Impact of COVID-19 on the course of chronic ischemic heart disease

December 9, 2022
1062
Resume

Patients with cardiovascular disease are at particular risk during the COVID-19 pandemic. The spread of coronavirus infection poses a particular danger in terms of decompensation of existing chronic diseases, specific damage to the cardiovascular system, especially in the case of a severe course of the disease and a high risk of adverse consequences in patients with chronic coronary heart disease (CHD). CHD is the leading cause of death and the most common cardiovascular disease worldwide. The number of cases of COVID-19 in patients with a history of CHD is increasing. CHD is a risk factor for a severe course of COVID-19, as SARS-CoV-2 induces endothelial inflammation, contributing to the progression of vascular dysfunction. The article discusses the main aspects of the impact of the coronavirus disease on the cardiovascular system, including the mechanism, pathogenesis, and important ways of impact of COVID-19 on the course of chronic CHD. The cause of exacerbation of CHD is the ulceration of the atherosclerotic plaque with the exposure of collagen fibers and the subsequent adhesion and aggregation of platelets on them. This leads to the formation of blood clots in the arteries of the heart and the release of thromboxane A2 from the platelets into the bloodstream, which causes spasm of the coronary arteries and the reduction or cessation of blood flow in them. When endothelium is damaged, plasma hemostasis is activated at the same time as platelet hemostasis. In patients with CHD, significant disturbances in the system of plasma hemostasis are noted, which increase as the disease progresses. Signs of blood hypercoagulation are noted: shortening of the activated partial thromboplastin time, increase in the content of fibrinogen, factors VII, VIII, XIII, the appearance in the bloodstream of fibrin-monomer complexes and fibrinogen/fibrin degradation products, a decrease in anticoagulant activity, inhibition of fibrinolysis.

References

  • 1. Guan W.-J., Ni Z.-Y., Hu Y. et al. (2020) Clinical characteristics of Coronavirus disease 2019 in China. N. Engl. J. Med., 382(18): 1708–1720. dx.doi.org/10.1056/nejmoa2002032.
  • 2. Driggin E., Madhavan M.V., Bikdeli B. et al. (2020) Cardiovascular considerations for patients, health care workers, and health systems during the COVID-19 pandemic. J. Am. Coll. Cardiol., 75(18): 2352–2371. dx.doi.org/10.1016/j.jacc.2020.03.03.
  • 3. Li B., Yang J., Zhao F. et al. (2020) Prevalence and impact of cardiovascular metabolic diseases on COVID-19 in China. Clin. Res. Cardiol., 109(5): 531–538. dx.doi.org/10.1007/s00392-020-01626-9.
  • 4. Wu Z., McGoogan J.M. (2020) Characteristics of and important lessons from the Coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72 314 cases from the Chinese center for disease control and prevention. JAMA, 323(13): 1239. dx.doi.org/10.1001/jama.2020.2648.
  • 5. Chen N., Zhou M., Dong X. et al. (2020) Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: a descriptive study. Lancet, 395(10223): 507–513. dx.doi.org/10.1016/s0140-6736(20)30211-7.
  • 6. Onder G., Rezza G., Brusaferro S. (2020) Case-Fatality Rate and Characteristics of Patients Dying in Relation to COVID-19 in Italy. JAMA, 323(18): 1775–1776. doi:10.1001/jama.2020.4683.
  • 7. Richardson S., Hirsch J.S., Narasimhan M. et al. (2020) Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. JAMA, 323(20): 2052–2059. doi: 10.1001/jama.2020.6775.
  • 8. GBD 2015 Mortality and Causes of Death Collaborators (2016) Global, regional, and national life expectancy, all-cause mortality, and causespecific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. doi.org/10.1016/S0140-6736(16)31012-1.
  • 9. Szabo S. (2020) COVID-19: new disease and chaos with panic, associated with stress. Med. Sci., 59(1). mspsss.org.ua/index.php/journal/article/view/281.
  • 10. Varga Z., Flammer A.J., Steiger P. et al. (2020) Endothelial cell infection and endotheliitis in COVID-19. Lancet, 395(10234): 1417–1418. dx.doi.org/10.1016/S0140-6736(20)30937-5.
  • 11. Коваленко С.В. (2020) Досвід застосування методів синдромно-патогенетичної терапії при пневмонії, спричиненій COVID-19, в умовах пульмонологічного відділення. Здоров’я України 21 сторіччя, 13–14: 481–482.
  • 12. Batah S.S., Fabro A.T. (2021) Pulmonary pathology of ARDS in COVID-19: a pathological review for clinicians. Resp. Med., 176: 106239. doi: 10.1016/j.rmed.2020.106239.
  • 13. Рудик Ю.С., Пивова С.М. (2021) COVID-19 і захворювання серцево-судинної системи: у фокусі — серцева недостатність. Здоров’я України, 4: 42–44.
  • 14. Sattar Y., Ullah W., Rauf H. et al. (2020) COVID-19 cardiovascular epidemiology, cellular pathogenesis, clinical manifestations and management. Int. J. Cardiol. Heart Vasc., 29: 100589. DOI: 10.1016/j.ijcha.2020.100589.
  • 15. Hemmat N., Derakhshani A., Bannazadeh Baghi H. et al. (2020) Neutrophils, crucial, or harmful immune cells involved in Coronavirus infection: a bioinformatics study. Front. Genet., 11. dx.doi.org/10.3389/fgene.2020.00641.
  • 16. Wu Q., Zhou L., Sun X. et al. (2017) Altered lipid metabolism in recovered sars patients twelve years after infection. Sci. Rep., 7(1): 1–12.
  • 17. Feng X., Li S., Sun Q. et al. (2020) Immune-inflammatory parameters in COVID-19 cases: A systematic review and meta-analysis. Front. Med. (Lausanne), 7. dx.doi.org/10.3389/fmed.2020.00301.
  • 18. Fovino L.N., Cademartiri F., Tarantinij G. (2020) Subclinical coronary artery disease in COVID-19 patients. Eur. Heart J. Cardiovasc. Imaging, 21(9): 1055–1056. doi: 10.1093/ehjci/jeaa202.
  • 19. Inciardi R.M., Adamo M., Lupi L. et al. (2020) Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy. Eur. Heart J., 41(19): 1821–1829. doi: 10.1093/eurheartj/ehaa388.
  • 20. Gatti A., Radrizzani D., Viganò P. et al. (2020) Decrease of non‐classical and intermediate monocyte subsets in severe acute SARS‐CoV‐2 infection. Cytometry A., 97(9): 887–890. dx.doi.org/10.1002/cyto.a.24188.