ArticleThe Journal of clinical investigation1992
Apolipoprotein(a) phenotypes, Lp(a) concentration and plasma lipid levels in relation to coronary heart disease in a Chinese population: evidence for the role of the apo(a) gene in coronary heart disease.
Article in The Journal of clinical investigation, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 163 citations in OpenAlex.
- Cytosine base editing of LPA in transgenic mice averts large deletions.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Lipoprotein(a): from Causality to Treatment.Current atherosclerosis reports · 2024Review
- Lp(a) and the Risk for Cardiovascular Disease: Focus on the Lp(a) Paradox in Diabetes Mellitus.International journal of molecular sciences · 2022Review
- The Use of Blood Biomarkers in Precision Medicine for the Primary Prevention of Atherosclerotic Cardiovascular Disease: a Review.Expert review of precision medicine and drug development · 2021Article
- Article
- Lipoprotein (a): a historical appraisal.Journal of lipid research · 2017Review
- Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology.Journal of lipid research · 2016Review
- Structure, function, and genetics of lipoprotein (a).Journal of lipid research · 2016Review
- Human Genetics and the Causal Role of Lipoprotein(a) for Various Diseases.Cardiovascular drugs and therapy · 2016Review
- Screening for and management of elevated Lp(a).Current cardiology reports · 2013Review
- Update on lipoprotein(a) as a cardiovascular risk factor and mediator.Current atherosclerosis reports · 2013Review
- Insulin sensitivity and Lp(alpha) concentrations in normoglycemic offspring of type 2 diabetic parents.Lipids in health and disease · 2003Article
- Silent coronary artery disease in type 2 diabetes mellitus: the role of Lipoprotein(a), homocysteine and apo(a) polymorphism.Cardiovascular diabetology · 2002Article
- Kringle-containing fragments of apolipoprotein(a) circulate in human plasma and are excreted into the urine.The Journal of clinical investigation · 1996Article
- A unique pattern of apo(a) polymorphism in an isolated east Greenlandic Inuit (Eskimo) population.European journal of epidemiology · 1995Article
- Sequence polymorphism in kringle IV 37 in linkage disequilibrium with the apolipoprotein (a) size polymorphism.Human genetics · 1995Article
- Genetic variation in lipoprotein (a) levels in families enriched for coronary artery disease is determined almost entirely by the apolipoprotein (a) gene locus.American journal of human genetics · 1995Article
- Lipoprotein(a): new insights into an atherogenic lipoprotein.The Clinical investigator · 1994Review
- Comparative analysis of the apo(a) gene, apo(a) glycoprotein, and plasma concentrations of Lp(a) in three ethnic groups. Evidence for no common "null" allele at the apo(a) locus.The Journal of clinical investigation · 1994Article
- Association of elevated lipoprotein(a) levels and coronary heart disease in NIDDM patients. Relationship with apolipoprotein(a) phenotypes.Diabetologia · 1994Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated lipoprotein(a) (Lp[a]) concentrations are associated with premature coronary heart disease (CHD). In the general population, Lp(a) levels are largely determined by alleles at the hypervariable apolipoprotein(a) (apo[a]) gene locus, but other genetic and environmental factors also affect plasma Lp(a) levels. In addition, Lp(a) has been hypothesized to be an acute phase protein. It is therefore unclear whether the association of Lp(a) concentrations with CHD is primary in nature. We have analyzed apo(a) phenotypes, Lp(a) levels, total cholesterol, and HDL-cholesterol in patients with CHD, and in controls from the general population. Both samples were Chinese individuals residing in Singapore. Lp(a) concentrations were significantly higher in the patients than in the population (mean 20.7 +/- 23.9 mg/dl vs 8.9 +/- 12.9 mg/dl). Apo(a) isoforms associated with high Lp(a) levels (B, S1, S2) were significantly more frequent in the CHD patients than in the population sample (15.9% vs 8.5%, P less than 0.01). Higher Lp(a) concentrations in the patients were in part explained by this difference in apo(a) allele frequencies. Results from stepwise logistic regression analysis indicate that apo(a) type was a significant predictor of CHD, independent of total cholesterol and HDL cholesterol, but not independent of Lp(a) levels. The data demonstrate that alleles at the apo(a) locus determine the risk for CHD through their effects on Lp(a) levels, and firmly establish the role of Lp(a) as a primary genetic risk factor for CHD.
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