Association of G894T eNOS 4G/5G PAI and T1131C APOA5 polymorphisms with susceptibility to myocardial infarction in Morocco

© Elsevier Masson SAS. All rights reserved.

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20 Archives of Cardiovascular Diseases Supplements (2017) 9, 11-28

Objective The aim of our study is to explore the potential association of C677T MTHFR (rs 1801133) and G20210A FIIprothrombin (rs1799963) polymorphisms with the susceptibility of Myocardial Infarction in Morocco.

Methods After being extracted by the standard salting out procedure, DNA samples of 100 MI patients and 182 apparently healthy controls were geno- typed by PCR-RFLP using respectively HinfI and HindIII restriction enzymes.

Results Our results show a significant association of the G20210T FII with MI risk; the frequencies of the heterozygote genotype GA, homo- zygous mutated AA and the 20210A allele was higher among patients than controls (GA: 59% vs 5.5%, P<0.001; AA: 10% vs 0%, P=0.003 and 20210A: 39.5% vs 2.7%, P<0.003), suggesting that this polymorphism may be a potential genetic marker for Myocardial Infarction in Morocco.

There was no significant association between the C677T MTHFR and MI occurrence, even there was more heterozygote CT in patients group com- paring to controls.

Conclusion As being a multifactorial disease, the development of Myocar- dial Infarction may be the result of many factors that influence synergistically its occurrence. Thus, further studies are merited to try to better assess these associations (gene – gene and gene – environment interactions).

Keywords Myocardial Infarction, Susceptibility, association, Moroccan population, C677T MTHFR, G20210A FII.

The authors hereby declare no conflict of interest

470

Association of G894T eNOS, 4G/5G PAI and T1131C APOA5 poly- morphisms with susceptibility to myocardial infarction in Morocco H. Hassani Idrissi (*)(2), W. Hmimech (2), B. Diakité (2), F. Korchi (1), D. Baghdadi (1), R. Habbal (1), S. Nadifi (2)

(1) Hôpital universitaire Ibn Rochd, Cardiologie, Casablanca, Maroc – (2) Université Hassan II, Faculté de Médecine et de Pharmacie, Géné- tique humaine et pathologies moléculaires, Casablanca, Maroc

*Corresponding author: hassani-idrissi-hind@hotmail.fr

Background Myocardial infarction (MI) is a common multifactorial dis- ease. Numerous studies have found that genetic plays an essential role in MI occurrence. The main objective of our case – control study is to explore the association of G894T eNOS (rs1799983), 4G/5G PAI (rs1799889) and T1131C APOA5 (rs662799) polymorphisms with MI susceptibility in the Moroccan population.

Methods and Results 118 MI patients were recruited vs 184 healthy con- trols. DNA samples were genotyped by PCR-RFLP method using MboI, BslI and MseI restriction enzymes respectively for the G894T eNOS, 4G/

5G PAI and T1131C APOA5 polymorphisms. Our results show that the G894T eNOS was significantly associated with increased risk of MI under the three genetic transmission models (dominant: OR=1.64, 95% CI=1.05- 2.58, P=0.003; recessive: OR=2.15, 95% CI=0.74–6.16, P=0.03; additive:

OR=1.54, 95% CI=1.06–2.23, P=0.001). The T1131C APOA5 polymor- phism was associated to MI risk in recessive and additive models (OR=1.53, 95% CI=0.72–3.2, P=0.04 and OR=1.78, 95% CI=1.26–2.51, P=0.03 respectively). For the 4G/5G PAI variant, even the cases and con- trols groups were not in Hardy – Weinberg Equilibrium (HWE), the dom- inant and additive models show a statistically significant association with MI risk (OR=7.96, 95% CI=3.83–16.36, P=0.01 and OR=1.96, 95%

CI=1.4–2.72, P=0.03 respectively).

Conclusion Our results suggest that G894T eNOS and T1131C APOA5 polymorphisms may be considered as genetic markers of MI among the Moroccan population. Further studies including larger sample sizes and exploring more genetic associations are needed to confirm our results and to better understand the susceptibility to MI.

The authors hereby declare no conflict of interest

474

G2691A and C2491T mutations of FV gene and predisposition to myocardial infarction in Morroco

W. Hmimech (1), B. Diakité (1), H. Hassani Idrissi (*)(1), KH. Hamzi (1), F. Korchi (2), D. Baghdadi (2), R. Habbal (2), S. Nadifi (1)

(1) Université Hassan II, Faculté de Médecine et de Pharmacie, Génétique humaine et pathologies moléculaires, Casablanca, Maroc – (2) Hôpital uni- versitaire Ibn Rochd, Cardiologie, Casablanca, Maroc

*Corresponding author: hassani-idrissi-hind@hotmail.fr

Background Coagulation factor Leiden mutation has been described as a common genetic risk factor for venous thrombosis. The frequency of this mutation was practically absent in African population. Recently, a new non- sense mutation in the gene encoding factor V, has been associated with the risk of occurrence of cardio cerebrovascular diseases such as stroke and venous thrombosis.

Objective The aim of our study is to investigate if the FVL and C2491T nonsense mutations modulate the risk of developing myocardial infarction.

Methods Genotyping of FVL and C2491T FV was performed by PCR- RFLP method on a sample of 100 patients with myocardial infarction and 211 controls.

Results The frequency of FVL mutation was practically nil in our study population. By cons with C2491T mutation, the TT genotype was associated with an increased risk of myocardial infarction (OR: 3.16, 95% CI=1.29-7.71;

Pc=0.03). There was a significant association between C2491T FV mutation and myocardial infarction risk in recessive (OR: 2.74, 95% CI=1.14-6.58;

Pc=0.04), dominant (OR: 1.85, 95% CI=1.13-3.04; Pc=0.02) and additive (OR: 1.88; 95% CI=1.25-2.80; Pc=0.004) models. According to the risk fac- tors of myocardial infarction, a positive correlation was found between the C2491T FV mutation and hypertension (P=0.02).

Conclusion The results of our study suggest that the C2491T nonsense mutation of FV gene could be a risk factor for myocardial infarction in Moroccan population.

Keywords: FVL, C2491T, nonsense, mutation, myocardial infarction.

The authors hereby declare no conflict of interest

535

The role of bile acids and gut microbiota in coronary artery disease:

results of the MABAC study in human (microbiota atheroma and bile acid in coronary disease)

C. Chong-Nguyen (*)(1), H. Duboc (2), D. Rainteau (3), L. Humbert (3), H. Sokol (3), A. Bado (2), S. Weber (1), O. Varenne (1), D. Duboc (1) (1) APHP-Hôpital Cochin, Cardiologie, Paris, France – (2) Université Paris Diderot, Inserm UMR 1149 CRI, Paris, France – (3) APHP-Hôpital Saint-Antoine, Université Pierre et Marie Curie, UMR 7203, Paris, France

*Corresponding author: caroline. ng87@gmail.com

Introduction In mice models of atherogenesis (Apo E-/-, LDL-/-), Bile acids (BA) signaling molecules acting on glucose and lipid homeostasis inhibit the plaque development through 2 specific receptors, FXR and TGR5.

BA are active metabolites of the gut microbiota, which has been recently asso- ciated with atheroma in human.

Purpose Describe the composition of the fecal microbiota and the BA in sera and feces in a coronary artery disease (CAD) population compared to non CAD subjects.

Methods between February and June 2015, all the patients hospitalized in

the department of Cardiology for a coronary angiogram were screened. The

exclusion criteria were: non fasting, hepatic diseases, cholecystectomy, antibi-

otic, lipid-lowering drugs or corticosteroids. The concentration of BA in sera

and feces was measured with high pressure liquid chromatography coupled

with tandem mass spectrometry. The gut microbiota was analyzed by 454

pyrosequencing of fecal DNA.