The thrombophilia and hypercoagulation at COVID-19 are rather well described, and the research conducted earlier showed that system anti-coagulation by heparin can reduce mortality when carrying out IVL at patients with COVID-19. Aspirin can make similar impact thanks to the antiagregantny and antiinflammatory properties as TsOG-1 inhibitor which reduces A2 thromboxane synthesis, aggregation of thrombocytes and a thrombogenesis. At injury of lungs of advantage of aspirin as believe, consist in reduction of aggregation of thrombocytes and neutrophils in lungs, decrease in inflammation and increase in formation of a lipoksin who restores function of cells of an endothelium of lungs. This protective influence can be used at COVID-19 when the tendency to hypercoagulation is extraordinary high and often dysfunction of endothelial cells takes place.
At COVID-19 antiinflammatory properties of aspirin can promote protection of lungs also. Aspirin showed decrease in production of interleukin-6 (IL-6), S-jet protein and a macrophagic colony stimulating factor at patients with cardiovascular diseases, and at COVID-19 these effects can reduce the frequency of emergence of a tsitokinovy storm. Aspirin also has an inhibiting effect on cyclooxygenase-2 (TsOG-2) that also reduces production of SILT-6 and S-jet protein.
In a number of researches the possible positive effect of aspirin in ARDS (acute respiratory distress syndrome) was studied. For example, Erlich and other authors studied 161 patients with risk of the acute injury of lungs (AIL), 79 of which at hospitalization received anti-modular therapy. At the same time 75 (94.9%) patients of anti-modular group took aspirin. The research showed that anti-modular therapy is connected with decrease in OPL and ORDS. The group of researchers led by doctor Chen studied 1149 patients with high risk of ORDS and found out that intake of aspirin before hospitalization is connected with decrease in frequency of ORDS after correction of factors hindrances. Decrease in frequency of ORDS remained at inspection of patients with sepsis. Other research of patients from group of high risk showed that though aspirin was associated with decrease in ORDS in one-factor analysis, communication was not statistically significant in the multiple-factor analysis. Meta-analysis of these three researches in total showed that aspirin was associated with the general decrease in frequency of ORDS.
In the analysis of mortality as outcome, it is revealed that before receipt in a hospital or during hospitalization use of aspirin for patients with ORDS is associated with decline in mortality in ORIT, but not hospital mortality. In clinical trial on prevention of damage of lungs with use of aspirin (LIPS-A) 390 patients with high risk of ORDS were examined. The participants selected in a random way received aspirin or placebo, and was established that within 7 days aspirin did not interfere with development of ORDS and did not improve survival within 28 days.
However exist one more interesting research from the USA which limited set of patients only to those which had the diagnosis of COVID-19, unlike other researches in which all patients with high risk of ORDS participated. When it was reported about factors of initial risk of ORDS, the range of diagnoses was wide: sepsis, not cardiogenic shock, aspiration, pancreatitis, pneumonia, positive shock index and trauma. This heterogeneity, perhaps, weakened and distorted effects of aspirin. Besides, not all reasons of ORDS are connected with hypercoagulation, as in a case with COVID-19. In a one-center research it is shown that the infection of SARS-CoV-2 was associated with an embolism of lungs with a frequency of 20.6% that is three times higher, than at all patients who came to ORIT during the same interval of time (20.6% of SARS-CoV-2 against 6.1% in control group). This indicator more than twice exceeded the indicator observed at the patients with flu who came to ORIT (against 7.5% patients with flu have 20.6% of SARS-CoV-2, increase in absolute risk for 13.1%). Moreover, on the available data, at autopsy of the patients who died after COVID-19, alveolar microblood clots are present by 9 times more often than at patients with flu. As hypercoagulation is widespread at COVID-19, the effect of aspirin can be more expressed at this category of the diseased; possibly therefore the discussed research in the USA statistically could reveal significant communication with decrease in the need for IVL, transfer to ORIT and the hospital mortality while some previous researches did not find these advantages.
It is obvious that COVID-19 is the general disease striking vascular network and that SARS-CoV-2 causes endoteliit with involvement of pulmonary capillaries. The submicroscopy and histologic analyses showed that the SARS-CoV-2 virus infects endotheliocytes of many bodies, causing endoteliit, microcirculation disturbance, apoptosis — in the sum leads it to inflammation and microthrombosis. Aspirin as an antiagregant, perhaps, interferes with aggregation of thrombocytes and the subsequent microthrombosis.