[Effect of polymorphisms on key enzymes in homocysteine metabolism, on plasma homocysteine level and on coronary artery-disease risk in a Tunisian population]. / Effet des polymorphismes des enzymes clés du métabolisme de l'homocystéine sur l'homocystéinémie et le risque coronarien chez une population tunisienne.

BACKGROUND: Hyperhomocysteinemia is known as an independent-risk factor for coronary-artery disease (CAD). However, the effect of homocystein metabolic enzymes polymorphisms on CAD is still controversed. We investigated the relation between homocystein metabolic key enzymes polymorphisms, homocystenemia and coronary stenosis in a Tunisian population. METHODS: Samples were collected from 251 CAD patients documented by angiography. Genotyping were performed for C677T methylene-tetrahydrofolate reductase (MTHFR), A2756G methionine-synthase (MS) and 844ins 68 cystathionine-beta-synthase (CBS). We measured fasting plasma tHcy, folate and vitamin B12. RESULTS: There was significant increase in homocysteinemia for homozygous genotypes of C677T MTHFR (p<0.001) and A2756G MS (p=0.01), but not for 844ins68 CBS (p=0.105). Potential confounders adjusted odds-ratios for significant coronary stenosis, associated with MTHFR TT, MS GG and CBS insertion, were respectively 1.78 (p=0.041); 2.33 (p=0.036) and 0.87 (p=0.823). The effect of mutated MTHFR genotype was more pronounced on homocysteinemia (21.4+/-9.1 micromol/L; p<0.001) and coronary stenosis (OR=2.73; p=0.033) at low folatemia (< or =6.1 ng/mL). CONCLUSION: MTHFR TT and MS GG genotypes increase tHcy concentration and coronary stenosis risk, especially with low folatemia.

[Arachidonate to saturated fatty acid ratio of circulating sterides and phospholipids: can it be risk marker of coronary stenosis? A Tunisian study]. / Le rapport arachidonate sur acides gras saturés des stérides et des phospholipides circulants: peut-il être un témon du risque de sténose coronarienne? Etude dans une population tunisienne.

The prevention and early diagnosis of cardiovascular diseases is a public health priority in Tunisia and actions are undertaken to evaluate biologic marquers in at risk populations. Concentrations of fatty acids in serum phospholipids and sterides have been measured using thin layer chromatography and gaz chromatography of transmethyled derivatives. The study concerned 98 coronarographed patients, presenting (n = 72) or not coronary artery disease (n = 26). The results have been compared to those of a reference population (n = 43) without any cardiac pathology. The mean concentrations of most of sterides fatty acids in coronarographed patients were higher than in controls, except for arachidonic acid which was slightly lower (68 +/- 34 mg/L versus 77 +/- 19,6 mg/L in controls). Considering concentrations of sterides fatty acids in the two subgroups of patients, coronary artery disease was associated with an increase of all these fatty acids, which was statistically significant for palmitate, linoleate and linolenate. Measurements of fatty acids in phospholipids showed a reduction of arachidonic acid in coronarographed patients (76 +/- 36,7 mg/L versus 135 +/- 49,3 mg/L in controls), but without correlation with the severity of the stenosis.

[Lipoprotein (a) and ischemic heart diseases in patients with type 2 diabetes]. / Lipoprotéine (a) et cardiopathies ischémiques chez les patients diabétiques de type 2.

Lipoprotein (a) is a new independent coronary risk factor, but the role of lipoprotein (a) in type 2 diabetes remains controversial. The objective of this study was to demonstrate the relationship between the level of lipoprotein (a) and the coronary artery diseases (CAD) in type 2 diabetes. Recruitment was carried out in 3 groups of patients: Group 1: 110 control subjects, Group 2: 115 diabetics (D), Group 3: 105 diabetics with CAD (DC). The mean age was, 51 + 7; 52 + 6; 56 + 6 respectively. Total cholesterol, triglyceride, HDL-C, LDL-C, Apo A-I, Apo B and lipoprotein (a) were measured for the patients. The Lp (a) level was significantly higher in the diabetic groups as compared to the controls (p < 0.05), but this level was different between D and DC: 312 + 232 vs 347.8 + (NS). However, when the Lp (a) level is higher than 300 mg/ml, there is a significant difference between DC and D (53% vs 42% p = 0.05). There is no correlation between Lp level and total cholesterol; however, there is a significant variation of Lp (a) level with LDL-C (r = -0.14, P = 0.01). There is a negative correlation between Lp (a) and HDL-C (r = -0.13, p = 0.03), Lp (a) and ApoA-I (r = - 0.11, p = 0.05); but there is a positive correlation between Lp (a) and ApoB (r = 0.14, p = 0.02). Lp(a) level higher than 300 mg/L constitutes a coronary risk factor in type 2 diabetes. This contributes, with the other lipid disorders, to the increase of the coronary risk factors in diabetes.