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Effects of red wine on risk factors for atherosclerosis
Abstracts/Atherosclerosis
AFOLIPOPROTEIN (a) GENETIC VARIATION CORONARY HEART DISEASE IN A WELSH
AND RISK COHORT
OF
263
112 11995) 261-267 Hypertension Audit of Risk Factor Therapy (HART) survey: lipid, lipoprotein and glucose concentrations in hypertensive patients in the United Kingdom.
R Morgan, AJ Bishop, A Rees Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XU
SR Fcnstcr, L Rltchic’, N Poulter, RS Fink* and DJ Betteridge, University College London Medical Mortimer Street, London WIN BAA, ‘Dept of Practice, Univ of Aberdeen, Foresterhill Health Aberdeen and ‘West Middlesex Hospital, Isleworth.
Elevated Iwells of apolipoprotein (a) (Ape(a)), the unique apoprotein of lipoprotein (a), are associated with an increased risk of coronary heart disease (CHD). The major determinant of Ape(a) levels is the Ape(a) gene which is located in close proximity to the plasminogen gene on chromosome 6. The Ape(a) gene exhibits a wide size heterogeneity which is determined by the number of Kringle 4 repeats in the gene. We have investigated variation at the Apo(a)/plasminogen locus in ao angiographically defined cohort consisting of 102 patients with severe CHD and 109 matched controls. An 800 bp genomic probe containing an exon encoding the amino-terminal half of Kringle 4 was used to identify an Ssll polymorphism at this lccos. Two alleles (Sl -15 Kb; S2 - 10 Kb and 5 Kb) were identified by the polymorphism. Allele frequencies for the CHD and control groups, respectively, were:S1S1-0.54,0.57;S1S2-0.42,0.36;S2S2-0.04,0.07. There was no significant difference in frequencies between the two groups. However, a sign&ant difference in Apo(a) levels was observed between the three genotypic groups SlSl - 245 U/l; SlS2 - 166 U/l; S2S2 - 69 U/l @=0.001). Thus, although the Sell polymorphism is not a genetic marker for CHD it is possible that the Sill alleles are in linkage disequihbrium with alleles at the Ape(a) locus which determine Ape(a) levels.
20,467 hypertensive patients (14-91 years; 9,605 males; 88.9% Caucasians) were recruited from 725 general practitioners in the UK. Clinical details were recorded and fastmg total and HDL cholesterol and triglycerides and glucose WC’TC mcasurcd centrally. Data were analyxxi by age, sex, race, region, body mash ir?dex, cval$t hip ratlo, reportctd exercise, diabetes, smoking, alcohol, clinical vascular dlseasc and type of therapy. Lipid data is presented for the age group 50-59 years (n=2193 men, 2631 women). Concentrations arc’ in mmol/l. 38.7% men had cholesterol level 6.5-7.7 and 13.3’% >7.8. For women the percentages were 40.3% and 24.6% rcspectivcly. men and 6% women had 10.8% calculated LDL cholesterol >4.5. 31% men and 23.5% women had triglyceride level between 2.3-5.6. Total to HDL cholesterol ratio was >5 in 67.9% men and 4Y.9% women. For the whole population 3% were known dlabctics but 13.5% had glucose levels between 6-7.9 and 5.6%, of >8 mmol/l. Percentages for Asians wcrc 15.2% and 12.1% respectively and for Afro-Caribbeans 17.2% and 11.4% The huge data base of the HART survey will enable detailed analysis of multiple risk factor interaction in a group at high risk ot vascular discasc.
PHYTOSTEROLAEMIA
EFFECTS OF RED WINE ATHEROSCLEROSIS
IN
THREE
UNRELATED
SOUTH AFRICAN FAMILIES G.M.B. Berger, W.M. Deppe, E. Kormuth, M. Biggs, A.D. Marais* Department of Chemical Pathology, University of Natal, *Department of Medicine, University of Cape Town, South Africa. Phytosterolaemia has recently been attributed to an inherited defect in HMG CoA reductasesynthesis. It has not hitherto been reported in SouthernAfrica. We report 4 new homozygotes,from 3 unrelated families. The noncholesterol sterol content of plasma was 16-30% (fisitosterol 6.6-11.3%, campesterol 2.2-4.6%). Three of the 4 patients had cutaneous and tendinous xanthomas within the first decade of life. All our patients were female bringing the male:female ratio in reported casesto 8:23. All were small and presentedat some stage with haematologic abnormalities. The oldest patient had evidenceof atherosclerosis. The patientsrespondedto the administration of cholestyramine and a diet restricted in phytosterolswith decreasesin plasmasterol concentrations of up to 68%, accompanied by marked regression of xanthomasin one patient.
ON RISK
FACTORS
School, General Ccntre,
FOR
Sharpe PC’, McGrath LT2, McClean E’, Archbold GPR’ 1 Department of Clinical Biochemistry, Belfast City Hospital, 2. Department of Therapeutics, Queens University, Belfast Epidemiological studies have pointed to the role of alcohol, and red wine in particular, in reducing the incidence of coronary heart disease. We attempted fo distinguish, in viva, the effects of components specific to red wine and alcohol on lipoproteins, antioxidant status and membrane fluidity. Volunteers (n = 201 were given 200 ml of red wine per day for 10 days. Following a 6 week washout this was repeated with white wine. Changes within treatment groups were analysed by paired t tests and repeated measures analysis of variance was used to distinguish effects of red wine components and alcohol. LDL was prepared by ultracentrifugation and all other assays were by conventional laboratory techniques. No effect with either treatment was detected on total cholesrerol, triglycerides, HDL or measures of antioxidant status. Both treatments reduced LDL cholesterol lp
AFOLIPOPROTEIN (a) GENETIC VARIATION CORONARY HEART DISEASE IN A WELSH
AND RISK COHORT
OF
263
112 11995) 261-267 Hypertension Audit of Risk Factor Therapy (HART) survey: lipid, lipoprotein and glucose concentrations in hypertensive patients in the United Kingdom.
R Morgan, AJ Bishop, A Rees Department of Medicine, University of Wales College of Medicine, Heath Park, Cardiff CF4 4XU
SR Fcnstcr, L Rltchic’, N Poulter, RS Fink* and DJ Betteridge, University College London Medical Mortimer Street, London WIN BAA, ‘Dept of Practice, Univ of Aberdeen, Foresterhill Health Aberdeen and ‘West Middlesex Hospital, Isleworth.
Elevated Iwells of apolipoprotein (a) (Ape(a)), the unique apoprotein of lipoprotein (a), are associated with an increased risk of coronary heart disease (CHD). The major determinant of Ape(a) levels is the Ape(a) gene which is located in close proximity to the plasminogen gene on chromosome 6. The Ape(a) gene exhibits a wide size heterogeneity which is determined by the number of Kringle 4 repeats in the gene. We have investigated variation at the Apo(a)/plasminogen locus in ao angiographically defined cohort consisting of 102 patients with severe CHD and 109 matched controls. An 800 bp genomic probe containing an exon encoding the amino-terminal half of Kringle 4 was used to identify an Ssll polymorphism at this lccos. Two alleles (Sl -15 Kb; S2 - 10 Kb and 5 Kb) were identified by the polymorphism. Allele frequencies for the CHD and control groups, respectively, were:S1S1-0.54,0.57;S1S2-0.42,0.36;S2S2-0.04,0.07. There was no significant difference in frequencies between the two groups. However, a sign&ant difference in Apo(a) levels was observed between the three genotypic groups SlSl - 245 U/l; SlS2 - 166 U/l; S2S2 - 69 U/l @=0.001). Thus, although the Sell polymorphism is not a genetic marker for CHD it is possible that the Sill alleles are in linkage disequihbrium with alleles at the Ape(a) locus which determine Ape(a) levels.
20,467 hypertensive patients (14-91 years; 9,605 males; 88.9% Caucasians) were recruited from 725 general practitioners in the UK. Clinical details were recorded and fastmg total and HDL cholesterol and triglycerides and glucose WC’TC mcasurcd centrally. Data were analyxxi by age, sex, race, region, body mash ir?dex, cval$t hip ratlo, reportctd exercise, diabetes, smoking, alcohol, clinical vascular dlseasc and type of therapy. Lipid data is presented for the age group 50-59 years (n=2193 men, 2631 women). Concentrations arc’ in mmol/l. 38.7% men had cholesterol level 6.5-7.7 and 13.3’% >7.8. For women the percentages were 40.3% and 24.6% rcspectivcly. men and 6% women had 10.8% calculated LDL cholesterol >4.5. 31% men and 23.5% women had triglyceride level between 2.3-5.6. Total to HDL cholesterol ratio was >5 in 67.9% men and 4Y.9% women. For the whole population 3% were known dlabctics but 13.5% had glucose levels between 6-7.9 and 5.6%, of >8 mmol/l. Percentages for Asians wcrc 15.2% and 12.1% respectively and for Afro-Caribbeans 17.2% and 11.4% The huge data base of the HART survey will enable detailed analysis of multiple risk factor interaction in a group at high risk ot vascular discasc.
PHYTOSTEROLAEMIA
EFFECTS OF RED WINE ATHEROSCLEROSIS
IN
THREE
UNRELATED
SOUTH AFRICAN FAMILIES G.M.B. Berger, W.M. Deppe, E. Kormuth, M. Biggs, A.D. Marais* Department of Chemical Pathology, University of Natal, *Department of Medicine, University of Cape Town, South Africa. Phytosterolaemia has recently been attributed to an inherited defect in HMG CoA reductasesynthesis. It has not hitherto been reported in SouthernAfrica. We report 4 new homozygotes,from 3 unrelated families. The noncholesterol sterol content of plasma was 16-30% (fisitosterol 6.6-11.3%, campesterol 2.2-4.6%). Three of the 4 patients had cutaneous and tendinous xanthomas within the first decade of life. All our patients were female bringing the male:female ratio in reported casesto 8:23. All were small and presentedat some stage with haematologic abnormalities. The oldest patient had evidenceof atherosclerosis. The patientsrespondedto the administration of cholestyramine and a diet restricted in phytosterolswith decreasesin plasmasterol concentrations of up to 68%, accompanied by marked regression of xanthomasin one patient.
ON RISK
FACTORS
School, General Ccntre,
FOR
Sharpe PC’, McGrath LT2, McClean E’, Archbold GPR’ 1 Department of Clinical Biochemistry, Belfast City Hospital, 2. Department of Therapeutics, Queens University, Belfast Epidemiological studies have pointed to the role of alcohol, and red wine in particular, in reducing the incidence of coronary heart disease. We attempted fo distinguish, in viva, the effects of components specific to red wine and alcohol on lipoproteins, antioxidant status and membrane fluidity. Volunteers (n = 201 were given 200 ml of red wine per day for 10 days. Following a 6 week washout this was repeated with white wine. Changes within treatment groups were analysed by paired t tests and repeated measures analysis of variance was used to distinguish effects of red wine components and alcohol. LDL was prepared by ultracentrifugation and all other assays were by conventional laboratory techniques. No effect with either treatment was detected on total cholesrerol, triglycerides, HDL or measures of antioxidant status. Both treatments reduced LDL cholesterol lp