Apolipoprotein(a) and ischaemic heart disease in familial hypercholesterolaemia

@article{Wiklund1990ApolipoproteinaAI,
  title={Apolipoprotein(a) and ischaemic heart disease in familial hypercholesterolaemia},
  author={Olov Wiklund and S-O. Olofsson and Gunnar Fager and Göran Bondjers and Bo Angelin and Mark Erikson and Lars F Berglund},
  journal={The Lancet},
  year={1990},
  volume={335},
  pages={1360-1363}
}
Lipoprotein (a) as an independent risk factor for myocardial infarction in patients with common hypercholesterolaemia.
TLDR
In middle aged men with common hypercholesterolaemia the serum concentration of Lp(a), a powerful and independent risk factor for MI, should probably be routinely measured in all patients referred to a lipid clinic.
Lipoprotein (a) concentrations in patients with various dyslipidaemias.
TLDR
Serum Lp(a) levels are different in various types of primary hyperlipidaemia and are modulated according to the type of lipid elevation, as well as in hypercholesterolaemic and hypertriglyceridaemic patients.
Lp(a) concentration and apo(a) isoform size. Relation to the presence of coronary artery disease in familial hypercholesterolemia.
TLDR
Study of the relation between the concentration of lipoprotein(a) in plasma, apolipoprotein (a) [apo(a)] phenotype, and the clinical expression of coronary artery disease (CAD) in a previously described cohort of patients with familial hypercholesterolemia and an appropriate population of control subjects shows that on the basis of Lp(a), there is no significant difference between FH patients with and without signs or symptoms of CAD.
Established and emerging coronary risk factors in patients with heterozygous familial hypercholesterolaemia
TLDR
The results indicate that emerging coronary risk factors appear not to be associated with CAD in adults with treated familial hypercholesterolaemia, but the strong association with smoking suggests that patients should be identified early in childhood and discouraged from ever starting to smoke.
Serum lipoprotein(a) in patients heterozygous for familial hypercholesterolemia, their relatives, and unrelated control populations.
TLDR
Elevated serum Lp(a) concentrations should probably now be regarded as a component of the clinical syndrome of FH, however, within the FH population Lp (a) did not distinguish those with clinically overt coronary heart disease from those without the disease.
Lp(a) levels and atherosclerotic vascular disease in a sample of patients with familial hypercholesterolemia sharing the same gene defect.
There is considerable variation in the severity of cardiovascular disease among patients with familial hypercholesterolemia (FH). Some reports have suggested that plasma lipoprotein(a) [Lp(a)] levels
Lipoprotein(a) determination and risk of cardiovascular disease in South African patients with familial hypercholesterolaemia.
TLDR
Measurements of Lp(a) using the RIA method differ significantly from those obtained by the reference ELISA technique, suggesting that misclassification could lead to inaccurate CHD risk assessment.
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References

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TLDR
It is concluded that Lp(a) is an important attribute that should often be considered when coronary heart disease risk is assessed and was not explained by differences in total cholesterol levels, high-density lipoprotein or low-density lipid levels, subscapular skin fold, systolic blood pressure, history of smoking, alcohol consumption, or age.
The Relationship of Lipoprotein (a) (Lp(a)) to Risk Factors of Coronary Heart Disease: Initial results of the prospective epidemiological study on Company employees in Westfalia
Lp(a) concentrations were determined in 987 male and 477 female company employees in Westfalia, in the age range 17-70 years. These values were then related to age and to the following risk factors:
Treatment of heterozygous familial hypercholesterolemia with lipid-lowering drugs.
Patients with heterozygous familial hypercholesterolemia (FH) constitute a unique population at high risk for the premature development of coronary artery disease (CAD) and in whom long-term
Turnover of lipoprotein (a) in man.
TLDR
The results of this study indicate that Lp(a) is not converted to other serum lipoproteins, and from the correlations between serum concentration and kinetic parameters of L p(a), it is concluded that an elevated Lp (a) level is the consequence of an increased Lp-a) apoprotein synthesis.
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