saku

Zhang

et al. 1999

Jpn Circ J

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ipoprotein(a) [Lp(a)] is a heterogeneous lipoprotein 1 that incorporates a low-density lipoprotein (LDL) particle and highly polymorphic apolipoprotein (a) [apo(a)], which is covalently linked to the apolipoprotein B moiety of the LDL by a single disulfide bridge. 2,3 Apo(a) is highly homologous to plasminogen and affects the human coagulation system. 4,5 The apo(a) gene locus is the major gene that controls plasma Lp(a) concentrations. 6,7 The alleles at this locus determine the size polymorphism of apo(a), which is the result of a variable number of expressed Japanese Circulation Journal Vol.63, September 1999 kringle IV repeats, 6-8 and is assessed by apo(a) genotyping. 7 Utermann et al first reported a size polymorphism of 6 apo(a) isoforms with different molecular weights, 8 and other researchers have detected additional apo(a) isoforms using different detection methods. 9,10 We recently detected 26 different apo(a) alleles, including a null allele, at the apo(a) locus by a sensitive high-resolution technique using sodium dodecyl sulfate (SDS)-agrose/gradient polyacrylamide gel electrophoresis (PAGE). 11 Approximately 75% of the subjects had a double band of apo(a), and the remaining subjects had a single band. An inverse relationship has been demonstrated between plasma Lp(a) concentrations and the size of apo(a), 8,11 and a smaller Lp(a) band was well correlated with Lp(a) levels in double-banded phenotypes. [11][12][13] High plasma levels of Lp(a) have been shown to be associated with myocardial infarction (MI), 14-17 although this association was not confirmed by 2 prospective studies. 18,19 Apo(a) size polymorphism has been shown to be inversely associated with the risk of coronary heart disease (CHD) in Jpn Circ J 1999; 63: 659 -665 (Received April 2, 1999; revised manuscript received May 24, 1999; accepted May 27, 1999 , age: 62±10 y) and control subjects (n=92, M/F: 53/39, age: 58±14 y) were classified into quintile groups (Groups I to V) according to Lp(a) levels. Apo(a) isoform phenotyping was performed by a sensitive, high-resolution technique using sodium dodecyl sulfate-agarose/gradient polyacrylamide gel electrophoresis (3-6%), which identified 26 different apo(a) phenotypes, including a null type. Groups with higher Lp(a) levels (Groups II, III, and V) had higher percentages of MI patients than that with the lowest Lp(a) levels (Group I) (54%, 56%, or 75% vs. 32%, p<0.05). Groups with different Lp(a) levels had different frequency distributions of apo(a) isoprotein phenotypes: Groups II, III, IV, and V, which had increasing Lp(a) levels, had increasingly higher percentages of smaller isoforms (A1-A4, A5-A9) and decreasingly lower percentages of large isoforms (A10-A20, A21-A25) compared to Group I. An apparent inverse relationship existed between Lp(a) and the apo(a) phenotype. Subjects with the highest Lp(a) levels (Group V) had significantly (p<0.05) higher serum levels of total cholesterol, apo B, and Lp(a). Patients with MI and the controls had different distributions of apo(a) phenot...

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confidence: 99%

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

Saku

Zhang

et al. 1999

Jpn Circ J

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“…Unlike plasminogen, apo(a) contains no kringles (K) 1-3; the apo(a) structure shows multiple copies of K4, followed by K5 and a protease domain [2]. Apo(a) contains ten distinct classes of K4 (classes [1][2][3][4][5][6][7][8][9][10]. Each K4 class is present as a single copy, except K4 class 2 that is present in multiple copies (from 3 to at least 30).…”

Section: Structure Of Apolipoprotein(a)mentioning

confidence: 99%

“…The progressive improvement of the electrophoretic separation techniques permitted the identification of increasingly larger numbers of isoforms [3]. Recent studies showed that apo(a) polymorphism has a very high predictive value for coronary artery disease (CAD), when apo(a) polymorphism is analyzed by high-resolution methods [9][10][11][12]. A study performed by Kraft et al [9] showed that, among the risk factors considered, apo(a) polymorphism was the best predictor of CAD.…”

Section: Apolipoprotein(a) Polymorphism and Cardiovascular Disease Riskmentioning

confidence: 99%

A New Emerging Risk Factor for Cardiovascular Disease: Apo(a) Polymorphism

2003

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Apolipoprotein(a) [apo(a)], the specific apolipoprotein of lipoprotein(a), is characterized by a high degree of genetic polymorphism. Recent studies have shown that apo(a) polymorphism may represent a powerful independent cardiovascular risk factor. Indeed, an association between apo(a) polymorphism and coronary artery disease (CAD) has been documented both in the general population and among subjects at high cardiovascular disease risk, such as hypertensive, uremic, hypercholesterolemic, and diabetic patients. In addition, apo(a) polymorphism seems to correlate well with age of onset and severity of CAD. Nevertheless, at present, some problems prohibit the utilization of apo(a) polymorphism in clinical practice. Indeed, apo(a) phenotyping methods are not standardized, and there is not a cutoff of apo(a) polymorphism for clinical purposes. Moreover, large prospective studies should confirm the predictive value of apo(a) polymorphism for CAD. When the above problems are solved, apo(a) polymorphism could be a reliable tool to discriminate subjects with genetic predisposition to CAD among people with a family history of CAD and among patients with diseases representing a high cardiovascular risk, such as hypercholesterolemia, hypertension, diabetes, and uremia.

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“…Accordingly, it is suggested that Lp(a) level may be increased in patients with atherothrombotic stroke, but not in those with lacunar infarction. 19 As small-sized apo(a) isoforms have been linked with atherothrombotic disease, 20,21 it is feasible that apo(a) phenotypes of low molecular weight (LMW) would be a risk factor only for atherothrombotic stroke and that any association with lacunar infarction would be less strong or absent.…”

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confidence: 99%

“…When the patient had a double band, only the smaller band was used to express the phenotype in the analysis. 21,28 To estimate the odds ratio (OR) for different stroke subtype, multivariate logistic regression analysis was performed. The following variables were introduced into the model: age, body mass index, and log-transformed Lp(a) level as continuous variables; gender, smoke, hypertension, diabetes, hypercholesterolemia, and the carriage of at least one apo(a) isoform of LMW as dichotomous variables.…”

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confidence: 99%

Inferior predilection of Lisch nodules with ptosis

Wood¹,

Egan²

2005

Neurology

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Abstract-Objective:To determine the distribution of apolipoprotein (a) (apo [a]) isoforms and their relation to the clinical severity of different ischemic stroke subtypes. Methods: Ninety-four hospital cases with a first-ever ischemic stroke and 188 randomly selected control subjects matched for age, gender, and ethnicity were enrolled. Stroke etiology was defined according to Trial of Org 10172 in Acute Stroke Treatment criteria. NIH Stroke Scale (NIHSS) was used to assess the severity of stroke on admission Results: In univariate analysis, the presence of at least one small apo(a) isoform was associated with ischemic stroke in men (p ϭ 0.02) but not in women (p ϭ 0.33). After allowance for age, gender and traditional vascular risk factors, subjects carrying at least one small apo(a) isoform were at increased risk of atherothrombotic stroke (odds ratio [OR] 7.1, 95% CI 2.8 to 17.5, p ϭ 0.00001) but not of lacunar infarction (OR 1.1, 95% CI 0.5 to 2.7, p ϭ 0.78). Multivariate logistic regression analysis revealed that in the atherothrombotic stroke group, the presence of at least one small-sized apo(a) phenotype was associated with an NIHSS score Ն6 (OR 13.6, 95% CI 1.6 to 111.9, p ϭ 0.015). Conclusion: Small apolipoprotein (a) isoforms distinguish atherothrombotic stroke from lacunar infarction and are associated with the severity of atherothrombotic stroke.

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Association of lipoprotein(a) levels and apolipoprotein(a) phenotypes with coronary heart disease in patients with essential hypertension

Cited by 33 publications

References 37 publications

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

Associations Among Serum Lipoprotein(a) Levels, Apolipoprotein(a) Phenotypes, and Myocardial Infarction in Patients With Extremely Low and High Levels of Serum Lipoprotein(a)

A New Emerging Risk Factor for Cardiovascular Disease: Apo(a) Polymorphism

Inferior predilection of Lisch nodules with ptosis

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