PO3-60 EFFECTS OF APOE POLYMORPHISM ON LDL AND HDL PARTICLE SIZES

PO3-60 EFFECTS OF APOE POLYMORPHISM ON LDL AND HDL PARTICLE SIZES

Poster Sessions PO3 Pathophysiology of lipids and lipoproteins small vessel disease. Reduced smoking showed benefit after a 5 year follow-up as renal ...

68KB Sizes 0 Downloads 30 Views

Poster Sessions PO3 Pathophysiology of lipids and lipoproteins small vessel disease. Reduced smoking showed benefit after a 5 year follow-up as renal small vessel disease recovered. PO3-60

EFFECTS OF APOE POLYMORPHISM ON LDL AND HDL PARTICLE SIZES

J. Vekic 1 , A. Topic 1 , A. Zeljkovic 1 , V. Spasojevic-Kalimanovska 1 , Z. Jelic-Ivanovic 1 , S. Spasic 1 , S. Veselinovic 2 . 1 Institute of Medical Biochemistry, Faculty of Pharmacy, Belgrade, Serbia; 2 Health Center Sabac, Sabac, Serbia

PO3-61

LOCATION OF TENDON XANTHOMATA AND PREVALENCE OF CORONARY ARTERY DISEASE AMONG HETEROZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA PATIENTS

J. Skoumas, L. Papadimitriou, C. Pitsavos, C. Masoura, C. Chrysohoou, N. Giotsas, M. Toutouza, M. Kambaxis, C. Stefanadis. 1st Cardiology Department, University of Athens, Hippokration Hospital, Athens, Greece Background and Aims: The accumulation of cholesterol in tendons lead to the development of Tendon xanthomata (TX) in heterozygous familial hypercholesterolemia (hFH) patients. The aim of this study was to investigate the association of the location of TX with the prevalence of Coronary Artery Disease (CAD) and other biochemical parameters. Methods: The study population consisted of 524 patients (234 men, 290 women) with hFH. All subjects were screened for the presence of TX, while the lipidemic profile and the prevalence of CAD were recorded. Results: 151 hFH persons (87 males, 64 females) exhibit TX. Among persons with TX, the frequency distribution of TX was 30.3% in the upper extremities, 38.1% in the lower, and 31.6% in both extremities. Among these three subgroups we conducted a multifactorial analysis, which revealed that the lowest levels of apolipoprotein A were observed in persons with TX in both upper and lower extremities (p=0.014). We also reported that the levels of Total Cholesterol (p=0.21) LDL-Cholesterol (p=0.16), HDL Cholesterol (p=0.2), Triglycerides (p=0.89), apolipoprotein B, glucose and of fibrinogen did not differ between hFH individuals with TX in upper, lower, and both extremities respectively. Another multifactorial analysis of our data showed that the prevalence of CAD statististically differed between persons with TX in the upper, lower and both extremities (30.8% vs. 20.5% vs. 48.7%, p=0.008, respectively). Conclusions: The simultaneous presence in upper and lower extremities seems to be related with an exacerbation of the prevalence of CAD.

TENDON XANTHOMATA, LIPIDEMIC PROFILE AND PREVALENCE OF CORONARY ARTERY DISEASE AMONG FAMILIAL HETEROZYGOUS HYPERCHOLESTEROLEMIA PATIENTS

L. Papadimitriou, J. Skoumas, C. Pitsavos, C. Masoura, C. Chryshoou, N. Giotsas, M. Toutouza, K. Paliou, C. Stefanadis. 1st Cardiology Department, University of Athens, Hippokration Hospital, Athens, Greece Background and Aims: Familial Heterozygous Hypercholesterolemia (hFH) is the only dyslipidemia with tendon xanthomata (TX), which are depositions of cholesterol in the tendons. The aim of this study was to investigate the association of the presence of TX with the prevalence of Coronary Artery Disease (CAD) and other biochemical parameters. Methods: The study population consisted of 524 patients (234 men, 290 women) with hFH. The lipidemic profile, the exhibition of TX and the presence of CAD among all participants was recorded. Results: Among hFH subjects 372 persons did not exhibit TX, while 151 individuals did. The TX positive hFH patients (TX+) were males (57.7% males vs. 39.2% females, p<0.001), had statistically higher levels of LDL-C (330.1mg/dl vs. 283.7mg/dl, p=0.001), apolipoprotein B (p=0.001) and of fibrinogen (p=0.016) and lower levels of HDL Cholesterol (p=0.014)and apolipoprotein A (p=0.044) compared to TX negative (TX-) subjects, respectively. Total cholesterol (p=0.1), Triglycerides (p=0.098), lipoprotein a (p=0.1) and glucose (96.4mg/dl vs. 92.3mg/dl, p=0.06) did not differ between the subgroups of hFH with and without TX respectively. The prevalence of CAD among TX+ hFH subjects was higher than TX- (25.8% vs. 12.6%, p<0.001). After adjusting for age, gender, waist circumference, smoking habits, lipidemic profile and glucose levels, the presence of TX was associated with a 2.2 fold higher risk for CAD. Conclusions: The presence of TX seems to double the risk for CAD, which could be attributed to the higher levels of LDL-Cholesterol and the lower levels of HDL-Cholesterol. PO3-63

APOLIPOPROTEIN B-48 IN LIPOPROTEIN FRACTION EXTRACTED FROM HUMAN AORTIC PLAQUE AND PLASMA FROM SUDDEN CARDIAC DEATH CASES

T. Nakano 1 , M. Niimi 1 , K. Nakajima 1 , M. Fujita 2 , Y. Nakajima 3 , S. Takeichi 3 , A. Tanaka 4 , T. Matsushima 5 , M. Kinoshita 6 , T. Teramoto 6 . 1 JIMRO Co., Ltd., Takasaki, Gunma, Japan; 2 Department of Forensic Medicine, Keio University School of Medicine, Tokyo, Japan; 3 Department of Forensic Medicine, Tokai University School of Medicine, Isehara, Kanagawa, Japan; 4 Kagawa Nutrition University, Saitama, Japan; 5 Internal Medicine, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan; 6 Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan Background: Apo B-48 is a chylomicron (CM) specific apolipoprotein. It is well known apo B-100 is always found in human plaque, but the presence of apo B-48 in human plaque is still unclear. We investigated whether apo B-48 is detected in human aortic plaque, and investigated the particle size of apo B-48 carrying lipoproteins in plasma in sudden cardiac death cases. Subjects and Methods: Human aortic plaques from five sudden cardiac death cases were analyzed. We extracted lipoprotein fractions from human aortic plaque by the method of Rapp et al. and separated lipoprotein fractions by HPLC method. The detection of apo B-48 was performed by an ELISA method using specific anti-human apo B-48 monoclonal antibody. Western blot analysis of plaque extraction was performed using same antibody. Results: Apo B-100 in plaque extracts was confirmed in the peaks of very low density lipoprotein (VLDL) and LDL. Apo B-48 was confirmed in the peaks of CM, VLDL and LDL, and was also detected in HDL. Apo B-48 in plasma from sudden cardiac death cases was detected in various particle sizes, often smaller size than HDL. As an immunoblotting of plaque extraction, small sized apo B-48 react with anti-human apo B-48 monoclonal antibody was detected between 25 and 150 kDa. Conclusions: Apo B-48 was found not only in the fraction of CM, VLDL and LDL, but also in HDL in plaque extracts. These results indicated the presence of apo B-48 containing particles in human aortic plaque and assumed the possibility of its atherogenesity.

76th Congress of the European Atherosclerosis Society, June 10–13, 2007, Helsinki, Finland

POSTER SESSIONS

Objective: To evaluate the effect of apolipoprotein E (apoE) phenotypes on lipoprotein size relative to that of other cardiovascular risk factors in the population of Serbia. Methods: LDL and HDL particle diameters were measured by gradient gel electrophoresis, and apoE phenotype was determined by isoelectric focusing in 192 asymptomatic subjects (108 men and 84 women). The effects of ε2 and ε4 alleles on lipoprotein particle sizes were assessed using multiple linear regression, after adjustment for demographic data, lipid, lipoprotein and apolipoprotein levels. Results: The allele frequencies for ε2, ε3 and ε4 were 6.8%, 78.1% and 15.1%, respectively. In men, the carriers of ε2 allele had the smallest LDL particle size (P<0.05), while apoE polymorphism had no effect on HDL size. Multiple regression analysis showed that the variations in LDL size were significantly associated with the changes in body mass index (P<0.05) and triglyceride concentrations (P<0.05), but not with the possession of ε2 allele (P=0.154). In women, apoE phenotype was significantly related to HDL size and the smallest HDL particles were found among the carriers of ε4 allele (P<0.05). ApoE phenotype had no effect on LDL size (P=0.548). The possession of ε4 allele (P<0.005) and LDL cholesterol concentration (P<0.05) remained significant predictors of HDL size in multiple regression analysis. Conclusions: Polymorphism in apoE phenotypes was associated with diverse effects on lipoprotein size in men and women. The observed changes in LDL size were not independent of triglycerides, while the influence on HDL size was modulated with LDL cholesterol concentration.

PO3-62

33