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Human lipoprotein lipase HindIII polymorphism in young patients with myocardial infarction
R Gambino1, L Scaglione, N Alemanno
1Dipartimento di Medicina Interna, Universita' di Torino, Italy.
Insights
The LPL HindIII polymorphism is linked to coronary artery disease (CAD) severity in young myocardial infarction (MI) survivors. The homozygous LPL HindIII(+) allele significantly increases the risk of multivessel disease in this population.
Area of Science:
- Cardiovascular Genetics
- Molecular Cardiology
- Human Genetics
Background:
- Conflicting evidence exists regarding the association between the lipoprotein lipase (LPL) gene HindIII polymorphism and coronary artery disease (CAD) severity.
- No previous studies have investigated this association in an Italian population of young myocardial infarction (MI) survivors.
Purpose of the Study:
- To investigate the association between the DNA HindIII polymorphism of the human LPL gene and the severity of CAD in young Italian MI survivors.
Main Methods:
- Retrospective analysis of 87 young MI survivors (mean age 40.1 years) who underwent coronary angiography.
- Genotyping for the LPL HindIII polymorphism and assessment of CAD severity based on the number of diseased coronary vessels.
Main Results:
- The allelic frequency for the HindIII H(-) and H(+) alleles was 0.37 and 0.63, respectively.
- A significant association was found between the LPL HindIII polymorphism and CAD severity.
- Patients with the HindIII(+/+) genotype had a fourfold increased risk of multivessel disease compared to other genotypes.
- This association remained significant and independent of smoking status, family history of CAD, and hypertension.
Conclusions:
- The homozygous LPL HindIII(+) allele is a significant risk factor for multivessel coronary artery disease in young Italian MI survivors.
- This genetic marker may contribute to predicting CAD severity in specific populations.
- Further research is needed to reconcile conflicting findings and understand the underlying mechanisms.
Abstract:
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.