Document Detail


Human lipoprotein lipase HindIII polymorphism in young patients with myocardial infarction.
MedLine Citation:
PMID:  10484057     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated the possibility that the DNA HindIII polymorphism of human lipoprotein lipase (LPL) is associated with the severity of coronary artery disease (CAD) determined by angiography in young patients who survived a myocardial infarction (MI). Conflicting studies have explored the relationship linking CAD severity to the HindIII restriction site polymorphism at the LPL gene locus, and to our knowledge, no data are available from Italy. The patients were aged less than 45 years (mean age, 40.1 +/- 3.9 years); 83 were male and four were female. The 87 case-patients had a Q-wave or non-Q-wave infarction (67.3% and 32.7%, respectively); the MI was anterior (50.5%), lateral (41.7%), or inferior (7.8%). Analysis of coronary angiograms showed the absence of critical stenosis in 13.8% and the presence of monovessel disease in 50.6% and multivessel disease in 35.6% of the case-patients. The allelic frequency of the HindIII H(-) and H(+) allele was 0.37 and 0.63, respectively. There was a striking association between the HindIII polymorphism and the number of diseased vessels. The patients with HindIII(+/+) genotypes were significantly more likely to have double- or triple-vessel disease and less likely to have no significantly diseased vessels. In this study, we demonstrated that the homozygous form of the LPL HindIII(+) allele increases the risk of multivessel disease by a factor of 4 in an Italian group of young MI survivors. This association was independent from the smoking status and a positive family history for CAD and hypertension, which are known to predict CAD severity. The discrepancies in the results of these studies are difficult to explain. The lack of homogeneity in the study populations (age at which CAD occurred, number of enrolled patients, and geographical origin) and differences in the assessment of CAD severity may account for these conflicting results.
Authors:
R Gambino; L Scaglione; N Alemanno; G Pagano; M Cassader
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Publication Detail:
Type:  Clinical Trial; Journal Article    
Journal Detail:
Title:  Metabolism: clinical and experimental     Volume:  48     ISSN:  0026-0495     ISO Abbreviation:  Metab. Clin. Exp.     Publication Date:  1999 Sep 
Date Detail:
Created Date:  1999-09-28     Completed Date:  1999-09-28     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  0375267     Medline TA:  Metabolism     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1157-61     Citation Subset:  IM    
Affiliation:
Dipartimento di Medicina Interna, Universita' di Torino, Italy.
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MeSH Terms
Descriptor/Qualifier:
Adult
Alleles
Coronary Angiography
Coronary Disease / etiology
Deoxyribonuclease HindIII
Electrocardiography
Female
Gene Frequency
Genotype
Humans
Italy
Lipids / blood
Lipoprotein Lipase / genetics*
Lipoproteins / blood
Male
Myocardial Infarction / enzymology,  genetics*
Polymorphism, Genetic*
Polymorphism, Restriction Fragment Length
Regression Analysis
Risk Factors
Chemical
Reg. No./Substance:
0/Lipids; 0/Lipoproteins; EC 3.1.1.34/Lipoprotein Lipase; EC 3.1.21.-/Deoxyribonuclease HindIII

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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