In order to examine the relationship between certain risk factors for atherosclerosis and family history of myocardial infarction, we compared a group of children (n=51) whose parents had survived myocardial infarction (n=34) with a control group of children (n=90) with a negative family history of atherosclerosis (62 parents). The study revealed a surprising fact that 26.7 % of control children had hypercholesterolaemia compared to 15.7 % incidence in "risk" children. "Risk" children differed from the controls most in the apo-A-l levels and a higher risk index expressed by the proportion of apo-B:apo-A-l (1.22, 1.34 g/1, p=0.001, 0.58, 0.46, p=0.05, respectively). Since the most frequent primary hyperlipoproteinaemia in myocardial infarction families was familial combined hyperlipoproteinaemia, we assume that this condition may be presented in affected children by an unfavourable proportion of apolipoproteins of the lipoprotein classes.
The objective of this study was to examine plasma homocysteine levels and C677T methylenetetrahydrofolate reductase (MTHFR) gene polymorphism in two ethnic groups from Slovakia. The samples consisted of general Slovak-Romany population (68 men and 81 women) from Southwestern Slovakia and the Slovak-Caucasians (174 men and 177 women) who participated in the CINDI project. The homocysteine levels were examined by HPLC, the analysis of MTHFR genotypes was done by PCR. The Slovak-Romany men (12.0±5.6 (S.D.) μmol/l) and women (9.2±2.6 μmol/l) have significantly lower plasma homocysteine levels (p<0.024 and p<0.00001) when compared to Caucasians (13.3±5.1 μmol/l in men and 11.3±4.3 μmol/l in women). The genetic equilibrium is assumed for the gene frequencies of the MTHFR polymorphism in both samples. The distribution of MTHFR genotypes did not differ between the two populations (TT 13 vs. 10.6 %; CT 46.6 vs. 41.7 %; CC 40.4 vs. 47.7%, zeta2 = 2.315, df=2, ns). The effect of MTHFR genotypes on homocysteine levels was not confirmed in the Slovak-Romanies and TT homozygosity significantly increased plasma homocysteine levels only in Slovak-Caucasians (11.5±4.4 mmol/l, ns; vs. 14.8±4.8 mmol/l, p<0.002, respectively). To our knowledge, this is the first epidemiological study in the Romany population examining distribution of the MTHFR genotypes and their effect on homocysteine levels. Further studies are needed to establish the variety of cardiovascular risk factors among Romanies in order to evaluate the significance of particular factors.
The oxidative modification of low density lipoprotein (LDL) plays an important role in the pathogenesis of atherosclerosis. LDL of subjects with atherogenic lipoprotein phenotype (ALP) is known to be more susceptible to oxidation. We studied the effect of the hypolipidaemic drug ciprofibrate on the susceptibility of LDL to in vitro oxidation. Nine patients with primary hypertriglyceridaemia and hypoalphalipoproteinaemia (mean plasma triglycerides 3.76 mmol.L1 and HDL-cholesterol 0.74 mmol.l-1) were treated with ciprofibrate for 12 weeks. The susceptibility of LDL to in vitro Cu2 +-mediated oxidation was assessed by measuring conjugated diene formation at 234 nm. Ciprofibrate therapy significantly prolonged the lag time (93±7 min vs. 102±11 min, P = 0.02). The maximal rate of diene production was 11 % lower, but the decrease was not significant. A significant positive correlation was observed between maximal rate and maximal amount of dienes formed. Thiobarbituric acid reacting substances (TBARS) and lipid hydroperoxides (LPO) in oxidatively-modified LDL, isolated from the plasma of patients before and after drug treatment, were unchanged. The results suggest that ciprofibrate therapy has a favourable effect by increasing the in vitro resistance of LDL against oxidation.