Influence of Plasma Hemostasis on Intracardiac Hemodynamics in Patients with Chronic Coronary Heart Disease and COVID-19
V.Z. Netiazhenko1,3, S.E. Mostovyi1,2, M.M. Zhaivoronok1,4
- Bogomolets National Medical University, Kyiv, Ukraine
- SE “Medbud”, Kyiv, Ukraine
- State Institution of Science “Center of innovative healthcare technologies” State Administrative Department, Ukraine
- P. L. Shupyk National Healthcare University of Ukraine, Ukraine
DOI: https://doi.org/10.15407/fz71.02.040

Abstract
In COVID-19 coronavirus disease, plasma hemostasis
dysfunction and intracardiac hemodynamics (ICH) are
observed, which increase the risk of thromboembolic
complications and cardiovascular events. The aim of our
study was to investigate the impact of COVID-19 on the
interdependence of changes in the plasma hemostasis system
and intracardiac hemodynamics in patients with chronic
coronary artery disease (CHD). We analyzed the laboratory
and instrumental results of 386 patients who were divided
into 3 groups: Group 1 - CHD without COVID-19 (n = 79);
Group 2 - CHD in combination with COVID-19 (n = 127);
Group 3 - COVID-19 without CHD (n = 180). The control
group included 37 conditionally healthy volunteers. Changes
in plasma hemostasis were studied using an automatic blood
coagulation analyzer K 3002 OPTIS (KSELMED), Poland.
Echocardiography was performed on the HDI 11XE and
MyLabXE8 XP. In patients with chronic coronary artery
disease with concomitant COVID-19, a wide range of plasma
hemostatic disorders were observed, including increased
levels of soluble fibrin monomer complexes, XII-a (Hageman)
dependent fibrinolysis, and decreased levels of protein C
and antithrombin III. The profile of CHD in combination
with COVID-19, in contrast to the “isolated” passing of
both conditions, was characterized by a more pronounced
disturbance of intracardiac hemodynamics. Patients with
chronic coronary artery disease, in particular in combination
with COVID-19, showed signs of left and right ventricular
remodeling and increased systolic pressure in the pulmonary
artery according to echocardiography. Patients with chronic
coronary artery disease who have had COVID-19 have a
more pronounced activation of plasma hemostasis compared
to patients with coronary artery disease alone or COVID-19.
COVID-19 contributes to the deterioration of left ventricular
systolic function and left ventricular remodeling in patients
with chronic CHD, which correlates with fibrinogen and
protein C and antithrombin III levels. Increased systolic
pressure in the pulmonary artery and right ventricular
dilatation in patients with CHD and COVID-19 may indicate
the development of pulmonary hypertension and an increased
risk of right ventricular failure. Thus, patients with chronic
CHD and concomitant COVID-19 along with dysfunction of
the plasma hemostasis system showed signs of intracardiac
hemodynamics of the left ventricle. Additional consideration
of the characteristics of plasma hemostasis and intracardiac
hemodynamics is advisable in managing such patients.
Keywords:
chronic coronary heart disease; COVID-19; intracardiac hemodynamics; left ventricular systolic function, plasma hemostasis.
References
- Zhu N, Zhang D, Wang W, et al. A novel coronavirus from patients with pneumonia in China. 2019. N Engl J Med. 2020
CrossRef
PubMed PubMedCentral
382(8): 727-33. doi: 10.1056/NEJMoa2001017. Epub 2020 Jan 24.
- Ackermann M, Verleden SE, Kuehnel M, et al. Pulmonary vascular endothelialitis, thrombosis, and angiogenesis in COVID-19. N Engl J Med. 2020; 383(2): 120-8. doi: CrossRef
PubMed PubMedCentral
10.1056/NEJMoa2015432. Epub 2020 May 21.
- Thompson BT, Chambers RC, Liu KD. Acute respiratory distress syndrome. N Engl J Med. 2017; 2017 Aug 10;377(6):562-72. doi: 10.1056/NEJMra1608077.
CrossRef
PubMed
- Zaim S, Chong JH, Sankaranarayanan V, Harky A. COVID-19 and multi-organ response. Curr Probl Cardiol. 2020; 45(8): 100618. PMID: 32439197 doi: 10.1016/j.cpcardiol.2020.100618
CrossRef
PubMed PubMedCentral
- Schulman S, Hu Y, Konstantinides S. Venous thromboembolism in COVID-19. Thromb Haemostas. 2020; 120 (12): 1642-53. doi: 10.1055/s-0040-1718532
CrossRef
PubMed PubMedCentral
- Katneni UK, Alexaki A, Hunt RC, Schiller T. Coagulopathy and thrombosis as a result of severe COVID-19 infection: A microvascular focus. Thromb Haemostas. 2020; 120(12): 1668-79. doi: 10.1055/s-0040-1715841
CrossRef
PubMed PubMedCentral
- Conti P, Ronconi G, Caraffa A, Gallenga C, Ross R, Frydas I, Kritas S. Induction of pro-inflammatory cytokines (IL1 and IL-6) and lung inflammation by Coronavirus-19 (COVI-19 or SARS-CoV-2): Anti-inflammatory strategies. J Biol Regul Homeost Agent. 2020;34(2):327-31. doi: 10.23812/CONTI-E.
CrossRef
PubMed
- Sayyadi M, Hassani S, Shams M, Dorgalaleh A. Status of major hemostatic components in the setting of COVID-19: the effect on endothelium, platelets, coagulation factors, fibrinolytic system, and complement. Ann Hematol. 2023 102:1307-22. CrossRef
CrossRef
PubMed PubMedCentral
- Anna Kalinskaya, et al. Targeted blood plasma proteomics and hemostasis assessment of post COVID-19 patients with acute myocardial infarction. Int J Mol Sci. 2023, 24, 6523. CrossRef
CrossRef
PubMed PubMedCentral
- Shari R Waldstein, Willem J Kop, Edward C Suarez, William R Lovallo, Leslie I Katzel. Handbook of cardiovascular behavioral medicine. New York: Springer; 2021. Сhapter 2. Section ІІ: Hemostasis and Endothelial Function. p. 861-90. CrossRef
- Zolotukhina Y.O. Fibrinolytic activity of blood in patients with coronary heart disease and concomitant type 2 diabetes mellitus. Ukr Med J. 2018;6(128):1-3. DOI: 10.32471/umj.1680-3051.128.134557 [Ukrainian].
- Krasnova AA, Ignatko YA, Derbak MA, Rishko OA. Features of the course of chronic coronary heart disease in the context of the COVID-19 pandemic (literature review). Probl Clin Pediatr. 2022;4 (58):.6-11. DOI: 10.24144/1998-6475.2022.58.6-11. [Ukrainian].
- Iba T, Levy JH, Levi M, Thachil J. (2020) Coagulopathy in COVID-19. J. Thromb. Haemost., 18(9): 2103-2109. J Thromb Haemost. 2020 Sep;18(9):2103-9. doi: 10.1111/jth.14975
CrossRef
PubMed PubMedCentral
- Lip GYH, Blann AD, et al. Fibrinogen and fibrin D-dimer in cardiovascular disease: Determinants and implications. J Am College Cardiol. 1998; 31(7): 1427- DOI:10.1016/S0735-1097(98)00128-8.
- Libby P, Lüscher T. «COVID-19 is, in the end, an endothelial disease. Eur Heart J. 2020; 41(32): 3038-44. DOI:10.1093/eurheartj/ehaa623.
CrossRef
PubMed PubMedCentral
- Long B, Brady WJ, Koyfman A, Gottlieb M. Cardiovascular complications in COVID-19. Am J Emerg Med. 2020;38(7):1504-7. DOI:10.1016/j.ajem.2020.04.048.
CrossRef
PubMed PubMedCentral
- Vilahur G, Fuster V, Ibanez B. Pathogenesis of coronary thrombosis and myocardial infarction. In: Fuster V, Narula J, Vaishnava P, Leon MB, Callans DJ, Rumsfeld JS, Poppas A, editors. Fuster and Hurst's The Heart. McGraw-Hill Education; 2022.
- Levi M, Thachil J, Iba T, Levy JH. Coagulation abnormalities and thrombosis in patients with COVID-19. Lancet Haematol. 2020;7(6):e438-40. doi:10.1016/S2352-3026(20)30145-9
CrossRef
PubMed
- Zeng JH, Liu YX, Yuan J, et al. First case of COVID-19 complicated with fulminant myocarditis: a case report and insights. Infection. 2020;48(5):773-7. doi:10.1007/s15010-020-01424-5.
CrossRef
PubMed PubMedCentral
- Tang N, Li D, Wang X, Sun Z. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18(4):844-7. doi:10.1111/jth.14768.
CrossRef
PubMed PubMedCentral
- Terpos E, Ntanasis-Stathopoulos I, Elalamy I, et al. Hematological findings and complications of COVID-19. Am J Hematol. 2020;95(7):834-47. doi:10.1002/ajh.25829
CrossRef
PubMed PubMedCentral
- Petersen SE, Friedrich MG, Leiner T, Elias MD, Ferreira VM, Fenski M, et al. Cardiovascular magnetic resonance for patients with COVID-19, JACC: Cardiovascul Imag. 2022;15(4): 685-99. CrossRef
CrossRef
PubMed PubMedCentral
- Hudák A, Pusztai D, Letoha A, Letoha T. Mutual inhibition of antithrombin III and SARS-CoV-2 cellular attachment to syndecans: Implications for COVID-19 treatment and vaccination. Int J Mol Sci. 2024; 25(14):7534. CrossRef
CrossRef
PubMed PubMedCentral
- Griffin JH, Lyden P. COVID-19 hypothesis: Activated protein C for therapy of virus-induced pathologic thromboinflammation. Res Pract Thromb Haemost. 2020;4(4):506-9. doi:10.1002/rth2.12362
CrossRef
PubMed PubMedCentral
- Hvas CL, Larsen JB. The fibrinolytic system and its measurement: history, current uses and future directions for diagnosis and treatment. Int J Mol Sci. 2023; 24(18):14179. CrossRef
CrossRef
PubMed PubMedCentral
- Mann KG, Brummel K, Butenas S. What is all that thrombin for? J Thromb Haemost. 2003;1(7):1504-14. doi:10.1046/j.1538-7836.2003.00298.x
CrossRef
PubMed
- Grobler C, Maphumulo SC, Grobbelaar LM, et al. Covid-19: The rollercoaster of fibrin(ogen), d-dimer, von willebrand factor, p-selectin and their interactions with endothelial cells, platelets and erythrocytes. Int J Mol Sci. 2020;21(14):5168. doi:10.3390/ijms21145168.
CrossRef
PubMed PubMedCentral
|