scholarly journals The role of markers of endothelial dysfunction, oxidative and cellular stress in the prediction of myocardial infarction in comorbid patients with stable coronary heart disease

2021 ◽  
Vol 12 (1) ◽  
pp. 23-27
Author(s):  
Yuliya A. Kotova ◽  
Anna A. Zuikova ◽  
Natalia V. Strahova ◽  
Olga N. Krasnorutskaya ◽  
Elena Y. Esina

Aim. To study the role of markers of endothelial dysfunction, oxidative and cellular stress in the prediction of myocardial infarction (MI) in comorbid patients with stable coronary heart disease (CHD). Material and methods. The study involved 336 patients with a diagnosis of CHD. The presence of CHD was confirmed by diagnostic coronary angiography with the calculation of the Gensini index. All patients were divided into 2 groups: group 1288 patients without a history of MI, group 248 patients with a history of MI. All patients were assessed for the levels of oxidized modified proteins, high-sensitivity C-reactive protein (hs-CRP), homocysteine, heat shock protein (HSP70), and superoxide dismutase activity. Results. All patients were comparable in age. For other clinical and anthropometric characteristics, we saw significant differences (according to the MannWhitney criterion): patients with previous MI had higher BMI, waist circumference, and blood pressure. The correlation analysis revealed positive significant average strength relationships between past MI and the Gensini index, low-density lipoprotein level, total cholesterol level, homocysteine level, hs-CRP level, and the level of oxidized modified proteins; and negative significant average strength relationships between past MI and SOD activity level (r=-0.374, p=6.4 E-07) and HSP70 level (r=-0.563, p=2.6 E-15). The ROC analysis revealed that not all markers were significant in predicting the risk of MI. It is shown that the most expected characteristics were shown by the hs-СRP. However, further analysis of the predictive significance of the markers demonstrated that the addition of HSP70 to hs-CRP increases the predictive significance of hs-CRP in relation to the risk of developing MI. Conclusion. We have demonstrated that a strategy using a cumulative risk assessment consisting of 2 biomarkers (individually involved in inflammation and stress-induced cellular responses) can identify patients with an established diagnosis of CHD who have an increased risk of acute MI.

2020 ◽  
Vol 6 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Sergey A. Demchenko ◽  
Ivan S. Koklin ◽  
Natalia Yu. Koklina

Introduction: The review provides relevant information about arginase 2, the role of this enzyme in the formation of endothelial dysfunction and, as a consequence, the development of cardiovascular diseases. History of the discovery of arginase and its functions: The discovery of arginase took place long before its active study as a substance that affects the formation of endothelial dysfunction. Role of arginase 2 in the development of a number of cardiovascular diseases: The role of NO synthase and arginase 2 in the formation of oxidative stress is determined. The pathophysiological mechanisms of the development of a number of cardiovascular diseases, such as coronary heart disease, atherosclerosis, and aortic aneurysm, are described. The modern possibilities of treatment of endothelial dysfunction in the pathology of the cardiovascular system and the possibility of creation of new drugs are considered. An increase in the activity of arginase 2 was proven to occur in the case of the development of coronary heart disease (CHD), hypertension, type II diabetes mellitus, hypercholesterolemia, as well as in the process of aging. According to the WHO, coronary heart disease and apoplectic attack have topped the list of causes of death worldwide over the past 15 years. Arginase 2 as a potential pharmacological target: The purpose of this literature review is to determine the possibilities of use of arginase 2 as a new target for the pharmacological correction of cardiovascular diseases.


2019 ◽  
Vol 1 (9) ◽  
pp. 33-37
Author(s):  
Yu. A. Kotova ◽  
A. A. Zuykova ◽  
N. V. Strakhova ◽  
O. N. Krasnorutskaya

The high incidence of stable coronary heart disease, the increasing frequency of myocardial infarction, disability and mortality determine the relevance of the search for new risk markers and laboratory criteria for predicting this severe complication. The aim of the study was to develop an information panel for diagnosing the risk of myocardial infarction in patients with stable coronary heart disease, including significant generally accepted and potentially possible new laboratory parameters characterizing various pathogenetic links of coronary atherosclerosis. The study included 168 patients who were divided into 2 groups: Group 1 - with a history of myocardial infarction, Group 2 - without a history of myocardial infarction. In addition to the standard laboratory and instrumental examination, all patients were identified parameters of endothelial dysfunction, oxidative stress and chaperone activity as potential markers of myocardial infarction in patients with stable coronary heart disease. Assessment of the risk of myocardial infarction in patients with stable coronary heart disease was carried out using a logical and mathematical model, which combined the most informative laboratory indicators of oxidative stress, endothelial dysfunction, and chaperone activity, which are important in the occurrence and progression of coronary atherosclerosis, according to the results of preliminary comparative and correlation analysis. The basis for the development of the information panel was the method of decision trees. The study confirmed the relationship between the severity of coronary atherosclerosis and the occurrence of myocardial infarction. Comparative analysis of the selected groups of patients showed a higher level of oxidative stress, serum homocysteine concentrations and lower values of chaperone activity in Group 1. In patients with a history of myocardial infarction, C-reactive protein was significantly higher than in Group 2, indicating a more pronounced inflammatory response in patients with large atherosclerotic lesions. The study suggests the possibility of using mathematical information panels based on decision trees as a system for assessing the risk of acute myocardial infarction in patients with stable coronary heart disease. As a result of the analysis of the obtained model, laboratory biochemical factors of high risk of myocardial infarction were identified. Such factors were chaperone activity, serum homocysteine level, serum C-reactive protein concentration and superoxide dismutase activity.


Author(s):  
Normunds Līcis ◽  
Gustavs Latkovskis ◽  
Baiba Krivmane ◽  
Milāna Zabunova ◽  
Marina Berzina ◽  
...  

Relation of the Leu40Arg variant of glycoprotein IIIA to personal and family history of myocardial infarction GPIIb/IIIa fibrinogen receptor is a key element of the thrombotic pathway. In this study, we investigated the possible relation of PlA1/A2 polymorphism (1565T>C; Leu33Pro) and a rare 1586T>G (Leu40Arg) variation of GPIIIa gene to personal and family history of myocardial infarction (MI) among 601 patients with angiographically confirmed coronary heart disease. Four hundred and fifteen patients had MI and 94 of individuals reported family history of premature MI. The Arg40 (1586G) variant (n = 4) was present exclusively in MI-patients and significantly correlated with a family history of premature MI (P = 0.013), whereas the Pro33 (1565C; PlA2) allele (n = 204) was similarly prevalent among different groups of patients. These data indicate the importance of the Arg40 variant but do not support a significant role of Pro33 allele in susceptibility to MI.


2018 ◽  
Vol 5 (4) ◽  
pp. 12-22
Author(s):  
A. V. Ponasenko ◽  
A. V. Tsepokina ◽  
M. V. Khutornaya ◽  
V. A. Dolgikh ◽  
I. Yu. Malshev ◽  
...  

Objective:to assess the probability of pathogenic effects OF Il-18 (IL18, IL18R1 and IL18RAP) gene polymorphism on the risk of myocardial infarction in patients with stable coronary heart disease.Materials and methods: the present study was performed with the inclusion of 260 patients with stable coronary heart disease (CHD), residents of the industrial region of Western Siberia. Molecular genetic testing was performed on nine polymorphic sites of il18, IL18R1, IL18RAP genes.Results:associations of polymorphic sites rs13015714 IL18R1 and rs917997 IL18RAP with risks of myocardial infarction were Determined (OR =1.95 (95% CI =1.06-3.58), p =0.029 and OR =2.01 (95% CI =1.11-3.64), p=0.018).Conclusion:to confirm the role of polymorphism IL18, IL18R1, IL18RAP in the pathogenesis of atherosclerosis, prospective monitoring of this group of patients is necessary to identify cases of manifestation of clinical signs in persons with adverse prognosis.


Angiology ◽  
2007 ◽  
Vol 58 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Hüseyin Oren ◽  
Ali R. Erbay ◽  
Mustafa Balci ◽  
Sengül Çehreli

2019 ◽  
Vol 4 (1) ◽  
pp. 31-39
Author(s):  
Eka Fithra Elfi ◽  
Yose Ramda Ilhami ◽  
Eryati Darwin

  Coronary heart disease (CHD) is caused by obstruction of coronary blood flow due to endothelial dysfunction triggered by various genetic and non-genetic risk factors such as hyperlipidemia, hypertension, hyperglycemia and obesity. Endothelial cell activation due to hyperglycaemia in diabetes mellitus induces production of pro-inflammatory factors that damage the cell membrane triggering the formation of membrane particles called microparticles. Endothe-lial microparticles contain proteins including endothelial nitric oxide synthase (eNOS) which plays a role in the production of nitric oxide (NO). To determine the role of microparticles in the occurrence of coro-nary heart disease in diabetes mellitus due to endothelial dysfunction, a study was conducted by comparing the levels of eNOS and NO in DM patients who had CHD with DM patients who had no CHD. Blood samples from 20 DM patients who had CHD and 20 DM patients who had no CHD of the outpatients in Cardiology Department and Inter-nal Medicine department of regional public hospital were included in this study. All patients were fulfilled inclusion and exclusion criteria and diagnosed by the appropriate specialist. The eNOS and NO lev-els were measured using the ELISA method. The results of this study show that eNOS levels in the group of DM patients who had CHD (21,292±12,415 ng/ml) were significantly lower (p <0.05) than those in the group of DM patients who had no CHD (29,721±11,952 ng/ml). Nitric oxide levels in DM patients who had CHD (0,053±0,021 nmol/ μl) were not statistically different to the levels in DM patients who had no CHD (0,047±0,032 nmol/μl). From the results of this study we concluded that endothelial microparticle protein eNOS plays a role in the occurrence of CHD due to the complications of diabetes mellitus 


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