Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 161
Filter
1.
Clinical and Experimental Dermatology ; 47(5):982-983, 2022.
Article in English | EMBASE | ID: covidwho-1822048
2.
Hemato ; 3(1):111, 2022.
Article in English | ProQuest Central | ID: covidwho-1818069

ABSTRACT

Background. Hypercoagulable state and endothelial cell activation are common alterations in patients with COVID-19. Nevertheless, the hypothesis of persistent hypercoagulability and endothelial cell activation following recovery from COVID-19 remains an unresolved issue. Objectives. To investigate the persistence of endothelial cell activation and hypercoagulability after recovery from COVID-19. Patients/Methods. COVID-19 survivors (n = 208) and 30 healthy individuals were enrolled in this study. The following biomarkers were measured: procoagulant phospholipid-dependent clotting time (PPL-ct), D-Dimer, fibrin monomers (FM), free Tissue factor pathway inhibitor (free-TFP)I, heparinase, and soluble thrombomodulin (sTM). Antibodies against SARS-CoV-2 (IgG and IgA) were also measured. Results. The median interval between symptom onset and screening for SARS-CoV-2 antibodies was 62 days (IQR = 22 days). Survivors showed significantly higher levels of D-Dimers, FM, TFPI, and heparanase as compared to that of the control group. Survivors had significantly shorter PPL-ct. Elevated D-dimer was associated with older age. Elevated FM was associated with female gender. Elevated heparanase was independently associated with male gender. Decreased Procoag-PPL clotting time was associated with female gender. One out of four of COVID-19 survivors showed increase at least one biomarker of endothelial cell activation or hypercoagulability. Conclusions. Two months after onset of COVID-19, a significant activation of endothelial cells and in vivo thrombin generation persists in at least one out of four survivors of COVID-19. The clinical relevance of these biomarkers in the diagnosis and follow-up of patients with long COVID-19 merits to be evaluated in a prospective clinical study.

3.
Clinical Neurosurgery ; 67(SUPPL 1):131, 2020.
Article in English | EMBASE | ID: covidwho-1816190

ABSTRACT

INTRODUCTION: Covid 19 infections has been shown to be associated with a range of thromboembolic disease that has implications for the neuro-endovascular management of large vessel occlusions. METHODS: Five consecutive Covid-19 positive patients presented with large vessel occlusions to our institution. Covid-19 testing was performed using nasal swab. All thrombectomy cases was performed under general endotracheal anesthesia using a stent-aspiration combination as primary thrombectomy technique. The technical details of each case and the angiographic outcome are described. Routine labs including D-dimer, platelet count, coagulation panel (aPTT, INR), Interleukin 6 (IL-6), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) were evaluated in all patients. Rotational thrombelastography (ROTEM) was performed on the patients' blood samples to assess real-time clot formation/dissolution properties. RESULTS: Four patients had anterior circulation large vessel occlusions and one patient had both anterior and posterior circulation occlusions. Mean age was 52.8 years and 80% were males. TICI 3 revascularization was achieved in one patient, TICI 2B achieved in two patients and TICI 2A in two patients. In our cohort, patients were on average 52.8 years old and presented with a median NIHSS of 27. All our patients had very proximal occlusions. Three patients presented with intra-cranial ICA occlusions. Two patients presented with a tandem carotid bulb thrombus in conjunction with an intracranial vessel occlusion. One patient had an ICA terminus occlusion with a concomitant basilar occlusion. Second, the intravascular clots in all our patients were prone to fragment and migrate into both new vascular territories and into distal downstream vasculature. Distal emboli into a different territory (anterior cerebral artery occlusion) was seen in two two of our five patients (40%) and distal emboli into a downstream territory was seen in all five patients (100%). An average of 2.7 pstent-retriever passes was needed to achieve a final TICI revascularization of IIb or better. CONCLUSION: Covid-19 patients are predisposed to a hypercoagulable state. When presenting with large vessel occlusions, these patients present unique challenges that make successful revascularization difficult.

4.
Int Med Case Rep J ; 14: 519-522, 2021.
Article in English | MEDLINE | ID: covidwho-1808852

ABSTRACT

BACKGROUND: Deep vein thrombosis (DVT) is commonly identified and diagnosed in the emergency department. Factors including sedentary life (immobility), pregnancy in women, cancer, postoperation, admission to ICU, smoking, and obesity are identified risks for thrombosis development. We report a case of a 35-year-old man who presented to the emergency department developing left lower leg swelling and pain, low-grade fever, and headache after he was treated and discharged, cured of severe COVID-19. Then venous and arterial Doppler ultrasound of the lower leg revealed dilated, absent flow and luminal thrombus in the distal popliteal, anterior and posterior tibial veins and perforator vessels were diagnosed as leg DVT. CONCLUSION: DVT is a hematological emergency that needs serious consideration in prevention as well early diagnosis in patients with possible risk factors. This case report aims to arouse the clinician's awareness of the occurrence of deep vein thrombosis during and after COVID-19.

5.
American Journal of Blood Research ; 12(1):43-53, 2022.
Article in English | EMBASE | ID: covidwho-1798258

ABSTRACT

Coronavirus disease 2019 (COVID-19) is caused by pathogenic and highly transmissible Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which is a single stranded RNA virus. It rapidly emerged from an epidemic to a global pandemic form spreading in alarming levels. The pathogenesis involving spike protein which is present on the viral surface, plays a key role in host attachment and penetration. SARS-CoV-2 infection significantly affects respiratory system, but may involve other systems including haematopoietic system and homeostasis. Aim of the review article is to discuss spectrum of haematological changes in the blood counts, coagulation, peripheral blood and bone marrow in COVID-19 for complete understanding the disease process, the knowledge of which is helpful in early diagnosis and management of these patients. An extensive immune profiling of B and T cell population with analysis of spectrum of immune changes during the period of infection were also discussed. In COVID-19, changes in laboratory parameters and hematologic abnormalities have been reported and its association with early diagnosis, disease prognosis and severity has been repeatedly discussed in the literature. Changes in laboratory investigations help in risk stratification and early intervention. The most common laboratory finding in COVID-19 is lymphopenia. COVID-19 patients presented with coagulopathy is at high risk of morbidity and mortality. In severe COVID-19 patients, bone marrow aspirate shows histiocytic proliferation with hemophagocytosis. To understand the correlations between immune responses and severity of COVID-19, immune profiling of B and T cell population was compared with extensive clinical data. A deep understanding of the laboratory findings and haematological abnormalities associated with SARS-CoV-2 infection would help to raise disease suspicion in absence of Real time polymerase chain reaction or antibody results. Also the blood counts along with the morphological changes in peripheral blood would be helpful in prompt screening, diagnosis, prognosis and management of COVID-19 patients.

6.
World J Crit Care Med ; 11(2):92-101, 2022.
Article in English | PubMed | ID: covidwho-1791996

ABSTRACT

BACKGROUND: Since December 2019, an outbreak of pneumonia caused by severe acute respiratory syndrome - coronavirus-2 (SARS-CoV-2) has led to a life-threatening ongoing pandemic worldwide. A retrospective study by Chow et al showed aspirin use was associated with decreased intensive care unit (ICU) admissions in hospitalized coronavirus disease 2019 (COVID-19) patients. Recently, the RECOVERY TRIAL showed no associated reductions in the 28-d mortality or the progression to mechanical ventilation of such patients. With these conflicting findings, our study was aimed at evaluating the impact of daily aspirin intake on the outcome of COVID-19 patients. AIM: To study was aimed at evaluating the impact of daily aspirin intake on the outcome of COVID-19 patients. METHODS: This retrospective cohort study was conducted on 125 COVID-19 positive patients. Subgroup analysis to evaluate the association of demographics and comorbidities was undertaken. The impact of chronic aspirin use was assessed on the survival outcomes, need for mechanical ventilation, and progression to ICU. Variables were evaluated using the chi-square test and multinomial logistic regression analysis. RESULTS: 125 patients were studied, 30.40% were on daily aspirin, and 69.60% were not. Cross-tabulation of the clinical parameters showed that hypertension (P = 0.004), hyperlipidemia (0.016), and diabetes mellitus (P = 0.022) were significantly associated with aspirin intake. Regression analysis for progression to the ICU, need for mechanical ventilation and survival outcomes against daily aspirin intake showed no statistical significance. CONCLUSION: Our study suggests that daily aspirin intake has no protective impact on COVID-19 illness-associated survival outcomes, mechanical ventilation, or progression to ICU level of care.

7.
Indian J Med Res ; 2022 Apr 14.
Article in English | MEDLINE | ID: covidwho-1789528

ABSTRACT

Background & objectives: Autopsy study has been considered the gold standard method for studying the effects of any disease on the body. Since COVID-19 is a novel disease, autopsy is crucial to understand its pathophysiology. This study was conducted to analyze the microscopic and macroscopic findings of various organs in COVID-19 and to associate those findings with clinical observations and laboratory findings. Methods: Conventional invasive autopsies were performed on 33 patients with COVID-19 from September 7, 2020 to December 23, 2020. All the organs were removed by routine dissection techniques and preserved in 10 per cent formalin. The tissues were processed and stained according to standard practices using haematoxylin-eosin (H & E) and periodic acid-schiff (PAS) stain. Results: The study included 28 males and 5 females with a median age of 61 yr (range 30-90 yr). Massive pulmonary oedema and thrombi in the lungs were the characteristic features macroscopically. On microscopic examination, diffuse alveolar damage in the exudative/proliferative phase was found in 29 (87.88%) cases. Among the other notable microscopic findings were bronchopneumonia and lung abscesses due to secondary bacterial infection (n=17, 51.52%), acute tubular injury (n=21, 63.64%) and thrombi in the lungs, heart, and kidneys. Interpretation & conclusions: COVID-19 primarily affected the respiratory and the renal systems in the vast majority of severely affected patients in our study. We also found signs of hypercoagulability, as evidenced by widespread thrombi in multiple organs, along with a raised d-dimer level and a hyperinflammatory state manifested by elevated inflammatory markers. Our autopsy findings and altered laboratory investigations support the role of immune-mediated cellular injury along with direct virus-mediated cellular damage.

8.
World Journal of Gastroenterology ; 28(11):1102-1112, 2022.
Article in English | EMBASE | ID: covidwho-1780095

ABSTRACT

Coronavirus disease 2019 (COVID-19) is, at present, one of the most relevant global health problems. In the literature hepatic alterations have been described in COVID-19 patients, and they are mainly represented by worsening of underlying chronic liver disease leading to hepatic decompensation and liver failure with higher mortality. Several potential mechanisms used by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to cause liver damage have been hypothesized. COVID-19 primary liver injury is less common than secondary liver injury. Most of the available data demonstrate how liver damage in SARSCoV-2 infection is likely due to systemic inflammation, and it is less likely mediated by a cytopathic effect directed on liver cells. Moreover, liver alterations could be caused by hypoxic injury and drugs (antibiotics and non-steroidal anti-inflammatory drugs, remdesivir, tocilizumab, tofacitinib and dexamethasone). SARS-CoV-2 infection can induce multiple vascular district atherothrombosis by affecting simultaneously cerebral, coronary and peripheral vascular beds. Data in the literature highlight how the virus triggers an exaggerated immune response, which added to the cytopathic effect of the virus can induce endothelial damage and a prothrombotic dysregulation of hemostasis. This leads to a higher incidence of symptomatic and confirmed venous thrombosis and of pulmonary embolisms, especially in central, lobar or segmental pulmonary arteries, in COVID-19. There are currently fewer data for arterial thrombosis, while myocardial injury was identified in 7%-17% of patients hospitalized with SARS-CoV-2 infection and 22%-31% in the intensive care unit setting. Available data also revealed a higher occurrence of stroke and more serious forms of peripheral arterial disease in COVID-19 patients. Hemostasis dysregulation is observed during the COVID-19 course. Lower platelet count, mildly increased prothrombin time and increased D-dimer are typical laboratory features of patients with severe SARS-CoV-2 infection, described as “COVID-19 associated coagulopathy.” These alterations are correlated to poor outcomes. Moreover, patients with severe SARS-CoV-2 infection are characterized by high levels of von Willebrand factor with subsequent ADAMTS13 deficiency and impaired fibrinolysis. Platelet hyperreactivity, hypercoagulability and hypofibrinolysis during SARS-CoV-2 infection induce a pathological state named as “immuno-thromboinflammation.” Finally, liver dysfunction and coagulopathy are often observed at the same time in patients with COVID-19. The hypothesis that liver dysfunction could be mediated by microvascular thrombosis has been supported by postmortem findings and extensive vascular portal and sinusoidal thrombosis observation. Other evidence has shown a correlation between coagulation and liver damage in COVID-19, underlined by the transaminase association with coagulopathy, identified through laboratory markers such as prothrombin time, international normalized ratio, fibrinogen, D-dimer, fibrin/fibrinogen degradation products and platelet count. Other possible mechanisms like immunogenesis of COVID-19 damage or massive pericyte activation with consequent vessel wall fibrosis have been suggested.

10.
J Hematol ; 11(1): 40-44, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1771849

ABSTRACT

A main feature of coronavirus disease 2019 (COVID-19) pathogenesis is the high frequency of thrombosis, predominantly pulmonary embolism (PE). Anticoagulation therapy is a crucial part of the management. Heparin use for anticoagulation could increase the risk of heparin-induced thrombocytopenia (HIT), a potentially fatal complication that presents with thrombocytopenia with or without thrombosis. We present a 69-year-old unvaccinated female patient with severe COVID-19 pneumonia. Initial laboratory investigation was significant for thrombocytopenia and low D-dimer levels. She was initially started on enoxaparin followed by unfractionated heparin. On hospital day 8, she developed left facial droop and dysarthria and was found to have non-occlusive thrombus in proximal middle cerebral artery as well as bilateral pulmonary emboli. She received intravenous thrombolysis followed by heparin infusion. On day 13 of hospitalization, platelet count dropped from 120,000/mm3 to 43,000/mm3, raising suspicion of HIT. Heparin was stopped and fondaparinux was started. After 3 days, HIT antibody testing returned positive, then a positive serotonin release assay confirmed the diagnosis. On discharge, she was transitioned to apixaban to complete 3 months of anticoagulation for provoked PE. This case represents the diagnostic challenge of HIT in COVID-19 patients. Thrombocytopenia after heparin infusion should raise clinical suspicion of HIT, which allows appropriate discontinuation of heparin products and initiation of alternative anticoagulants to limit devastating complications. To our knowledge, this is the first case report of a COVID-19 patient presenting with venous thrombosis as well as arterial thrombotic event in the context of underlying HIT.

11.
Cureus ; 14(3): e22796, 2022 Mar.
Article in English | MEDLINE | ID: covidwho-1753940

ABSTRACT

Calciphylaxis is a rare dermatologic condition that is primarily associated with end-stage renal disease (ESRD). Nonuremic calciphylaxis has been reported in patients with autoimmune disorders such as systemic lupus erythematosus and other hypercoagulable states such as anti-phospholipid syndrome. New research throughout the COVID-19 pandemic has shown an increased inflammatory and coagulopathic complication of COVID-19. We present a case of a patient with nonuremic calciphylaxis following treatment for severe COVID-19 and no known cause of hypercoagulability. A 40-year-old Caucasian female with a history of recent COVID-19 infection requiring hospitalization, hypertension, alcohol abuse, anxiety, and one prior spontaneous miscarriage presented to the hospital with bilateral lower extremity wounds. The wounds were seen to have necrosis and eschar formation, as well as blackened mottled skin, and were extremely painful to the patient. The initial lesions were on the anterior thighs bilaterally and spread laterally and to the lower back. Initial autoimmune workup was non-specific, and biopsy confirmed calciphylaxis. Calciphylaxis is a known dermatologic disease that has high mortality and morbidity, but it is usually associated with ESRD. Some cases have been reported for autoimmune or hypercoagulable states. The disease presents with non-healing, painful skin ulcers that are at a high risk of infection and have poor healing. The case presented shows biopsy-confirmed calciphylaxis in the absence of known etiologies, and we hypothesize that it is due to COVID-19 or COVID-19 aggravating an underlying but unidentified hypercoagulable condition.

12.
Cureus ; 14(2): e22155, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1753936

ABSTRACT

We report a case of atherothrombotic microembolism in a 53-year-old male diagnosed with coronavirus disease 2019 (COVID-19) prior to hospital admission. Upon admission, Day 9 after diagnosis, he presented with COVID-19 pneumonia and mottling of the lower extremities. The patient was treated with anticoagulation therapy. The lower extremity angiogram showed a patent posterior tibial artery and a patent peroneal artery. Despite initial anticoagulation therapy, toe and transmetatarsal amputations were required. However, a below-the-knee amputation was subsequently required due to continued worsening and extension of mottling. Unfortunately, the patient ultimately expired from cardiopulmonary arrest before any other surgical intervention could be done.

13.
Clinics (Sao Paulo) ; 77: 100012, 2022.
Article in English | MEDLINE | ID: covidwho-1748123

ABSTRACT

There is increasing evidence that COVID-19 can be associated with ischemic stroke (COVID-stroke). The frequency and pathogenesis of COVID-stroke, however, remains largely unknown. This narrative review aimed at summarizing and discussing current knowledge about frequency and pathogenesis of COVID-stroke in 455 patients collected from the literature. COVID-stroke occurs in all age groups and predominantly in males. The anterior circulation is more frequently affected than the posterior circulation. COVID-stroke is most frequently embolic. The severity of COVID-stroke ranges from NIHSS 3 to 32. Cardiovascular risk factors are highly prevalent in patients with COVID-stroke. COVID-stroke occurs simultaneously with the onset of pulmonary manifestations or up to 40 days later. Clinical manifestations of COVID-19 are most frequently mild or even absent. The majority of patients with COVID-stroke achieve complete or partial recovery, but in one-quarter of patients, the outcome is fatal. In conclusion, the frequency of ischemic stroke has not increased since the outbreak of the SARS-CoV-2 pandemic. COVID-stroke predominantly affects males and the anterior circulation. COVID-stroke is multifactorial but predominantly embolic and more frequently attributable to cardiovascular risk factors than to coagulopathy.


Subject(s)
COVID-19 , Ischemic Stroke , Stroke , COVID-19/complications , Humans , Male , Pandemics , SARS-CoV-2 , Stroke/complications
14.
Open Forum Infectious Diseases ; 8(SUPPL 1):S277, 2021.
Article in English | EMBASE | ID: covidwho-1746648

ABSTRACT

Background. COVID 19 is associated with a hypercoagulable state with cytokine storm syndrome and thrombocytopenia leading to complications across various systems. COVID-19 infection, its treatment, resultant immunosuppression, and pre-existing comorbidities have made patients vulnerable to secondary infections Methods. We systematically reviewed COVID-19 cases between Jan to May 2021 for pulmonary and extrapulmonary complications. Patients with recent COVID-19 vaccination and neurological symptoms were also included. Results. Neurological complications: Neurological complications include ischemic and haemorrhagic strokes. Other complications are encephalopathy, encephalitis, Guillain-Barré syndrome, acute hemorrhagic necrotizing encephalopathy. Demyelination and radiculopathies are seen as post vaccination complications. Mucormycosis: Unprecedented high rate of invasive fungal sinusitis in association with COVID -19 is reported from the Indian subcontinent. This has a propensity for intra orbital and intracranial extension. COVID -19 associated coagulopathy: COVID -19 is a pro-inflammatory hypercoagulable state. Pulmonary thromboembolism, deep venous thrombosis and catheter related thrombosis are well documented. Cardiac complications: Cardiac manifestations include Myocardial Injury with non-obstructed coronary arteries (MINOCA), myocarditis, myocardial ischemia, cardiomyopathy. Pulmonary complications and sequelae of COVID -19: Progression of lung injury to ARDS during the initial phase and fibrosis of parenchyma in the recovery phase. Spontaneous pneumomediastinum, pneumatoceles and pneumothorax and secondary infections are identified in our study. COVID- 19 associated gastrointestinal complications: Patients evaluated for renal colic, pancreatitis, cholecystitis showed, ground glass opacities or subpleural bands in typical Covid-19 distribution. COVID-19 may lead of acute kidney and bowel injury due to arterial thrombosis. COVID - 19 associated myonecrosis: Ischemia of the small caliber vessels may result in myonecrosis. Conclusion. Awareness of these unusual manifestations will facilitate an early diagnosis, improve management and help reduce morbidity and mortality.

15.
Journal of the Hong Kong College of Cardiology ; 28(2):105, 2020.
Article in English | EMBASE | ID: covidwho-1743807

ABSTRACT

Objectives: To have a comprehensive review on effects of novel coronavirus on heart. Methods: review article. Results: The novel coronavirus may affect cardiac tissue via three main mechanisms: 1-direct myocardial injury and myocarditis caused by the virus, 2-hyper-inflammation and immunopathology, and 3-respiratory failure, acute respiratory distress syndrome, and effects of hypoxemia on cardiac tissue. In a large number of patients, all three mechanisms are involved. Hypercoagulability is a mechanism for coronary artery stenosis and acute coronary syndrome or myocardial infarction. Also, blood pressure abnormalities, either hypertension or hypotension are frequent in severely ill patients. A high proportion of critically ill patients develop arrhythmias. Arrhythmias may arise due to hypoxemia, metabolic derangements, systemic inflammation, or myocarditis. In a postmortem study, real-time polymerase chain reaction analyses on heart tissue detected the viral genome in nearly one third of patients. Interleukin-6, serum ferritin, brain natriuretic peptide, and high sensitivity cardiac troponin are among the various biomarkers elevated during the course of the disease. It has been shown that as the disease severity increases and in the 3rd stage of the disease-host response-inflammatory and cardiac markers show elevations. Cardiac involvement ad elevated cardiac biomarkers are prominent features in COVID-19 and associated with a worse prognosis and increased mortality. In a survey in Wuhan, 40% of deaths were attributed to myocardial damage or heart failure, alone or in combination with respiratory failure. In autopsies, mononuclear infiltrates of macrophages and CD4+ T cells have been shown in areas of cardiac necrosis. It has been proposed that acute cardiac involvement is a stronger risk factor for increased mortality than age, diabetes mellitus, chronic pulmonary disease, or even history of cardiovascular disease. Since the virus is new-emerging, we do not know much about its long term consequences. So, its effects on heart in the convalescent and chronic phases are not well-known. Delayed myocarditis, cardiac arrest, hyperlipidemia and pulmonary fibrosis are possible long term consequences of the disease. Conclusion: We have to be aware of cardiac consequences of COVID-19 to manage the disease optimally.

16.
Cureus ; 14(2): e22496, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1744639

ABSTRACT

A 46-year-old male with a history of SARS-CoV-2 infection one month ago presented to the hospital due to acute onset left flank pain. He was found to have an acute left renal embolic infarction from a large 15mm ascending aortic thrombus, which may have formed due to a transient hypercoagulable state from his recent SARS-CoV-2 infection along with tobacco use. He was medically managed with anticoagulation for six months. Subsequent imaging after three months of therapeutic anticoagulation showed complete resolution of the ascending aortic thrombus.

17.
Revista Mexicana de Angiologia ; 48(3):70-76, 2020.
Article in Spanish | EMBASE | ID: covidwho-1737534

ABSTRACT

Since the beginning of the COVID-19 pandemic there has been many reports regarding venous and arterial thrombotic complications in patients infected with the SARS-CoV-2 virus, however the exact mechanisms for patients with COVID-19 to develop hypercoagulability states are still unknown. Prophylactic anticoagulation is considered a fundamental strategy to avoid the aforementioned complications. The objective of the present review is to guide the treatment of thromboembolic venous disease in hospitalized patients infected with SARS-CoV-2.The present article aims to review on specific recommendations of thromboembolic prophylaxis for the treatment of venous thrombotic disease in COVID-19 hospitalized patients. Hence, we differentiate between critically and non-critically ill patients as well as the duration of treatment and the recommended strategies when discharging these patients.There is still uncertainty regarding treatment options for the aforementioned complications, until an effective strategy is found, international recommendations are our best option to follow.

18.
Blood ; 138:3207, 2021.
Article in English | EMBASE | ID: covidwho-1736286

ABSTRACT

Background: COVID-19 has been associated with hypercoagulability, endothelial cell injury and frequent thrombotic complications resulting both from direct effects of the virus on the endothelium and from the ‘cytokine storm’ resulting from the host's immune response. Since the COVID-19 vaccines have been shown to effectively prevent symptomatic infection including hospital admissions and severe disease, the risk of COVID-19-related thrombosis should be expected to (almost) disappear in vaccinated individuals. However, some rare cases of venous thrombosis have been reported in individuals vaccinated with mRNA vaccines. Thus, there is a sharp contrast between the clinical or experimental data reported in the literature on COVID-19 and on the rare thrombotic events observed after the vaccination with these vaccines. This phenomenon raised some scepticism of even some fear about the safety of these vaccines which could compromise the adhesion of the citizens in the vaccination program. Aims: We conducted a prospective observational study, to explore the impact of vaccination with the BNT162b2 (Pfizer/BioNTech) on blood hypercoagulability and endothelial cell activation and to investigate if this is modified by the presence of active cancer. Methods: In total 229 subjects were prospectively included in the study from April to June 2021. Subjects were stratified in three predefined groups: 127 vaccinated patients with active cancer (VOnco group), 72 vaccinated health care workers (VHcw group) and 30 non vaccinated health individuals (Control group). Blood samples were obtained 2 days after the administration of the first dose of BNT162b2 vaccine and collected in Vacutainer® tubes (0.109 mol/L trisodium citrate). Platelet poor plasma (PPP) was prepared by double centrifugation at 2000 g for 20 minutes at room temperature and plasma aliquots were stored at -80°C until assayed. Samples of PPP were assessed for thrombin generation (TG) with PPP-Reagent® (Thrombogram-Thrombinoscope assay with PPP-Reagent®TF 5pM), E-selectin, D-dimers, (D-Di), Tissue Factor (TFa), procoagulant phospholipid-dependent clotting time (Procag-PPL) and von Willebrand factor (vWF), thrombomodulin (TM), tissue factor pathway inhibitor (TFPI), and platelet factor 4 (PF4). All assays were from Diagnostica Stago (France). The upper and lower normal limits (UNL and LNL) for each biomarker were calculated by the mean±2SD for the control group. Results: All vaccinated subjects showed significantly increased levels of PF4 (71% >UNL, p<0.001), D-Dimers (74% >UNL, p<0.01), vWF (60% >UNL, p<0.01), FVIII (62% >UNL, p<0.01) and shorter Procoag-PPL clotting time (96% <LNL, p<0.001), as compared to controls. Thrombin generation showed significantly higher Peak (60% >UNL, p<0.01), ETP (38% >UNL, p<0.01) and MRI (66% >UNL, p<0.01) but no differences in lag-time in vaccinated subjects as compared to the control group. Vaccinated subjects did not show any increase at the levels of TFa, TFPI, TM and E-selectin in comparison with the control group. The studied biomarkers were not significantly different between the VOnco and VHcw groups. Conclusion: The ROADMAP-COVID-19-Vaccine study shows that administration of the first dose of the BNT162b2 vaccine induced significant platelet activation documented by shorter Procoag-PPL associated with increased levels of PF4. Plasma hypercoagulability was less frequent in vaccinated individuals whereas there was no evidence of significant endothelial cells activation after vaccination. Interestingly, the presence of active cancer was not associated with an enhancement of platelet activation, hypercoagulability, or endothelial cell activation after the vaccination. Probably, the generated antibodies against the spike protein or lead to platelet activation in a FcyRIIa dependent manner that results in PF4 release. The implication of the mild inflammatory reaction triggered by the vaccination could be another possible pathway leading to platelet activation. Nevertheless, vaccination does not provoke endothelial activation even n patients with cancer. The findings of the ROADMAP-COVID-19-Vaccine study support the concept administration of mRNA based vaccines does not directly cause a systematic hypercoagulability. Disclosures: Gligorov: Roche-Genentech: Research Funding;Novartis: Research Funding;Onxeo: Research Funding;Daichi: Research Funding;MSD: Research Funding;Eisai: Research Funding;Genomic Heatlh: Research Funding;Ipsen: Research Funding;Macrogenics: Research Funding;Pfizer: Research Funding. Terpos: Novartis: Honoraria;Janssen: Consultancy, Honoraria, Research Funding;Genesis: Consultancy, Honoraria, Research Funding;Celgene: Consultancy, Honoraria, Research Funding;BMS: Honoraria;Amgen: Consultancy, Honoraria, Research Funding;Takeda: Consultancy, Honoraria, Research Funding;Sanofi: Consultancy, Honoraria, Research Funding;GSK: Honoraria, Research Funding. Dimopoulos: Amgen: Honoraria;BMS: Honoraria;Janssen: Honoraria;Beigene: Honoraria;Takeda: Honoraria.

19.
Diagnostics (Basel) ; 12(3)2022 Feb 24.
Article in English | MEDLINE | ID: covidwho-1736850

ABSTRACT

Hemostasis is a finely tuned process of which dysregulation can lead either to bleeding or thrombotic complications. The latter is often caused by the hypercoagulable state as it is also seen in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, i.e., in COVID-19 patients. COVID-19 patients requiring hospitalization often suffer from thrombotic events that could not be predicted using routine coagulation assays. Recently, several studies have reported ROtational ThromboElastoMetry (ROTEM) as a promising tool to predict outcomes in COVID-19 patients. In this review we give an overview of ROTEM with a particular focus on the interpretation of the symmetrical clot formation curve in relation to coagulopathy in COVID-19 patients. Furthermore, we have introduced new parameters that might help to better distinguish between COVID-19 patients and outcomes.

20.
Annals of Emergency Medicine ; 78(4):S32, 2021.
Article in English | EMBASE | ID: covidwho-1734168

ABSTRACT

Study Objectives: The primary objective of the study was to use thromboelastography (TEG) to evaluate coagulation dynamics in patients hospitalized with COVID-19 and to investigate TEG as a predictive tool for clinical course of infection. Methods: Adult patients admitted to Naval Medical Center Portsmouth with the diagnosis of SARS-CoV-2 were eligible for enrollment. TEG was performed on admission and trended daily with other laboratory tests through the hospitalization. Charts were reviewed for demographic, medical history, daily progress notes, clinical status, lab values, and anticoagulation medication use for each patient. Treatment teams were blinded to TEG values. Results: A total of 53 patients were enrolled, with three patients having two separate admissions. There were 31 males and 22 females with a mean age of 48. The preponderance of individual TEG components showed progression towards hypercoagulation as days of illness progressed, with 92% of subjects having at least one TEG value outside the reference range, even with the vast majority of patients receiving either therapeutic or prophylactic anticoagulants. The maximum amplitude (MA) and TEG coagulation indexes (CI) best correlated with day of illness (r = 0.45 and r = 0.32, respectively). Peak CI also correlated with length of hospital stay (r = 0.38). The majority (91%) remained hypercoagulable on discharge. Conclusions: The use of TEG measurements in those hospitalized at NMCP with COVID-19 infection confirms the hypercoagulable state previously reported in COVID-19 patients. It may have a role as a tool to predict clinical courses or to direct anticoagulation or antiplatelet therapy to reduce morbidity and mortality.

SELECTION OF CITATIONS
SEARCH DETAIL