Abstract
A better understanding of the pathogenetic mechanisms triggered by SARS-CoV-2 infection may contribute to a more effective management of patients with COVID-19. Coagulation dysfunction is a key pathogenetic element of this disease as well as a challenge for practitioners. Marked inflammatory process found in severe forms of COVID-19, the complement activation, the cytokine storm, and disruption of the renin-angiotensin-aldosterone system are involved in the onset of thrombotic microangiopathy and large vessel coagulopathy. Virus-induced procoagulant activity occurs at the systemic level. Intravascular microthrombi disrupt vascularization in various tissues and organs, contributing to the occurrence of multiorgan failure and explain the higher morbidity and all-cause mortality of patients. It is estimated that almost 20% of patients with COVID-19 have significant coagulation disorders, and about a quarter of those hospitalized in intensive care units are prone to develop thrombosis events under prophylactic anticoagulant treatment. Some of patients who have been immunized after healing from the SARS-CoV-2 infection have a hypercoagulable state and are prone to develop thrombosis. Hypercoagulability is supported by thrombelastographic analysis: patients have an acceleration of the propagation phase of blood clot formation and higher clot strength. Markers of coagulation dysfunction in SARS-CoV2 are: decreased platelet count, increased INR, presence of fibrin degradation products, and especially higher plasma levels of D-dimers, which predict unfavorable outcome in these patients. Age, pre-existing diseases and associated risk factors, together with careful monitoring of clinical evolution and laboratory parameters allow the choice of the best personalized prophylactic or curative anticoagulant treatment.
Highlights
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic began in China and spread around the world in a matter of months[1].Collaboration between teams of researchers around the world has been and is essential for conducting clinical trials in coronavirus disease 2019 (COVID-19) infected patients in order to understand the pathophysiological features of this new viral challenge[2].Coronavirus disease 2019 (COVID-19) is pathogenetically associated with inflammation, cytokine storm, and frequent lung injury[3] but multiple tissues and viscera can be affected, a situation which acquires a systemic character
Thrombosis discovered at autopsy An autopsy performed in 12 consecutive patients with confirmed COVID-19 detected the presence of deep venous thrombosis in 58%, it was not suspected before death[25]
The prophylactic anticoagulant treatment, or, if the situation requires it, the curative one, is indicated throughout the hospitalization in all patients with COVID-19. It seems to decrease the morbidity of patients with coagulation dysfunction induced by sepsis or with high plasma D-dimers levels[36]
Summary
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic began in China and spread around the world in a matter of months[1]. Deregulation of coagulation and fibrinolysis The risk of arterial and venous thrombosis in patients with severe forms of COVID-19 or with systemic manifestations is explained by the presence of expressed inflammatory syndrome, hypercoagulability, endothelial dysfunction, platelet activation, and blood stasis[14]. An early and accurate diagnosis of COVID-19 is essential to ensure appropriate treatment, to limit the worsening of viral disease, and, at the same time, contribute to the control and elimination of the SARS-Cov-2 epidemic[16] This viral infection may be asymptomatic or Thrombotic microangiopathy Thrombotic microangiopathy of the heart is responsible for the occurrence of myocarditis, various forms of cardiac arrhythmias, acute coronary syndrome, heart failure, and even sudden death, complications that occur more frequently in patients with pre-existing cardiovascular disease[9]. Thrombosis discovered at autopsy An autopsy performed in 12 consecutive patients with confirmed COVID-19 detected the presence of deep venous thrombosis in 58%, it was not suspected before death[25]
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