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Peculiarities of Hemostasis and Proteomics in Patients With Acute Myocardial Infarction and Healthy Volunteers After
A I Kalinskaya1, A K Elizarova1, A S Anisimova1
1Davydovsky Municipal Clinical Hospital, Moscow.
Insights
Patients with acute myocardial infarction (AMI) after COVID-19 show a weaker immune response but prolonged platelet activation. This suggests long-term effects of SARS-CoV-2 on hemostasis, primarily driven by platelets.
Area of Science:
- Cardiovascular Medicine
- Infectious Diseases
- Hematology
Background:
- COVID-19 can have long-term effects on cardiovascular health and hemostasis.
- Understanding post-COVID-19 changes in patients with acute myocardial infarction (AMI) is crucial for risk stratification and management.
Purpose of the Study:
- To investigate the hemostatic and proteomic profiles of patients with AMI who have had COVID-19 compared to those who have not.
- To assess the impact of a prior SARS-CoV-2 infection on blood plasma features in AMI patients and healthy volunteers.
Main Methods:
- Comparative analysis of patients with AMI (post-COVID and control) and healthy volunteers (post-COVID and control).
- Assessment of hemostasis using thromboelastometry, thrombodynamics, fibrinolysis, and impedance aggregometry.
- Proteomic analysis of blood plasma to identify key protein changes.
Main Results:
- Both AMI groups exhibited enhanced thrombus formation and density compared to controls.
- Patients with AMI post-COVID showed lower thrombus density and higher lysis rates but increased platelet aggregation compared to AMI controls.
- Post-COVID healthy volunteers displayed higher thrombus size and platelet aggregation compared to controls without COVID-19.
Conclusions:
- Patients with AMI post-COVID exhibit a less pronounced immune response, potentially due to chronic inflammation and immune system depletion after SARS-CoV-2 infection.
- Long-term activation of the hemostasis system in individuals post-COVID-19, including AMI patients, is predominantly linked to platelet function.
Aim:
To identify the features of plasma, platelet hemostasis, and proteomic composition of the blood plasma in patients with acute myocardial infarction (AMI) and healthy volunteers after COVID-19.
Material And Methods:
The study included patients with AMI who have recently had COVID-19 (AMI-post-COVID, n=56) and patients with AMI who have not recently had COVID-19 (AMI-control, n=141). Healthy volunteers constituted the control groups and were also divided into control-post-COVID (n=32) and control-control (n=71) groups. Previous SARS-CoV-2 infection was determined by anti-N IgG in the blood serum, the level of which persists for 6-10 months after the disease. Hemostasis was evaluated by thromboelastometry (on whole blood), thrombodynamics (on platelet-poor plasma), fibrinolysis, impedance aggregometry, and proteomic analysis.
Results:
The AMI-post-COVID and AMI-control groups had higher values of thrombus growth rate, size and density based on the data of thromboelastometry and thrombodynamics, as well as increased concentrations of the complement system components, proteins regulating the state of the endothelium, and a number of acute-phase and procoagulant proteins compared to the control groups. Furthermore, in the AMI-post-COVID group, compared to the AMI-control group, the thrombus density was lower, and its lysis rates were higher when measured by the thrombodynamics method on platelet-poor plasma, while the platelet aggregation induced by ADP and thrombin was higher. Also, in the control-post-COVID group, compared to the control-control group, the thrombus formation rate was lower, whereas, in contrast, the thrombus size as measured by the thrombodynamics method and the platelet aggregation induced by arachidonic acid and thrombin were higher. In addition, in the AMI-post-COVID group, compared to the AMI-control group, the concentrations of proteins involved in inflammation and hemostasis were lower.
Conclusion:
Patients with AMI who have recently had COVID-19 are characterized by a less pronounced activation of the immune response compared to patients with AMI who have not had COVID-19. This may be due to long-term chronic inflammation and depletion of components of the immune activation system after SARS-CoV-2 infection. Long-term activation of the hemostasis system in both patients with AMI and healthy volunteers after COVID-19 is primarily due to the platelet component of hemostasis.
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