Hypercoagulability and thrombosis in COVID-19: a modifiable cause for mortality?
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ABSTRACT:
SUBMITTER: Chan N
PROVIDER: S-EPMC8344546 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:A striking feature of COVID-19 is the high frequency of thrombosis, particularly in patients who require admission to intensive care unit because of respiratory complications (pneumonia/adult respiratory distress syndrome). The spectrum of thrombotic events is wide, including in situ pulmonary thrombosis, deep-vein thrombosis and associated pulmonary embolism, as well as arterial thrombotic events (stroke, myocardial infarction, limb artery thrombosis). Unusual thrombotic events have also been reported, e.g., cerebral venous sinus thrombosis, mesenteric artery and vein thrombosis. Several hematology abnormalities have been observed in COVID-19 patients, including lymphopenia, neutrophilia, thrombocytopenia (usually mild), thrombocytosis, elevated prothrombin time and partial thromboplastin times (the latter abnormality often indicating lupus anticoagulant phenomenon), hyperfibrinogenemia, elevated von Willebrand factor levels, and elevated fibrin d-dimer. Many of these abnormal hematologic parameters-even as early as the time of initial hospital admission-indicate adverse prognosis, including greater frequency of progression to severe respiratory illness and death. Progression to overt disseminated intravascular coagulation in fatal COVID-19 has been reported in some studies, but not observed in others. We compare and contrast COVID-19 hypercoagulability, and associated increased risk of venous and arterial thrombosis, from the perspective of heparin-induced thrombocytopenia (HIT), including the dilemma of providing thromboprophylaxis and treatment recommendations when available data are limited to observational studies. The frequent use of heparin-both low-molecular-weight and unfractionated-in preventing and treating COVID-19 thrombosis, means that vigilance for HIT occurrence is required in this patient population.
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Project description:Since December 2019, a novel Coronavirus (SARS-CoV-2) was confirmed as the etiologic agent of a worldwide outbreak of a pneumonia that can result in severe respiratory failure. This clinical entity seems to be associated with a marked hypercoagulable state that causes both arterial and venous thromboembolic complications. Therefore, an adequate anti-thrombotic prophylaxis is recommended in hospitalized COVID-19 patients. Although rapidly worsening respiratory symptoms in a patient with SARS-CoV-2 respiratory infection may correlate with worsening pneumonia itself, it may also mask a pulmonary embolism. We report the case of a 50-year-old man affected by SARS-CoV-2 pneumonia, who developed acute pulmonary embolism.
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| S-EPMC7874424 | biostudies-literature
Project description:During the coronavirus disease 2019 (COVID?19) pandemic, some patients with severe COVID?19 exhibited complications such as acute ischemic stroke (AIS), which was closely associated with a poor prognosis. These patients often had an abnormal coagulation, namely, elevated levels of D?dimer and fibrinogen, and a low platelet count. Certain studies have suggested that COVID?19 induces AIS by promoting hypercoagulability. Nevertheless, the exact mechanisms through which COVID?19 leads to a hypercoagulable state in infected patients remain unclear. Understanding the underlying mechanisms of hypercoagulability is of utmost importance for the effective treatment of these patients. The present review aims to summarize the current status of research on COVID?19, hypercoagulability and ischemic stroke. The present review also aimed to shed light into the underlying mechanisms through which COVID?19 induces hypercoagulability, and to provide therapies for different mechanisms for the more effective treatment of patients with COVID?19 with ischemic stroke and prevent AIS during the COVID?19 pandemic.
| S-EPMC7849983 | biostudies-literature
Project description:The SARS-CoV-2 virus, which causes Coronavirus disease 2019 (COVID-19), has resulted in millions of worldwide deaths. When the SARS-CoV-2 virus emerged from Wuhan, China in December 2019, reports of patients with COVID-19 revealed that hospitalized patients had acute changes in mental status, cognition, and encephalopathy. Neurologic complications can be a consequence from overall severity of the systemic infection, direct viral invasion of the SARS-CoV-2 virus in the central nervous system, and possible immune mediated mechanisms. We will examine the landscape regarding this topic in this review in addition to current understandings of COVID-19 and hemostasis, treatment, and prevention, as well as vaccination.
| S-EPMC8547944 | biostudies-literature
Project description:Thrombotic complications are frequent in COVID-19 and contribute significantly to mortality and morbidity. We review several mechanisms of hypercoagulability in sepsis that may be upregulated in COVID-19. These include immune-mediated thrombotic mechanisms, complement activation, macrophage activation syndrome, antiphospholipid antibody syndrome, hyperferritinemia, and renin-angiotensin system dysregulation. We highlight biomarkers within each pathway with potential prognostic value in COVID-19. Lastly, recent observational studies have evaluated a role for the expanded use of therapeutic anticoagulation in COVID-19. We review strengths and weaknesses of these studies, and we also discuss the hypothetical benefit and anticipated challenges of fibrinolytic therapy in COVID-19.
| S-EPMC7674272 | biostudies-literature
Project description:While the COVID-19 pandemic sweeps the world, much evidence is being gathered regarding its novel pathological mechanisms. It is the authors’ clinical experience that patients in the intensive care unit suffering from COVID-19 are extremely pro-coagulable, with venous and arterial thromboembolism frequently observed, and losses of vascular access lines and filtration circuits to thrombosis now commonplace. Here, we explore the evidence for hypercoagulability in this group, presenting evidence of both a localised pulmonary hypercoagulability, and a systemic hypercoagulability resulting in thrombosis distant to the pulmonary vasculature. Furthermore, we discuss the possible risk factors exacerbated by, or selected for in COVID-19. We review the available evidence for use of plasma D-dimer as a prognostic marker, exploring the possibility that it acts as a marker of a COVID-19-associated hypercoagulability. We review the evidence for a pro-coagulant subtype of disseminated intravascular coagulation, discussing its clinical significance. Finally, we discuss the current evidence surrounding treatment of COVID-19 hypercoagulability, including prophylactic and treatment-dose heparin, thrombolytic agents, antiplatelet agents, and direct thrombin inhibitors, among others. We suggest areas in which further investigation is urgently needed to reduce the startling incidence of thrombosis in this group, a complication no doubt contributing to morbidity and mortality.
| S-EPMC7346831 | biostudies-literature
Project description:The SARS-CoV-2 virus caused a global pandemic within weeks. Many patients with severe COVID-19 present with coagulation abnormalities, including increase D-dimers. This coagulopathy is associated with an increased risk of death. Furthermore, a substantial proportion of patients with severe COVID-19 develop sometimes unrecognized, venous thromboembolic complications. A better understanding of COVID-19 pathophysiology, in particular hemostatic disorders, will help to choose appropriate treatment strategies. A rigorous thrombotic risk assessment and the implementation of a suitable anticoagulation strategy are required. We review here the characteristics of COVID-19 coagulation laboratory findings in affected patients, the incidence of thromboembolic events and their specificities, and potential therapeutic interventions.
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Project description:The purpose of this study is to determine the effect of melatonin on thrombosis, sepsis, and mortality rate in adult patients with severe coronavirus infection (COVID-19). Methods: This single-center, prospective, randomized clinical trial was conducted from 1 December 2020 to 1 June 2021 at Al-Shifaa hospital in Mosul, Iraq. There were 158 patients with severe COVID-19 included in the study, 82 in the melatonin group (who received 10 mg melatonin in addition to standard therapeutic care), and 76 in the control group (given standard therapeutic care only). Patients were chosen by blocked randomization design. The physician then evaluated and recorded the incidence of thrombosis, sepsis, and mortality rate on days 5, 11, and 17 of symptoms. Results: The intervention group consisted of 82 patients, while the control group consisted of 76 patients. In comparison to the control group, thrombosis and sepsis developed significantly less frequently (P < 0.05) in the melatonin group during the second week of infection, while mortality was significantly higher in the control group (P < 0.05). Conclusions: Adjuvant use of Melatonin may help reduce thrombosis, sepsis, and mortality in COVID-19 patients.
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Project description:Treatment protocols, treatment availability, disease understanding, and viral characteristics have changed over the course of the Covid-19 pandemic; as a result, the risks associated with patient comorbidities and biomarkers have also changed. We add to the ongoing conversation regarding inflammation, hemostasis and vascular function in Covid-19 by performing a time-varying observational analysis of over 4000 patients hospitalized for Covid-19 in a New York City hospital system from March 2020 to August 2021 to elucidate the changing impact of thrombosis, inflammation, and other risk factors on in-hospital mortality. We find that the predictive power of biomarkers of thrombosis risk have increased over time, suggesting an opportunity for improved care by identifying and targeting therapies for patients with elevated thrombophilic propensity.
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