The pandemic of coronavirus disease 2019 (COVID-19) has posed a major health challenge for over 2 years. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that causes it belongs to single-stranded ribonucleic acid viruses and causes acute respiratory distress syndrome. The initial outbreak was discovered in December 2019 in Wuhan province, where SARS-CoV-2 quickly spread to other countries. In addition to respiratory disorders, it has been shown that during and after COVID-19 infection, cardiovascular diseases are often developed or exacerbated, such as: arterial hypertension, coronary artery disease, arrhythmias, heart failure and thromboembolic complications. In view of the higher prevalence of atherosclerosis in patients with COVID-19, we described the pathomechanisms of the development of this infection and the possible correlations between SARS-CoV-2 infection and thromboembolic complications. We focused on the role of the inflammatory response, renin-angiotensin system and endothelial dysfunction in the development of atherosclerosis in patients with COVID-19. A thorough understanding of the hemodynamic mechanisms and the impact of the infection on the cardiovascular system will allow for the proper selection of appropriate therapy in patients after SARS-CoV-2 infection.Abbreviations: ACE2 = angiotensin-converting enzyme 2, ACS = acute coronary syndromes, ARDS = acute respiratory distress syndrome, COVID-19 = coronavirus disease 2019, EC = endothelial cells, IL-10 = interleukin 10, IL-1β = interleukin 1 β, IL-6 = interleukin 6, NO = nitric oxide, SARS-CoV-2 = severe acute respiratory syndrome coronavirus 2, TNFα = tumor necrosis factor α.
Cardiovascular diseases remain the leading cause of death worldwide for the past 20 years. Of these, ischemic heart disease has the highest mortality rate. In over 98% of cases it is caused by atherosclerosis of the coronary arteries. Homocysteine is an amino acid, containing a sulfhydryl group, which is formed as a result of the metabolism of the amino acids methionine and cysteine, which is supplied with protein-containing foods. A small amount of it is necessary for the proper functioning of the body, however, an increased concentration in blood plasma, which hyperhomocysteinemia, negatively affects blood vessels leading to the development of atherosclerosis and thrombotic com¬plications. The adverse effect on blood vessels results from various mechanisms, such as: excessive activation of Toll-like 4 receptor, activation N-methyl-d-aspartate receptors, increased production of reactive oxygen species, and impairment of nitric oxide synthesis. Elevated levels of reactive oxygen species are associated with increased expression of proinflammatory cytokines such as IL-1β, IL-6, TNF-α (tumor necrosis tumor necrosis factor), MCP-1 and intracellular adhesion molecule-1. Another factor contributing to hyperhomocysteinemia is mutation of the MTHFR gene, which in normal conditions is responsible for maintaining homocysteine levels within the normal range. People with MTHFR mutation are more prone to develop atherosclerosis and the following complications: myocardial infarction, stroke, thrombotic episodes and coronary artery disease. The aim of this paper is to present evidence supporting the role of homocysteine in the development of many cardiovascular diseases.
The feeling of pain accompanies a significant proportion of Medical Emergency Teams (METs) and emergency depart¬ment patients, especially those with trauma. Modern medicine focuses on combating this unpleasant sensation, as it can negatively affect the patient’s condition. Paramedics, who are the first on the scene, in today’s emergency care system work in primary teams, i.e. without a doctor, so it is their responsibility to implement appropriate pharmacotherapy. Assessment and treatment of pain in the pre-hospital care setting are among the key aspects of the role of paramedics. In view of the scarcity of diagnostic tools, decisions are made on the basis of simple clinical tests, so the knowledge and experience of medical personnel seem to be paramount here. It is important to keep in mind the current state of the pa¬tient, as well as potential disorders that may occur during transport to the hospital. Massive injuries to organs, multiple areas of the body, as well as an advanced stage of disease, require the administration of strong analgesics. The use of appropriate analgesia in the prehospital setting, significantly improves the patient’s comfort and often contributes to a huge improvement in the clinical condition. Undertaking pain management from an ethical and moral point of view is one of the essential tasks of medical personnel, and also demonstrates commitment and professionalism.
On March 11, 2020, the World Health Organization (WHO) announced the COVID-19 pandemic, caused by the SARS-CoV-2 virus. It caused chaos in public spaces in almost every country, and the public was forced to reorganize their daily functioning. People began to experience severe stress due to the risk of infection from an unexplored and dangerous pathogen. During this specific period, working in health care became extremely difficult. One of the groups particularly exposed to stress factors turned out to be paramedics. Having daily contact with an infected person, they became the first link in the fight against this virus. Therefore, it was extremely important to develop appropriate ways to cope with stress. The following strategies proved to be effective: active coping strategy, learning, and acceptance, understood as acceptance of the situation. A significant factor in mitigating the effects of traumatic events was the ability to respond to stress in a healthy way, which depended on many factors, i.e. personality dispositions, defense mechanisms, and health-promoting behaviors.
Apelin is a biologically active protein encoded by the APLN gene. It was first isolated in 1998 as a ligand for the APJ receptor. It exists in several isoforms differing in polypeptide chain length and biological activity. It is secreted by white adipose tissue, and its expression has been identified in many body tissues, including the cardiovascular system, kidneys, lungs, CNS (especially the hypothalamus, suprachiasmatic and ventricular nuclei), skeletal muscle, mammary glands, adrenal glands, ovaries, stomach, liver cells, placenta, and breast milk. However, the highest concentrations were observed in the endocardium and endothelium of vascular smooth muscle cells. In myocardial tissue, apelin has a positive inotropic effect and exerts an opposing effect to the RAA (renin-angiotensin-aldosterone) system, lowering blood pressure. Therefore, its positive role in early stages of heart failure, in patients with hypertension and ischemic heart disease is emphasized. The synthesis and secretion of apelin by adipocytes makes it possible to classify this peptide as an adipokine. Therefore, its production in adipose tissue is enhanced in obesity. Furthermore, apelin has been shown to increase cellular sensitivity to insulin and improve glucose tolerance in the onset of type 2 diabetes, and therefore appears to play a significant role in the pathogenesis of metabolic disease. An accurate assessment of the importance of apelin in cardiovascular disease requires further studies, which may contribute to the use of apelin in the treatment of heart failure.
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