Genetic Variant Showing a Positive Interaction With β-Blocking Agents With a Beneficial Influence on Lipoprotein Lipase Activity, HDL Cholesterol, and Triglyceride Levels in Coronary Artery Disease Patients

Circulation ◽  
1997 ◽  
Vol 95 (12) ◽  
pp. 2628-2635 ◽  
Author(s):  
Björn E. Groenemeijer ◽  
Michael D. Hallman ◽  
Paul W.A. Reymer ◽  
Eric Gagné ◽  
Jan Albert Kuivenhoven ◽  
...  
The Lancet ◽  
1985 ◽  
Vol 325 (8440) ◽  
pp. 1242-1244 ◽  
Author(s):  
CH. Breier ◽  
H. Drexel ◽  
H.-J. Lisch ◽  
V. Mühlberger ◽  
M. Herold ◽  
...  

2007 ◽  
Vol 23 (3) ◽  
pp. 161-166 ◽  
Author(s):  
Penbe Cagatay ◽  
Belgin Susleyici-Duman ◽  
Cavlan Ciftci

Our aim was to determine whether lipoprotein lipase gene PvuII polymorphism can be considered as an independent risk factor for coronary artery disease (CAD) by conducting a meta-analysis of all available published trials, including our own study. In 7 seperate studies, 3289 subjects were screened for this substitution; meta-analysis included only some of these individuals. Among the 7 studies, 6 were performed on white subjects, whereas 1 was on patients with Saudi Arabic descent.Subgroup analysis indicated that individuals with PvuII substitution does not have an increased risk for CAD. The LPL-PvuII genotype and allele frequency distributions did not differ significantly between CAD patients and healthy controls. There was no difference in the distribution of LPL-PvuII genotypes between the healthy subjects and the patients with CAD. However, no significant differences in lipid variables (triglyceride and HDL-cholesterol) were determined for the PvuII polymorphisms in the patients with CAD. No significant differences were found in serum triglyceride and HDL-cholesterol levels for LPL-PvuII genotypes when the control and CAD groups were pooled. In conclusion, LPL-Pvu II polymorphism cannot be used as independent genetic risk factor for CAD.


2001 ◽  
Vol 100 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Ll. MASANA ◽  
G. FEBRER ◽  
J. CAVANNA ◽  
M. G. BARONI ◽  
W. MARZ ◽  
...  

Fifteen common polymorphic variants at six loci (apolipoproteins AI, B, CIII and E, hepatic lipase and lipoprotein lipase) involved in plasma lipid transport have been studied in 210 northern Spanish men, of whom 98 had proven coronary artery disease. The other 112 men were clinically free from coronary artery disease and acted as controls. The genotypes were investigated for relationships with plasma lipid and lipoprotein levels, as well as for the presence of coronary artery disease. As expected, the mean levels of plasma triacylglycerols (triglycerides) and lipoprotein (a) and the number of smokers were significantly higher in the disease group, and high-density lipoprotein (HDL)-cholesterol was significantly lower. Surprisingly, plasma cholesterol and low-density lipoprotein cholesterol were not different between the two groups. With regard to the common mutations, plasma triacylglycerol levels were related to the HindIII variants of lipoprotein lipase (P < 0.05), to the apolipoprotein CIII variant (C3175G in exon 4) and to the apolipoprotein AI XmnI polymorphisms (P < 0.05 and P < 0.02 respectively). The apolipoprotein E variants were related to plasma cholesterol (P < 0.05), HDL-cholesterol (P < 0.02), plasma triacylglycerols (P < 0.05) and the triacylglycerol/HDL ratio (P < 0.01). Only the three-codon insertion/deletion variants of the apolipoprotein B signal peptide region discriminated between the two groups with or without arterial disease (P = 0.02). The possible functional effects of these common mutations are discussed.


2007 ◽  
Vol 119 (15-16) ◽  
pp. 476-482 ◽  
Author(s):  
Martin Javorský ◽  
Daniela Gašperíková ◽  
Jozef Ukropec ◽  
Barbora Sedláková ◽  
Igor Riečanský ◽  
...  

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