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2.
Clin Respir J ; 15(12): 1259-1274, 2021 Dec.
Article in English | MEDLINE | ID: covidwho-1550812

ABSTRACT

The SARS-CoV-2 is a new coronavirus responsible for the COVID-19 disease and has caused the pandemic worldwide. A large number of cases have overwhelmed the healthcare system worldwide. The COVID-19 infection has been associated with a heightened risk of thromboembolic complications. Various mechanisms are leading to the high thrombotic risk in COVID-19 patients such as inflammation, endotheliitis, hyperviscosity, and hypercoagulability. We searched PubMed, EMBASE, and CINAHL from January 2020 to December 2020. We used the following search terms: COVID-19, coagulopathy, and thrombosis. We reviewed the epidemiology, clinical features, mechanisms, and treatment of COVID-19-associated coagulopathy.


Subject(s)
COVID-19 , Thromboembolism , Thrombophilia , Humans , Pandemics , SARS-CoV-2 , Thrombophilia/complications , Thrombophilia/epidemiology
3.
Rev Clin Esp (Barc) ; 221(10): 587-591, 2021 12.
Article in English | MEDLINE | ID: covidwho-1415752

ABSTRACT

BACKGROUND AND OBJECTIVES: A new coronavirus disease in humans, COVID-19, caused by SARS-CoV-2, emerged in December 2019. It has been associated with the development of thrombotic phenomena. Retinal vein occlusion (RVO) is mainly a consequence of vascular risk factors (VRF). This study aimed to analyze cases of COVID-19 in a cohort of patients with RVO (Valdecilla cohort). PATIENTS AND METHODS: Between December 2008 and December 2020, 429 patients with RVO were attended to in our clinic. Ten patients had COVID-19, one of which did not have VRF or thrombophilia. The remaining nine patients had RVO prior to the infection and VRF, six had carotid atherosclerosis, and four had antiphospholipid syndrome. The infection did not cause thrombotic phenomena in any of them. CONCLUSIONS: RVO is a rare manifestation of COVID-19. In our cohort of patients with RVO, COVID-19 disease did not lead to thrombotic events.


Subject(s)
Antiphospholipid Syndrome , COVID-19 , Retinal Vein Occlusion , Thrombophilia , Humans , Pandemics , Retinal Vein Occlusion/epidemiology , Risk Factors , SARS-CoV-2 , Thrombophilia/epidemiology
6.
PLoS One ; 15(12): e0243409, 2020.
Article in English | MEDLINE | ID: covidwho-983910

ABSTRACT

BACKGROUND: A significant proportion of patients with coronavirus disease 19 (COVID-19) suffer from excessive coagulation activation and coagulopathy which is associated with an increased risk of venous and arterial thromboembolism and adverse outcome. Our study investigates coagulation markers and the incidence of thromboembolic events in COVID-19 patients receiving recommended anticoagulation strategies. METHODS: In a retrospective single-center analysis at the University Hospital Zurich, Switzerland, we investigated 31 adult COVID-19 patients between April 6th and May 13th, 2020 and with at least one laboratory assessment of the coagulation markers prothrombin time/Quick, thrombin time, fibrinogen and D-dimers. For antithrombotic prophylaxis low-molecular-weight-heparin or unfractionated heparin was administered and two patients with heparin-induced thrombocytopenia received argatroban. RESULTS: We analyzed 31 patients (68% male, mean age 60± SD 15 years). 22 (71%) of these required intensive care unit treatment, 5 (16%) were hospitalized in a ward, and 4 (13%) were outpatients. Mean fibrinogen levels were markedly elevated to 6.4± SD 1.8g/l, with a peak in the third week of the disease and no significant decrease over time. D-dimers were elevated to a mean value of 5.1±4.4mg/l with peak levels of 6.8±5.3mg/l in the fourth week of disease, and a subsequent decrease. Platelet count (308±136G/l) and PT/Quick (85±22%) showed no significant changes over time. Sensitivity analyses for patients treated in the ICU showed that D-dimer levels were higher in this group. The results of other sensitivity analyses were comparable. Thromboembolic events were diagnosed in 4 (13%) patients and 5 (16%) patients died during the observation period. CONCLUSION: We find coagulation alterations in COVID-19 patients indicating significant hypercoagulability. These alterations are visible despite antithrombotic treatment, and peak around week 3-4 of the disease.


Subject(s)
Blood Coagulation , COVID-19 , Fibrin Fibrinogen Degradation Products/metabolism , Heparin, Low-Molecular-Weight/administration & dosage , SARS-CoV-2/metabolism , Thrombophilia , Adult , Aged , Biomarkers/blood , COVID-19/blood , COVID-19/complications , COVID-19/drug therapy , COVID-19/epidemiology , Critical Care , Female , Humans , Male , Middle Aged , Platelet Count , Retrospective Studies , Thrombin Time , Thrombophilia/blood , Thrombophilia/drug therapy , Thrombophilia/epidemiology , Thrombophilia/etiology
7.
Cytokine Growth Factor Rev ; 58: 75-81, 2021 04.
Article in English | MEDLINE | ID: covidwho-971009

ABSTRACT

Emerging evidence has documented that multisystem organ failure in coronavirus disease 2019 (COVID-19) patients is strongly associated with various coagulopathies. Treatments for COVID-19-associated coagulopathy are still a clinical challenge. An advancement in the knowledge of mechanisms of the excessive or inappropriate activation of the complement cascade involved in the genesis of COVID-19-associated coagulopathy might be a fundamental approach for developing novel classes of anticoagulant drugs. In this context, there is emerging evidence indicating that C5a, a component of the complement system, and its receptors (C5aRs) play a critical role in the genesis of the COVID-19-associated hypercoagulable state. Thus, this review describes the mechanisms by which C5a/C5aR signaling participates in the cascade of events involved in the pathophysiology of COVID-19-associated coagulopathy. Furthermore, it highlights the current possibilities for the development of a novel therapeutic approach for COVID-19 patients that targets C5a/C5aRs signaling.


Subject(s)
COVID-19/therapy , Complement C5a/physiology , Complement C5a/therapeutic use , Thrombophilia/therapy , Animals , COVID-19/blood , COVID-19/complications , COVID-19/epidemiology , Complement Activation/physiology , Humans , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Signal Transduction , Thrombophilia/epidemiology , Thrombophilia/etiology
8.
Br J Anaesth ; 126(3): 590-598, 2021 03.
Article in English | MEDLINE | ID: covidwho-965444

ABSTRACT

BACKGROUND: Critically ill coronavirus disease 2019 (COVID-19) patients present with a hypercoagulable state with high rates of macrovascular and microvascular thrombosis, for which hypofibrinolysis might be an important contributing factor. METHODS: We retrospectively analysed 20 critically ill COVID-19 patients at Innsbruck Medical University Hospital whose coagulation function was tested with ClotPro® and compared with that of 60 healthy individuals at Augsburg University Clinic. ClotPro is a viscoelastic whole blood coagulation testing device. It includes the TPA test, which uses tissue factor (TF)-activated whole blood with added recombinant tissue-derived plasminogen activator (r-tPA) to induce fibrinolysis. For this purpose, the lysis time (LT) is measured as the time from when maximum clot firmness (MCF) is reached until MCF falls by 50%. We compared COVID-19 patients with prolonged LT in the TPA test and those with normal LT. RESULTS: Critically ill COVID-19 patients showed hypercoagulability in ClotPro assays. MCF was higher in the EX test (TF-activated assay), IN test (ellagic acid-activated assay), and FIB test (functional fibrinogen assay) with decreased maximum lysis (ML) in the EX test (hypofibrinolysis) and highly prolonged TPA test LT (decreased fibrinolytic response), as compared with healthy persons. COVID-19 patients with decreased fibrinolytic response showed higher fibrinogen levels, higher thrombocyte count, higher C-reactive protein levels, and decreased ML in the EX test and IN test. CONCLUSION: Critically ill COVID-19 patients have impaired fibrinolysis. This hypofibrinolytic state could be at least partially dependent on a decreased fibrinolytic response.


Subject(s)
COVID-19/blood , COVID-19/epidemiology , Critical Illness/epidemiology , Fibrinolysis/drug effects , Thrombophilia/blood , Thrombophilia/epidemiology , Adult , Aged , Anticoagulants/administration & dosage , Blood Coagulation Tests/methods , COVID-19/diagnosis , Female , Fibrinolysis/physiology , Humans , Male , Middle Aged , Retrospective Studies , Thrombophilia/diagnosis , Tissue Plasminogen Activator/administration & dosage
9.
Clin Appl Thromb Hemost ; 26: 1076029620962853, 2020.
Article in English | MEDLINE | ID: covidwho-873836

ABSTRACT

Thrombotic complications of the novel coronavirus (COVID-19) are a concerning aspect of the disease, due to the high incidence in critically ill patients and poor clinical outcomes. COVID-19 predisposes patients to a hypercoagulable state, however, the pathophysiology behind the thrombotic complications seen in this disease is not well understood. Several mechanisms have been proposed and the pathogenesis likely involves a host immune response contributing to vascular endothelial cell injury, inflammation, activation of the coagulation cascade via tissue factor expression, and shutdown of fibrinolysis. Treatments targeting these pathways may need to be considered to improve clinical outcomes and decrease overall mortality due to thrombotic complications. In this review, we will discuss the proposed pathophysiologic mechanisms for thrombotic complications in COVID-19, as well as treatment strategies for these complications based on the current literature available.


Subject(s)
Betacoronavirus , Blood Coagulation/physiology , Coronavirus Infections/complications , Pandemics , Pneumonia, Viral/complications , Thrombophilia/etiology , COVID-19 , Coronavirus Infections/epidemiology , Global Health , Humans , Incidence , Pneumonia, Viral/epidemiology , SARS-CoV-2 , Thrombophilia/blood , Thrombophilia/epidemiology
10.
J Thromb Thrombolysis ; 51(4): 961-965, 2021 May.
Article in English | MEDLINE | ID: covidwho-813353

ABSTRACT

The rate of venous and arterial thrombotic events among patients infected with severe acute respiratory syndrome coronavirus-2 (SAR-CoV-2) is high. This may be due to a hypercoagulable state induced by the severe inflammation that results from the SAR-CoV-2 infection. We aimed to determine hypercoagulable states' incidence based on thromboelastography study and its association with thrombotic events in critically ill patients with coronavirus disease 2019 (COVID-19). Fifty-two COVID-19 patients who had thromboelastography study were retrospectively included. All patients received pharmacologic thromboprophylaxis. The hypercoagulable state was observed in 16 patients (30.8%). Among them, maximum amplitude and a-angle were elevated in 75% and 25%, respectively. Reaction time and K were low in only 12.5% for both of them. Inflammatory and coagulation markers, as well as thromboprophylaxis regimens, were not associated with a hypercoagulable state. Fourteen patients (27%) experienced a total of 16 thrombotic events, including 8 (57%) deep venous thrombosis, 6 (43%) pulmonary embolism, and 2 (14.3%) arterial thrombosis. The hypercoagulable state was not significantly associated with thrombotic events. In summary, we observed a lower rate of hypercoagulable state on thromboelastography study in critically ill COVID-19 patients. Also, the hypercoagulable state was not associated with the occurrence of thrombotic events.


Subject(s)
COVID-19 , Critical Illness , Pulmonary Embolism , Thrombelastography/methods , Thrombophilia , Venous Thromboembolism , Biomarkers/blood , COVID-19/blood , COVID-19/diagnosis , COVID-19/epidemiology , COVID-19/physiopathology , Chemoprevention/methods , Critical Illness/epidemiology , Critical Illness/therapy , Female , Humans , Incidence , Inflammation/blood , Inflammation/etiology , Male , Middle Aged , Outcome and Process Assessment, Health Care , Pulmonary Embolism/diagnosis , Pulmonary Embolism/epidemiology , Pulmonary Embolism/etiology , Risk Assessment , SARS-CoV-2/isolation & purification , Severity of Illness Index , Thrombelastography/statistics & numerical data , Thrombophilia/blood , Thrombophilia/epidemiology , Thrombophilia/etiology , United Arab Emirates/epidemiology , Venous Thromboembolism/diagnosis , Venous Thromboembolism/epidemiology , Venous Thromboembolism/etiology
11.
Pediatr Blood Cancer ; 67(12): e28745, 2020 12.
Article in English | MEDLINE | ID: covidwho-812651

ABSTRACT

Infection from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), though mainly a respiratory disease, can impair many systems, including causing hematological complications. Lymphopenia and hypercoagulability have been reported in adults with coronavirus disease 2019 (COVID-19) and are considered markers of poor prognosis. This review summarizes the hematological findings in children with SARS-CoV-2 infection. The majority of infected children had a normal leukocyte count, while the most common white blood cell abnormality was leukopenia. Lymphopenia, which may be a marker of severe disease, was rarer in children than in adults, possibly due to their immature immune system or due to the less severe manifestation of COVID-19 in this age group. Age may have an impact, and in neonates and infants the most common abnormality was lymphocytosis. Abnormalities of red blood cells and platelets were uncommon. Anemia and hypercoagulability were reported mainly in children presenting the novel multisystem inflammatory syndrome (MIS) associated with SARS-CoV-2.


Subject(s)
Anemia/blood , Betacoronavirus/metabolism , Coronavirus Infections/blood , Lymphopenia/blood , Pandemics , Pneumonia, Viral/blood , Thrombophilia/blood , Adolescent , Anemia/epidemiology , Anemia/immunology , Betacoronavirus/immunology , Biomarkers/blood , Blood Platelets/immunology , Blood Platelets/metabolism , COVID-19 , Child , Child, Preschool , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Erythrocytes/immunology , Erythrocytes/metabolism , Female , Humans , Infant , Infant, Newborn , Leukocyte Count , Lymphopenia/epidemiology , Lymphopenia/immunology , Male , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , SARS-CoV-2 , Thrombophilia/epidemiology , Thrombophilia/immunology
12.
J Stroke Cerebrovasc Dis ; 29(12): 105325, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-811980

ABSTRACT

INTRODUCTION: Coronavirus disease 2019 has been associated with stroke, particular characteristics of these patients are not fully understood. The adequate management of these patients depends on the comprehension of factors such as temporality, clinical presentation and etiology. We hypothesize there is an important temporal relationship between COVID-19 severity and stroke onset. METHODS: a systematic review of the available literature was conducted using Pubmed and Scopus, studies reporting patients with Coronavirus disease 19 and stroke were included. Clinical, sociodemographic and laboratory characteristics of patients were extracted and analyzed. RESULTS: Forty-seven studies and 176 patients were included, with a mean age of 63.1 years (SD= 16 n=122), most of them were males (63.2% n=171). The most frequent etiology was cryptogenic 40.9% n=66), and a mean National Institute of Health Stroke Scale of 14.4 points was found (SD= 8.6 n=73). Large vessel occlusion was reported in 65.9% patients (n=91) and these patients were younger with greater stroke severity. D-dimer, C-reactive protein, fibrinogen, ferritin and lactate dehydrogenase were elevated in most patients with reported findings. Most patients had severe Coronavirus disease 2019. The mean time from onset of respiratory symptoms to stroke was 9 days (SD=9.9), the shortest time was noted in those with mild and moderate disease. CONCLUSIONS: There is a trend between the severity of Coronavirus disease 2019 and time to stroke onset. Also, age and stroke severity were found to be related to the development of large vessel occlusion. Inflammation and hypercoagulability markers are elevated in this disease, we propose to not discard hypercoagulability secondary to severe acute respiratory syndrome-coronavirus-2 as an underlying cause of stroke in these patients.


Subject(s)
COVID-19/epidemiology , Global Health , Stroke/epidemiology , Adult , Age Factors , Aged , Aged, 80 and over , COVID-19/diagnosis , Female , Humans , Male , Middle Aged , Prognosis , Risk Assessment , Risk Factors , Severity of Illness Index , Stroke/diagnosis , Thrombophilia/epidemiology , Time Factors
13.
Am J Hematol ; 95(12): 1578-1589, 2020 12.
Article in English | MEDLINE | ID: covidwho-763015

ABSTRACT

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.


Subject(s)
COVID-19/complications , SARS-CoV-2 , Thrombosis/epidemiology , Anticoagulants/therapeutic use , Antiphospholipid Syndrome , COVID-19/drug therapy , COVID-19/immunology , COVID-19/therapy , Complement Activation , Critical Illness/epidemiology , Cytokine Release Syndrome/epidemiology , Disseminated Intravascular Coagulation , Ferritins/blood , Humans , Hyperferritinemia/epidemiology , Macrophage Activation , Pulmonary Embolism/epidemiology , Renin-Angiotensin System/physiology , Thrombophilia/blood , Thrombophilia/epidemiology , Thrombophilia/immunology , Thrombosis/blood , Thrombosis/immunology
15.
Thromb Res ; 194: 101-115, 2020 10.
Article in English | MEDLINE | ID: covidwho-608547

ABSTRACT

The 2019 coronavirus disease (COVID-19) presents with a large variety of clinical manifestations ranging from asymptomatic carrier state to severe respiratory distress, multiple organ dysfunction and death. While it was initially considered primarily a respiratory illness, rapidly accumulating data suggests that COVID-19 results in a unique, profoundly prothrombotic milieu leading to both arterial and venous thrombosis. Consistently, elevated D-dimer level has emerged as an independent risk factor for poor outcomes, including death. Several other laboratory markers and blood counts have also been associated with poor prognosis, possibly due to their connection to thrombosis. At present, the pathophysiology underlying the hypercoagulable state is poorly understood. However, a growing body of data suggests that the initial events occur in the lung. A severe inflammatory response, originating in the alveoli, triggers a dysfunctional cascade of inflammatory thrombosis in the pulmonary vasculature, leading to a state of local coagulopathy. This is followed, in patients with more severe disease, by a generalized hypercoagulable state that results in macro- and microvascular thrombosis. Of concern, is the observation that anticoagulation may be inadequate in many circumstances, highlighting the need for alternative or additional therapies. Numerous ongoing studies investigating the pathophysiology of the COVID-19 associated coagulopathy may provide mechanistic insights that can direct appropriate interventional strategies.


Subject(s)
Blood Coagulation , COVID-19 , Inflammation/drug therapy , Thrombophilia , Thrombosis , Venous Thromboembolism , Animals , Anti-Inflammatory Agents/therapeutic use , Anticoagulants/therapeutic use , Blood Coagulation/drug effects , COVID-19/blood , COVID-19/drug therapy , COVID-19/epidemiology , COVID-19/physiopathology , Humans , Incidence , Inflammation/blood , Inflammation/epidemiology , Inflammation/physiopathology , Thrombophilia/blood , Thrombophilia/epidemiology , Thrombophilia/physiopathology , Thrombophilia/prevention & control , Thrombosis/blood , Thrombosis/epidemiology , Thrombosis/physiopathology , Thrombosis/therapy , Venous Thromboembolism/blood , Venous Thromboembolism/epidemiology , Venous Thromboembolism/physiopathology , Venous Thromboembolism/therapy
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