PECULIARITIES OF OXIDATIVE STRESS IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION WITH IRON DEFICIENCY ANEMIA

  • I. P. Vakalyuk Ivano-Frankivsk National Medical University, Department of Internal Medicine №2 and Nursing, Ivano-Frankivsk, Ukraine https://orcid.org/0000-0002-4430-6816
  • O. S. Boichuk Ivano-Frankivsk National Medical University, Department of Internal Medicine №2 and Nursing, Ivano-Frankivsk, Ukraine https://orcid.org/0000-0003-2954-9868
Ключові слова: acute coronary syndrome, acute myocardial infarction, iron deficiency anemia, oxidative stress, antioxidant system

Анотація

The article presents changes in hemogram and oxidative stress in patients with acute myocardial infarction (AMI) on the background of iron deficiency anemia (IDA). Iron deficiency anemia is an additional factor that contributes to the deepening of myocardial ischemia and deepens the processes of peroxidation and damage to cardiomyocytes, which is an important factor in the unfavorable course, both acute period and recovery processes in myocardial necrosis. In order to study the indicators of the general analysis of blood and functional state of the antioxidant system in patients with acute myocardial infarction with IDA, 36 patients with AMI with IDA were examined, including 39% men and 61% women. The first group consisted of 10 patients with AMI without IDA, the second 26 patients with AMI and IDA of varying severity, the control group consisted of 30 healthy individuals. Hemogram parameters, glutathione system function, oxyproline, arginase and magnesium levels in the blood were determined. It has been established that women with mild and moderate anemia predominate among patients with acute myocardial infarction with concomitant iron deficiency anemia. Among men, half of the patients have severe anemia. In addition to a decrease in Hb levels, patients with ACS with IDA have the following laboratory signs of anemia: a tendency to increase the average concentration of hemoglobin in one erythrocyte, low serum iron levels and an increase in serum transferrin levels. In the presence of IDA in patients with ACS there are changes in the antioxidant system. Anemic syndrome in such patients is accompanied by increased concentrations of glutathione transferase and peroxidase, as well as decreased concentrations of oxyproline.

Anemia can trigger oxidative stress, and an increase in OS may be associated with changes in cardiac function. Possible cardiovascular effects in patients with comorbid conditions should also be considered.

Iron deficiency is the most prevalent micronutrient disorder globally. When severe, iron deficiency leads to anemia, which can be deleterious to cardiac function. Given the central role of iron and oxygen in cardiac biology, multiple pathways are expected to be altered in iron-deficiency anemia, and identifying these requires an unbiased approach.

Oxidative stress is an imbalance between free radicals and antioxidant molecules that can play an important role in the pathogenesis of iron-deficiency anemia (IDA).

Maintenance of the iron homeostasis is essential for metabolic and physiological processes. Iron plays a critical role in erythropoiesis, is incorporated into erythroblasts and reticulocytes, and has a crucial role in oxygen transport and oxygen storage. Moreover, iron is essential for cardiac and skeletal muscle metabolism, the synthesis and degradation of proteins, lipids, ribonucleic acids, and mitochondrial function.

Research has now focused on non-traditional cardiovascular risk factors and the roles of iron and iron deficiency (ID) in patients with cardiovascular disease.

The Iron required for immune response, hormonal balance, and plays an important role in regulating oxidative stress and aerobic metabolism. The myocardial tissue has a mainly aerobic cellular metabolism, which depends of mitochondria's Krebs cycle enzymes that need iron as an essential cofactor. In this regard, there is some evidence that myocardial iron deficiency is highly prevalent in HF and may play a role in the progression of the disease.

Опубліковано
2022-04-09
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