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1.
Blood Cells Mol Dis ; 94: 102653, 2022 05.
Article in English | MEDLINE | ID: covidwho-1676413

ABSTRACT

Abnormal coagulation dynamics, including disseminated intravascular coagulopathy, pulmonary embolism, venous thromboembolism and risk of thrombosis are often associated with the severity of COVID-19. However, very little is known about the contribution of platelets in above pathogenesis. In order to decipher the pathophysiology of thrombophilia in COVID-19, we recruited severely ill patients from ICU, based on the above symptoms and higher D-dimer levels, and compared these parameters with their asymptomatic counterparts. Elevated levels of platelet-derived microparticles and platelet-leukocyte aggregates suggested the hyperactivation of platelets in ICU patients. Strikingly, platelet transcriptome analysis showed a greater association of IL-6 and TNF signalling pathways in ICU patients along with higher plasma levels of IL-6 and TNFα. In addition, upregulation of pathways like blood coagulation and hemostasis, as well as inflammation coexisted in platelets of these patients. Further, the increment of necrotic pathway and ROS-metabolic processes in platelets was suggestive of its procoagulant phenotype in ICU patients. This study suggests that higher plasma IL-6 and TNFα may trigger platelet activation and coagulation, and in turn aggravate thrombosis and hypercoagulation in severe COVID-19 patients. Therefore, the elevated IL-6 and TNFα, may serve as potential risk factors for platelet activation and thrombophilia in these patients.


Subject(s)
COVID-19 , Cell-Derived Microparticles , Thrombophilia , Blood Platelets/metabolism , COVID-19/complications , Cell-Derived Microparticles/metabolism , Cytokines/metabolism , Humans , SARS-CoV-2 , Thrombophilia/complications , Up-Regulation
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.
J Thromb Thrombolysis ; 53(3): 586-593, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1491307

ABSTRACT

This study aims to review the available literature pertinent to vascular complications in COVID-19. A systematic search was performed using PubMed and Google Scholar to identify all relevant studies based on our study objective. Multiple studies have reported widespread systemic inflammation and procoagulant/hypercoagulable state in COVID-19, including thrombotic microangiopathy, endothelial dysfunction, bleeding disorder, and thrombosis. However, large specialised studies on vascular complications are lacking despite current evidence indicating dysfunctional coagulation pathways. Furthermore, there are no clear and definitive recommendations regarding thromboprophylaxis or full therapeutic anticoagulation in COVID-19. Several studies have reported hypercoagulability and vascular complications as important predictors of patient outcome in COVID-19. Therefore, it is important to understand the pathogenesis, epidemiology, management, and outcomes of patients who develop venous or arterial thrombosis and those with a pre-existing thrombotic disease who contract COVID-19 for risk stratification, thromboprophylaxis, optimal antithrombotic therapy during active infection and long-term anticoagulation following discharge or recovery.


Subject(s)
COVID-19 , Cardiovascular Diseases , Thrombophilia , Thrombosis , Venous Thromboembolism , Anticoagulants/therapeutic use , Blood Coagulation , COVID-19/complications , Cardiovascular Diseases/drug therapy , Humans , Thrombophilia/complications , Thrombosis/chemically induced , Venous Thromboembolism/prevention & control
4.
Card Electrophysiol Clin ; 14(1): 41-52, 2022 03.
Article in English | MEDLINE | ID: covidwho-1487627

ABSTRACT

COVID-19 is an acute respiratory disease of viral origin caused by SARS-CoV-2. This disease is associated with a hypercoagulable state resulting in arterial and venous thrombotic events. The latter are more frequent, especially in patients who develop a severe form of the disease and are associated with an increased mortality rate. It is therefore essential to identify patients at higher risk to initiate antithrombotic therapy. Hospitalized patients treated with treatment dose of anticoagulants had better outcomes than those treated with prophylactic dose. However, several trials are ongoing to better define the therapeutic and prevention strategies for this insidious complication.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Anticoagulants/therapeutic use , COVID-19/complications , Humans , SARS-CoV-2 , Thrombophilia/complications , Thrombophilia/drug therapy , Thrombosis/drug therapy
5.
J Am Acad Dermatol ; 85(2): 301-310, 2021 08.
Article in English | MEDLINE | ID: covidwho-1379127

ABSTRACT

The skin often provides initial clues of hypercoagulability with features such as livedo reticularis, livedo racemosa, retiform purpura, necrosis, and ulcerations. Because these cutaneous manifestations are nonspecific, laboratory testing is often needed to evaluate for underlying causes of hypercoagulability. Importantly, these disorders are reported to be the most common mimicker, resulting in an erroneous diagnosis of pyoderma gangrenosum. Understanding inherent properties of, and indications for, available tests is necessary for appropriate ordering and interpretation of results. Additionally, ordering of these tests in an indiscriminate manner may lead to inaccurate results, complicating the interpretation and approach to management. This second article in this continuing medical education series summarizes information on methodology, test characteristics, and limitations of several in vitro laboratory tests used for the work up of hypercoagulability and vasculopathic disease as it pertains to dermatologic disease.


Subject(s)
Skin Diseases/blood , Skin Diseases/diagnosis , Thrombophilia/blood , Thrombophilia/diagnosis , Clinical Laboratory Techniques , Humans , Skin Diseases/etiology , Thrombophilia/complications
7.
Pharmacol Res ; 158: 104950, 2020 08.
Article in English | MEDLINE | ID: covidwho-1318942

ABSTRACT

Patients affected by severe coronavirus induced disease-2019 (Covid-19) often experience hypoxemia due to alveolar involvement and endothelial dysfunction, which leads to the formation of micro thrombi in the pulmonary capillary vessels. Both hypoxemia and a prothrombotic diathesis have been associated with more severe disease and increased risk of death. To date, specific indications to treat this condition are lacking. This was a single center, investigator initiated, compassionate use, proof of concept, case control, phase IIb study (NCT04368377) conducted in the Intermediate Respiratory Care Unit of L. Sacco University Hospital in Milano, Italy. Our objective was to explore the effects of the administration of anti-platelet therapy on arterial oxygenation and clinical outcomes in patients with severe Covid-19 with hypercoagulability. We enrolled five consecutive patients with laboratory confirmed SARS-CoV-2 infection, severe respiratory failure requiring helmet continuous positive airway pressure (CPAP), bilateral pulmonary infiltrates and a pro-thrombotic state identified as a D-dimer > 3 times the upper limit of normal. Five patients matched for age, D-dimer value and SOFA score formed the control group. Beyond standard of care, treated patients received 25 µg/Kg/body weight tirofiban as bolus infusion, followed by a continuous infusion of 0.15 µg/Kg/body weight per minute for 48 hours. Before tirofiban, patients received acetylsalicylic acid 250 mg infusion and oral clopidogrel 300 mg; both were continued at a dose of 75 mg daily for 30 days. Fondaparinux2.5 mg/day sub-cutaneous was given for the duration of the hospital stay. All controls were receiving prophylactic or therapeutic dose heparin, according to local standard operating procedures. Treated patients consistently experienced a mean (SD) reduction in A-a O2 gradient of -32.6 mmHg (61.9, P = 0.154), -52.4 mmHg (59.4, P = 0.016) and -151.1 mmHg (56.6, P = 0.011; P = 0.047 vs. controls) at 24, 48 hours and 7 days after treatment. PaO2/FiO2 ratio increased by 52 mmHg (50, P = 0.172), 64 mmHg (47, P = 0.040) and 112 mmHg (51, P = 0.036) after 24, 48 hours and 7 days, respectively. All patients but one were successfully weaned from CPAP after 3 days. This was not true for the control group. No major adverse events were observed. Antiplatelet therapy might be effective in improving the ventilation/perfusion ratio in Covid-19 patients with severe respiratory failure. The effects might be sustained by the prevention and interference on forming clots in lung capillary vessels and by modulating megakaryocytes' function and platelet adhesion. Randomized clinical trials are urgently needed to confirm these results.


Subject(s)
Betacoronavirus , Coronavirus Infections/drug therapy , Hypoxia/drug therapy , Platelet Aggregation Inhibitors/therapeutic use , Pneumonia, Viral/drug therapy , Thrombophilia/drug therapy , Aged , Aspirin/therapeutic use , COVID-19 , Clopidogrel/therapeutic use , Compassionate Use Trials , Coronavirus Infections/complications , Female , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Hypoxia/complications , Male , Middle Aged , Pandemics , Pneumonia, Viral/complications , Proof of Concept Study , SARS-CoV-2 , Thrombophilia/blood , Thrombophilia/complications , Tirofiban/therapeutic use
8.
9.
Med Hypotheses ; 152: 110621, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1253390

ABSTRACT

The inflammatory component of Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) creates a pro-thrombotic state that necessitates a thrombophylactic strategy for hospitalized patients. Such strategies are difficult to be standardized because certain individuals can have pro-thrombotic conditions, such as inherited thrombophilia, which pre-dispose them to an additional coagulative risk. Whether outside the hospital or when admitted, patients with inherited thrombophilia need special anticoagulant and antiplatelet attention. Identifying such patients, especially in susceptible populations like the eastern Mediterranean (EM) region, will aid primary providers in risk stratification for choosing the optimal anticoagulation or antiplatelet plan.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Anticoagulants/therapeutic use , Humans , SARS-CoV-2 , Thrombophilia/complications
10.
Neurologist ; 26(3): 86-89, 2021 May 05.
Article in English | MEDLINE | ID: covidwho-1214712

ABSTRACT

INTRODUCTION: The concurrency of both, acute stroke and acute myocardial infarction in normal conditions, outside the pandemic is rare. Coagulopathy has been associated with the inflammatory phase of coronavirus disease (COVID-19) and might be involved in this concurrency. CASES REPORT: We describe 2 patients with previous mild or no symptoms of COVID-19, admitted for acute stroke with recent/simultaneous myocardial infarction in whom admission polymerase chain reaction was negative but serologic testing diagnosed COVID-19. In these patients, concurrent stroke and myocardial infarction could have been promoted by COVID-19 infection. Management and evolution are detailed, and their contacts to confirm the COVID-19 infection. Pathogenic analysis of possible hypercoagulation state is described suggesting the hypothesis of endothelial dysfunction as the strongest mechanism involved in thrombus formation after the acute phase of COVID-19 infection. CONCLUSIONS: Our experience with these cases suggests that patients with mild symptoms can also present thromboembolic complications once the acute phase of COVID-19 infection has passed.


Subject(s)
COVID-19/complications , Ischemic Stroke/etiology , Myocardial Infarction/etiology , Humans , Severity of Illness Index , Thrombophilia/complications , Thrombophilia/etiology
11.
Clin Appl Thromb Hemost ; 27: 10760296211002274, 2021.
Article in English | MEDLINE | ID: covidwho-1191430

ABSTRACT

The purpose of this article is to address several challenging questions in the management of young patients (those age 60 and under) who present with ischemic stroke. Do genetic thrombophilic states, strongly associated with venous thrombosis, independently cause arterial events in adults? Should cases of patent foramen ovale be closed with mechanical devices in patients with cryptogenic stroke? What are the optimal treatments for cerebral vein thrombosis, carotid artery dissection, and antiphospholipid syndrome and are DOACs acceptable treatment for these indications? What is the mechanism underlying large vessel stroke in patients with COVID-19? This is a narrative review. We searched PubMed and Embase and American College of physicians Journal club database for English language articles since 2000 looking mainly at randomized clinical trials, Meta analyses, Cochran reviews as well as some research articles viewed to be cutting edge regarding anticoagulation and cerebrovascular disease. Searches were done entering cerebral vein thrombosis, carotid dissection, anticoagulation therapy and stroke, antiphospholipid antibody and stroke, stroke in young adults, cryptogenic stroke and anticoagulation, patent foramen ovale and cryptogenic stroke, COVID-19 and stroke.


Subject(s)
COVID-19/complications , Ischemic Stroke/etiology , Ischemic Stroke/therapy , SARS-CoV-2 , Adult , Aneurysm, Dissecting/complications , Anticoagulants/adverse effects , Anticoagulants/therapeutic use , Antiphospholipid Syndrome/complications , Cervical Vertebrae/blood supply , Female , Foramen Ovale, Patent/complications , Foramen Ovale, Patent/surgery , Humans , Intracranial Thrombosis/etiology , Intracranial Thrombosis/therapy , Ischemic Stroke/prevention & control , Male , Middle Aged , Pandemics , Prognosis , Risk Factors , Thrombophilia/complications
12.
Eur J Clin Invest ; 51(5): e13546, 2021 May.
Article in English | MEDLINE | ID: covidwho-1142880
13.
Sci Rep ; 11(1): 1793, 2021 01 19.
Article in English | MEDLINE | ID: covidwho-1065942

ABSTRACT

COVID-19 caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) and other respiratory viral (non-CoV-2-RV) infections are associated with thrombotic complications. The differences in prothrombotic potential between SARS-CoV-2 and non-CoV-2-RV have not been well characterised. We compared the thrombotic rates between these two groups of patients directly and further delved into their coagulation profiles. In this single-center, retrospective cohort study, all consecutive COVID-19 and non-CoV-2-RV patients admitted between January 15th and April 10th 2020 were included. Coagulation parameters studied were prothrombin time and activated partial thromboplastin time and its associated clot waveform analysis (CWA) parameter, min1, min2 and max2. In the COVID-19 (n = 181) group there were two (1.0 event/1000-hospital-days) myocardial infarction events while one (1.8 event/1000-hospital-day) was reported in the non-CoV-2-RV (n = 165) group. These events occurred in patients who were severely ill. There were no venous thrombotic events. Coagulation parameters did not differ throughout the course of mild COVID-19. However, CWA parameters were significantly higher in severe COVID-19 compared with mild disease, suggesting hypercoagulability (min1: 6.48%/s vs 5.05%/s, P < 0.001; min2: 0.92%/s2 vs 0.74%/s2, P = 0.033). In conclusion, the thrombotic rates were low and did not differ between COVID-19 and non-CoV-2-RV patients. The hypercoagulability in COVID-19 is a highly dynamic process with the highest risk occurring when patients were most severely ill. Such changes in haemostasis could be detected by CWA. In our population, a more individualized thromboprophylaxis approach, considering clinical and laboratory factors, is preferred over universal pharmacological thromboprophylaxis for all hospitalized COVID-19 patients and such personalized approach warrants further research.


Subject(s)
COVID-19/pathology , Thrombophilia/diagnosis , Virus Diseases/pathology , Adult , COVID-19/complications , COVID-19/virology , Female , Humans , Male , Myocardial Infarction/complications , Myocardial Infarction/diagnosis , Partial Thromboplastin Time , Prothrombin Time , Retrospective Studies , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index , Thrombophilia/complications , Virus Diseases/complications
15.
Turk J Haematol ; 38(1): 15-21, 2021 02 25.
Article in English | MEDLINE | ID: covidwho-1045314

ABSTRACT

Objective: The defective interplay between coagulation and inflammation may be the leading cause of intravascular coagulation and organ dysfunction in coronavirus disease-19 (COVID-19) patients. Abnormal coagulation profiles were reported to be associated with poor outcomes. In this study, we assessed the prognostic values of antithrombin (AT) activity levels and the impact of fresh frozen plasma (FFP) treatment on outcome. Materials and Methods: Conventional coagulation parameters as well as AT activity levels and outcomes of 104 consecutive critically ill acute respiratory distress syndrome (ARDS) patients with laboratory-confirmed COVID-19 disease were retrospectively analyzed. Patients with AT activity below 75% were treated with FFP. Maximum AT activity levels achieved in those patients were recorded. Results: AT activity levels at admission were significantly lower in nonsurvivors than survivors (73% vs. 81%). The cutoff level for admission AT activity was 79% and 58% was the lowest AT for survival. The outcome in those patients who had AT activity levels above 75% after FFP treatment was better than that of the nonresponding group. As well as AT, admission values of D-dimer, C-reactive protein, and procalcitonin were coagulation and inflammatory parameters among the mortality risk factors. Conclusion: AT activity could be used as a prognostic marker for survival and organ failure in COVID-19-associated ARDS patients. AT supplementation therapy with FFP in patients with COVID-19-induced hypercoagulopathy may improve thrombosis prophylaxis and thus have an impact on survival.


Subject(s)
Antithrombins/blood , COVID-19/blood , COVID-19/therapy , Critical Illness/mortality , Aged , Aged, 80 and over , Antithrombins/physiology , Antithrombins/therapeutic use , Blood Coagulation Tests/methods , C-Reactive Protein/analysis , COVID-19/diagnosis , COVID-19/mortality , Case-Control Studies , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/prevention & control , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/prevention & control , Plasma , Procalcitonin/analysis , Prognosis , Retrospective Studies , SARS-CoV-2/genetics , Thrombophilia/complications , Thrombophilia/physiopathology , Turkey/epidemiology
16.
Medicina (Kaunas) ; 56(12)2020 Dec 03.
Article in English | MEDLINE | ID: covidwho-963621

ABSTRACT

Pulmonary embolism (PE) is a commonly encountered clinical entity in patients with coronavirus disease 2019 (COVID-19). Up to 1/3 of patients have been found to have PE in the setting of COVID-19. Given the novelty of the virus causing this pandemic, it has not been easy to address diagnostic and management issues in PE. Ongoing research and publications of the scientific literature have helped in dealing with COVID-19 lately and this applies to PE as well. In this article, we attempt to succinctly yet comprehensively discuss PE in patients with COVID-19 with a review of the prevailing literature.


Subject(s)
COVID-19/blood , Pulmonary Embolism/diagnosis , Pulmonary Embolism/therapy , Thrombophilia/blood , Anticoagulants/therapeutic use , COVID-19/complications , Computed Tomography Angiography , Disease Management , Disseminated Intravascular Coagulation/blood , Echocardiography , Extracorporeal Membrane Oxygenation , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinogen/metabolism , Humans , Lower Extremity/diagnostic imaging , Partial Thromboplastin Time , Platelet Count , Point-of-Care Systems , Prothrombin Time , Pulmonary Embolism/blood , Pulmonary Embolism/etiology , Thrombolytic Therapy , Thrombophilia/complications , Ultrasonography, Doppler, Duplex , Venous Thrombosis/diagnostic imaging , Ventilation-Perfusion Scan
17.
J Stroke Cerebrovasc Dis ; 29(12): 105307, 2020 Dec.
Article in English | MEDLINE | ID: covidwho-753198

ABSTRACT

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) initially most appreciated for its pulmonary symptoms, is now increasingly recognized for causing multi-organ disease and stroke in the setting of a hypercoagulable state. We report a case of 33-year-old African American woman with COVID-19 who developed acute malignant middle cerebral artery infarction due to thromboembolic occlusion of the left terminal internal carotid artery and middle cerebral artery stem. Mechanical thrombectomy was challenging and ultimately unsuccessful resulting in limited reperfusion of <67% of the affected vascular territory, and thrombectomized clot was over 50 mm in length, at least three times the average clot length. The final stroke size was estimated at 224 cubic centimeters. On admission her D-dimer level was 94,589 ng/mL (normal 0-500 ng/ml). Throughout the hospitalization D-dimer decreased but never reached normal values while fibrinogen trended upward. Hypercoagulability panel was remarkable for mildly elevated anticardiolipin IgM of 16.3 MPL/mL (normal: 0-11.0 MPL/mL). With respect to remaining stroke workup, there was no evidence of clinically significant stenosis or dissection in the proximal internal carotid artery or significant cardioembolic source including cardiomyopathy, atrial fibrillation, cardiac thrombus, cardiac tumor, valvular abnormality, aortic arch atheroma, or patent foramen ovale. She developed malignant cytotoxic cerebral edema and succumbed to complications. This case underscores the importance of recognizing hypercoagulability as a cause of severe stroke and poor outcome in young patients with COVID-19 and highlights the need for further studies to define correlation between markers of coagulopathy in patients with COVID-19 infection and outcome post stroke.


Subject(s)
Blood Coagulation , COVID-19/complications , Carotid Stenosis/etiology , Infarction, Middle Cerebral Artery/etiology , Thrombophilia/etiology , Adult , Biomarkers/blood , Brain Edema/etiology , COVID-19/blood , COVID-19/diagnosis , COVID-19/therapy , Carotid Stenosis/blood , Carotid Stenosis/diagnostic imaging , Carotid Stenosis/therapy , Disease Progression , Fatal Outcome , Female , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Infarction, Middle Cerebral Artery/blood , Infarction, Middle Cerebral Artery/diagnostic imaging , Infarction, Middle Cerebral Artery/therapy , Thrombectomy , Thrombophilia/complications , Thrombophilia/diagnosis , Treatment Outcome
18.
Med Hypotheses ; 144: 110231, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-741425

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic has increased exponentially in numbers with more than 20 million people infected around the globe. It is clear that COVID-19 is not a simple viral pneumonia, but presents with unusual pathophysiological effects. Of special interest is that SARS-CoV-2 utilises the angiotensin-converting enzyme-2 (ACE2) for cell entry and therefore has a direct effect on the renin angiotensin system (RAS). The RAS is primarily responsible for blood pressure control via the classic pathway. Recently numerous other pathological processes have been described due to stimulation of this classic pathway. There is also a protective RAS pathway medicated by ACE2 which may be suppressed in COVID-19. This leads to overstimulation of the classic pathway with adverse cardiovascular and respiratory effects, hypercoagulation, endothelial dysfunction, inflammation and insulin resistance. We hypothesize that overreaction of the renin-angiotensin-aldosterone may account for the myriad of unusual biochemical and clinical abnormalities noted in patients infected with SARS-CoV-2.


Subject(s)
COVID-19/metabolism , Gene Expression Regulation , Inflammation/metabolism , Renin-Angiotensin System/physiology , Aged , Angiotensin-Converting Enzyme 2/metabolism , Blood Pressure , COVID-19/complications , COVID-19/virology , Cardiovascular Diseases/complications , Critical Illness , Cytokines/metabolism , Female , Humans , Insulin Resistance , Intensive Care Units , Male , Models, Theoretical , Obesity/complications , Pandemics , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/virology , SARS-CoV-2 , Thrombophilia/complications
20.
Korean J Anesthesiol ; 74(4): 350-354, 2021 08.
Article in English | MEDLINE | ID: covidwho-705874

ABSTRACT

BACKGROUND: Coronavirus disease (COVID-19)-associated coagulopathy is most often characterized by elevated D-dimer, interleukin-6, and plasma fibrinogen concentrations as well as hypercoagulability in thromboelastometry with increased clot firmness in the EXTEM, INTEM, and FIBTEM assays. Clinically, it manifests with a very high incidence of thrombosis, particularly in the pulmonary system, whereas bleeding complications are infrequent. CASE: Here, we describe two critically ill patients with COVID-19 admitted to our intensive care unit demonstrating different thromboelastometry and biomarker patterns. One patient presented with hypercoagulability and the other patient with hypocoagulability and fibrinolysis shutdown in thromboelastometry. The pathophysiology and the potential impact on treatment options are discussed. CONCLUSIONS: A combination of biomarkers and thromboelastometry results can be helpful in the future to decide which therapeutic strategy might be most appropriate for critically ill patients with COVID-19. This would be an important step to establish precision medicine in this high-risk patient population.


Subject(s)
Blood Coagulation Disorders/complications , Blood Coagulation Disorders/diagnosis , COVID-19/complications , Thrombelastography/methods , Thrombophilia/complications , Thrombophilia/diagnosis , Aged , Blood Coagulation Disorders/pathology , Fatal Outcome , Female , Humans , Male , Middle Aged , SARS-CoV-2 , Thrombophilia/pathology
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