eNOS Gene Variants and the Risk of Premature Myocardial Infarction

BACKGROUND: Endothelial nitric oxide synthase (eNOS) as well as nitric oxide play an important role in the regulation of cardiovascular function. There are limited and controversial data regarding the impact of polymorphisms of eNOS gene that is implicated in the vasoconstrictive properties of the endothelium in the pathogenesis of premature myocardial infarction (MI).OBJECTIVE: We examined whether two common polymorphisms of eNOS gene (G894T and T786C) are associated with the development of premature MI.METHODS: We recruited 107 patients with premature MI and compared them to 103 age- and sex- matched controls. All patients underwent coronary angiogram and were classified into the subgroup of patients with ‘normal’ or ‘near normal’ coronary arteries and the subgroup of patients with significant coronary artery disease (≥ 50% stenosis in lumen diameter of coronary arteries). The genetic polymorphisms of eNOS gene were assayed with polymerase chain reaction and reverse hybridization.RESULTS: Nineteen patients (17.8%) had ‘normal’ or ‘near normal’ coronary arteries. A significantly higher frequency of homozygosity for the 786C (32%) and the 894T (21%) alleles of the eNOS gene in patients who develop early MI in the setting of angiographically 'normal' or 'near normal' coronary arteries were found.CONCLUSIONS: Our data suggest that the T786C and the G894T genetic polymorphisms are associated with the development of MI in very young individuals, whose coronary arteries are characterized by very small atheromatic burden.

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Genetic polymorphisms G894T on the eNOS gene is associated with endothelial function and vWF levels in premature myocardial infarction survivors

International Journal of Cardiology ◽

10.1016/j.ijcard.2005.02.039 ◽

2006 ◽

Vol 107 (1) ◽

pp. 95-100 ◽

Cited By ~ 21

Author(s):

Charalambos Antoniades ◽

Dimitris Tousoulis ◽

Carmen Vasiliadou ◽

Christos Pitsavos ◽

Marina Toutouza ◽

...

Keyword(s):

Myocardial Infarction ◽

Endothelial Function ◽

Genetic Polymorphisms ◽

Enos Gene ◽

Premature Myocardial Infarction

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Abstract 3457: Methylenetetrahydrofolate Reductase Gene Polymorphism C677T And The Risk Of Premature Myocardial Infarction With “Normal” Coronary Arteries.

Circulation ◽

10.1161/circ.116.suppl_16.ii_781-d ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Loukianos Rallidis ◽

Christoforos Komborozos ◽

Argyri Gialeraki ◽

Maria Zolindaki ◽

Panagiotis Vavoulis ◽

...

Keyword(s):

Myocardial Infarction ◽

Coronary Arteries ◽

Methylenetetrahydrofolate Reductase ◽

Young Patients ◽

Mthfr C677t ◽

C677t Polymorphism ◽

Mthfr C677t Polymorphism ◽

Normal Coronary Arteries ◽

Methylenetetrahydrofolate Reductase Gene Polymorphism ◽

The Impact

Purpose: the pathogenetic mechanism of acute myocardial infarction (AMI) in young patients remains unknown. We explored the impact of homocysteine and its main genetic modulator Table 2 methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism in patients who sustained AMI under the age of 36 years. Methods: we recruited 136 consecutive patients who had survived their first AMI before the age of 36 years (mean age=32 ± 3.1 years, range 23–35 years, 121 men). Blood was taken for lipids and homocysteine levels within 12 hours from admission. The MTHFR C677T polymorphism was also determined with polymerase chain reaction. All patients underwent cardiac catheterization. One hundred-three healthy individuals without a family history of coronary heart disease (CHD), matched for age and sex served as controls. Results: coronary angiogram revealed significant CHD in 104 patients while 32 (23.5%) had no significant CHD. The prevalence of homozygotes for C677T polymorphism [T/T genotype] was 27.2% in patients and 14.6% in controls (p=0.02). In the subgroup of patients who had AMI and “normal” coronary arteries the frequency of homozygotes was 43.8% (p=0.001 versus controls and p=0.02 versus patients with significant CHD). The table presents lipids and homocysteine levels in AMI patients with “normal” coronary arteries and controls. Logistic regression model showed that the odds ratio for a young individual with T/T genotype to develop AMI with “normal” coronary arteries was 5.2 (confidence interval 1.2–23, p=0.03) adjusted for smoking habits, body mass index, hypertension and diabetes mellitus. Conclusions: the presence of homozygocity for MTHFR C677T polymorphism is associated with 5-fold higher risk for premature AMI with “normal” coronary arteries. This suggests that homocysteine may be involved in the formation of an obstructive thrombus in coronary arteries, especially in young individuals without significant underlying atheromatic burden.

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Mean platelet volume is elevated in patients with myocardial infarction with normal coronary arteries, as in patients with myocardial infarction with obstructive coronary artery disease

Scandinavian Journal of Clinical and Laboratory Investigation ◽

10.1080/00365510902829354 ◽

2009 ◽

Vol 69 (5) ◽

pp. 570-574 ◽

Cited By ~ 13

Author(s):

Ercan Varol ◽

Atıilla Iclı ◽

Mehmet Ozaydıin ◽

Dogan Erdogan ◽

AkıIf Arslan

Keyword(s):

Myocardial Infarction ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Coronary Arteries ◽

Mean Platelet Volume ◽

Obstructive Coronary Artery Disease ◽

Platelet Volume ◽

Normal Coronary Arteries ◽

Artery Disease

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The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530320666200621174858 ◽

2020 ◽

Vol 20 ◽

Author(s):

Sarah Abdullah ◽

Yazun Jarrar ◽

Hussam Alhawari ◽

Eyada Abed ◽

Malek Zihlif

Keyword(s):

Nitric Oxide ◽

Nitric Oxide Synthase ◽

Lipid Profile ◽

Genetic Polymorphisms ◽

Endothelial Nitric Oxide Synthase ◽

Diabetic Patients ◽

Enos Gene ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Background: Endothelial nitric oxide synthase (eNOS) plays a major role in the response of antihypercholesterol statin drugs. Genetic polymorphisms in the eNOS gene affect the activity of eNOS and thereby modulate statin response. Objectives: This study investigated the influence of major functional eNOS gene polymorphisms (rs2070744, rs1799983, and rs61722009) on the lipid profile of type 2 diabetes mellitus (T2DM) Jordanian patients treated with atorvastatin. Methods: The sample comprised 103 T2DM patients who attended the diabetes clinic of Jordan University Hospital. The T2DM patients had regularly been taking 20 mg atorvastatin. The atorvastatin response was calculated by measuring the lipid profile before and after three months of atorvastatin treatment. The eNOS genotypes of the subjects were analyzed using polymerase chain reaction (PCR) followed by restriction fragment length polymorphism (RFLP) assay. Results: No significant association was found between eNOS genetic polymorphisms and the response to atorvastatin (ANOVA, p > 0.05). In addition, no significant difference in the frequency of eNOS genotypes was found between T2DM patients and healthy subjects. However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05). The eNOS rs1799983 and rs61722009 polymorphisms were in complete linkage disequilibrium (D' = 1). Conclusion: Although no association was found between eNOS genetic polymorphisms and atorvastatin response, there was a significant association between the rs1799983 and rs61722009 genotypes and baselines levels of TC and LDL in Jordanian T2DM patients. These genetic variants affect cholesterol levels and may play a role in the susceptibility to cardiovascular diseases in T2DM patients. Further studies are needed to validate these findings.

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