Key result
The 9Asn (with -93G) lipoprotein lipase genotype was associated with an increased risk of ischemic heart disease compared to noncarriers (HR 1.6; 95% CI 1.2-2.3).
Why the study?
Do lipoprotein lipase genetic variants affect triglycerides, HDL, and the risk of ischemic heart disease in the general population?
Observational (n=9,004)
Do lipoprotein lipase genetic variants affect triglycerides, HDL, and the risk of ischemic heart disease in the general population?
Hazard Ratio: 1.6 (95% CI 1.2–2.3)
Genetic variation in lipoprotein lipase is associated with significant differences in plasma triglycerides and HDL cholesterol, and the 9Asn variant increases the risk of ischemic heart disease.
May inform genetic IHD risk assessment; leaves open clinical utility pending prospective validation.
CONTEXT: Genetic variants in lipoprotein lipase may affect triglycerides, high-density lipoprotein (HDL), and risk of ischemic heart disease (IHD). OBJECTIVE: The objective of this study was to investigate the influence of T(-93)G, G(-53)C, Asp9Asn, Gly188Glu, Asn291Ser, and Ser447Ter lipoprotein lipase genotypes on triglycerides, HDL, and IHD. DESIGN: The cross-sectional study involved 9004 adults. The prospective study consisted of 8817 adults developing 1001 IHD events over 23 yr. The case-control study involved 7818 non-IHD individuals vs. cohorts of 915 and 1062 IHD patients, respectively. SETTING: The study was performed in the Danish general population (the Copenhagen City Heart Study). PARTICIPANTS: IHD was angina pectoris or myocardial infarction. MAIN OUTCOME MEASURES: Triglycerides, HDL, and IHD were the main outcome measures. RESULTS: Cross-sectionally, triglycerides varied by genotype with 1.27 mmol/liter in women and 1.22 mmol/liter in men. HDL cholesterol varied by genotype with 0.49 mmol/liter in women and 0.60 mmol/liter in men. Prospectively, 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers had a hazard ratio for IHD of 1.6 [95% confidence interval (CI), 1.2-2.3]; 291Ser and 447Ter did not change IHD risk. In the case-control study, combining the cohorts of IHD patients, 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers had an odds ratio for IHD of 1.5 (CI, 1.2-2.1). 291Ser and 447Ter did not change IHD risk. Stratified for apolipoprotein E genotype, the odds ratios for IHD in 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers were 2.6 (CI, 1.2-5.5) among epsilon32 individuals and 2.4 (CI, 1.4-4.1) among epsilon43 individuals. CONCLUSIONS: Genetic variation in lipoprotein lipase is associated with differences in plasma triglycerides greater than 1 mmol/liter and differences in HDL cholesterol greater than 0.5 mmol/liter. A 1.6-fold risk of IHD in 9Asn (with -93G) heterozygotes and homozygotes combined is influenced by apolipoprotein E genotype.
No takes yet. Share an insight, caveat, or question.
Wittrup et al. (2006) conducted an observational in Ischemic heart disease (n=9,004). 9Asn (with -93G) lipoprotein lipase genotype vs. Noncarriers was evaluated on Ischemic heart disease (HR 1.6, 95% CI 1.2-2.3). The 9Asn (with -93G) lipoprotein lipase genotype was associated with an increased risk of ischemic heart disease compared to noncarriers (HR 1.6; 95% CI 1.2-2.3).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: