Association of Polymorphisms in Endothelial Nitric Oxide Synthesis and Renin–Angiotensin–Aldosterone System with Developing of Coronary Artery Disease in Bulgarian Patients

Mokretar, Katya; Velinov, H.; Postadzhiyan, Arman; Apostolova, Margarita D.

doi:10.1089/gtmb.2015.0195

Cited by 18 publications

(15 citation statements)

References 36 publications

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“…However, this relationship occurred for the TT genotype (P = 0.05) and the T allele (P = 0.014). Mokretar et al (2016) in a cohort study of Bulgarian patients presented a high percentage of T894 alleles in patients with coronary ischemia (N = 171) compared to the control group (N = 123) (P = 0.006). Antoniades et al (2005) in their studies with 229 patients who underwent AMI in the early age (before 55 years old) found the TT homozygous polymorphism for G894T with a significant difference, as well as Isordia-Salas et al (2009) who described Glu298ASP as an independent risk factor for early AMI.…”

Section: Discussionmentioning

confidence: 92%

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

Campedelli¹,

Silva²,

Rodrigues³

et al. 2017

Genet. Mol. Res.

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ABSTRACT. Atherosclerotic and its cardiovascular complications are responsible for 17.5 million deaths a year, according to the World Health Organization. There is consensus that atherosclerosis involves multiple pathogenic processes initiated by endothelial dysfunction, with inflammation and vascular proliferation determining alterations in the matrix, with consequent formation of the atheromatous plaque and its clinical implications. Risk factors such as hypertension, diabetes mellitus, dyslipidemia, and smoking are widely known. Currently, genotyping, which is not directly related to these factors, is not accepted to estimate the risk of cardiovascular diseases, but strong evidence indicates several polymorphic genes as factors of risk and progression leading to complications of the disease. Among the genes involved, eNOS (endothelial nitric oxide synthase gene), which is responsible for the production of endothelial nitric oxide (an important arterial vasodilator), when presented in polymorphic variation can determine production, malfunction, and predisposition to atherosclerosis. In the present study, we analyzed the G894T polymorphism of the eNOS gene in groups of individuals diagnosed with atherosclerosis and in a control group. We collected 200 blood samples from patients previously diagnosed with atherosclerosis and 100 samples formed the control group. The genotyping analysis for polymorphism of the eNOS gene was determined by PCR. We considered variables such as gender, smoking, smoking history, and alcohol consumption; statistical differences were found in the distribution of case and control groups (P = 0.0378) and in non-smoking patients (P = 0.0263). In the other associations, no statistically significant difference was found. In the population studied, the frequency of the heterozygous genotype (GT) was much higher than in the other populations (GG and TT) in both groups (case and control). The GG genotype showed greater susceptibility to atherosclerosis. Association of the GG genotype in non-smokers also showed greater susceptibility. Gender, alcohol consumption, smoking, and smoking history did not influence atherosclerosis.

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Section: Discussionmentioning

confidence: 92%

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

Campedelli¹,

Silva²,

Rodrigues³

et al. 2017

Genet. Mol. Res.

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“…In addition, L-arginine 9 g/d ameliorates symptomatic vasospastic angina among patients with Prinzmetal's angina 15,16 and L-citrulline 800 mg/d increases flowmediated dilation of the brachial artery among patients with vasospastic angina. 19 To the extent that nitric oxide plays an important etiologic role in osteonecrosis, 1,2,7,10-14 in a fashion similar to Prinzmetal's angina, [15][16][17][18][19] L-arginine or L-citrulline should be therapeutic for osteonecrosis, reducing arterial, arteriolar, and endothelial disease. Along with venous occlusion, this disease promotes primary osteonecrosis.…”

Section: Discussionmentioning

confidence: 99%

“…The use of L-arginine 5 to 15 g/d restores physiologic levels of nitric oxide and augments nitric oxide-dependent signaling. 24 It is therapeutic for Prinzmetal's angina [15][16][17][18][19] and may be therapeutic for primary osteonecrosis if initiated before joint collapse occurs (Ficat stage I-II). 1,2,7,10-14…”

Section: Discussionmentioning

confidence: 99%

T786C Mutation in the Endothelial Nitric Oxide Synthase Gene in Patients With Primary Osteonecrosis

Khan¹,

Choi²,

Freiberg³

et al. 2017

Orthopedics

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Mutations in the T786C endothelial nitric oxide synthase gene (eNOS) are associated with osteonecrosis and Prinzmetal's angina. Nitric oxide is necessary for bone health and ameliorates Prinzmetal's angina. This study compared mutations of T786C eNOS in 146 patients with primary osteonecrosis, 114 patients with Prinzmetal's angina, and 83 normal control subjects. Patients with osteonecrosis had more mutant eNOS alleles than control subjects (42% vs 22%, respectively; P<.0001) but had the same number of mutant alleles as patients with Prinzmetal's angina (42% vs 41%, respectively; P=.7), who in turn had more mutant eNOS alleles than control subjects (41% vs 22%, respectively; P=.0001). Of 146 patients with primary osteonecrosis, 65 (45%) had none of the 5 thrombophilias (Factor V Leiden heterozygosity, high levels of Factors VIII and XI, anticardiolipin antibody immunoglobulin M, and homocysteine) that otherwise distinguished patients with osteonecrosis from control subjects (P<.05). No associations were found between eNOS hetero-homozygosity and the 5 major thrombophilias in primary osteonecrosis. Of the 65 patients who had osteonecrosis but no major thrombophilias, for 41 (28% of the total sample of 146), eNOS hetero-homozygosity was the only abnormality. Normalization of nitric oxide levels with l-arginine 9 g/d or l-citrulline 800 mg/d, both of which relieve vasospastic angina in Prinzmetal's angina, which has the same eNOS genotype as primary osteonecrosis, may slow or stop the progression of osteonecrosis. Placebo-controlled trials of patients with primary osteonecrosis who are hetero-homozygous for the T786C eNOS mutation and have no major thrombophilias are needed to assess the safety and efficacy of this treatment. [Orthopedics. 2017; 40(5):e898-e903.].

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“…A recent study indicated that high ACE and angiotensinogen affect the structure and function arteries and the heart. The D allele of ACE was reported to influence plasma level and activity of the ACE enzyme, resulting in elevation of Ang-II sensitivity; this is believed to involve the interaction of MI/R, ventricular hypertrophy, and hypertension [35]. ECG elevation in patients is not the only parameter used to diagnose acute MI/R; it also has to be measured by a series of ECG for diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia

et al. 2016

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BackgroundMyocardial ischemia and reperfusion lead to impairment of electrolyte balance and, eventually, lethal arrhythmias. The aim of this study was to investigate the effects of pharmacological inhibition of angiotensin-II (Ang-II) production on heart tissue with ischemia-reperfusion damage, arrhythmia, and oxidative stress.Material/MethodsRats were divided into 4 groups: only ischemia/reperfusion (MI/R), captopril (CAP), aliskiren (AL), and CAP+AL. The drugs were given by gavage 30 min before anesthesia. Blood pressure and electrocardiography (ECG) were recorded during MI/R procedures. The heart tissue and plasma was kept so as to evaluate the total oxidant (TOS), antioxidant status (TAS), and creatine kinase-MB (CK-MB).ResultsCreatine kinase-MB was not different among the groups. Although TAS was not affected by inhibition of Ang-II production, TOS was significantly lower in the CAP and/or AL groups than in the MI/R group. Furthermore, oxidative stress index was significantly attenuated in the CAP and/or AL groups. Captopril significantly increased the duration of VT during ischemia; however, it did not have any effect on the incidence of arrhythmias. During reperfusion periods, aliskiren and its combinations with captopril significantly reduced the incidence of other types of arrhythmias. Captopril alone had no effect on the incidence of arrhythmias, but significantly increased arrhythmias score and durations of arrhythmias during reperfusion. MAP and heart rate did not show changes in any groups during ischemic and reperfusion periods.ConclusionsAngiotensin-II production appears to be associated with elevated levels of reactive oxygen species, but Ang-II inhibitions increases arrhythmia, mainly by initiating ventricular ectopic beats.

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Association of Polymorphisms in Endothelial Nitric Oxide Synthesis and Renin–Angiotensin–Aldosterone System with Developing of Coronary Artery Disease in Bulgarian Patients

Abstract: The eNOS G894T and ACE I/D polymorphisms are associated with an increased risk of developing ACS after adjusting for classical risk factors for atherosclerosis in the Bulgarian cohort.

Cited by 18 publications

References 36 publications

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

Polymorphism of the gene eNOS G894T (Glu298Asp) in symptomatic patients with aterosclerosis

T786C Mutation in the Endothelial Nitric Oxide Synthase Gene in Patients With Primary Osteonecrosis

Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia

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