Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 280
Filter
1.
Eur Rev Med Pharmacol Sci ; 26(9): 3399-3405, 2022 May.
Article in English | MEDLINE | ID: covidwho-1856627

ABSTRACT

OBJECTIVE: COVID-19 patients have been shown to be hypercoagulable, increasing the risk for thromboembolic events. The kinetics of the blood coagulation process were monitored daily throughout hospitalization in COVID-19 positive patients. PATIENTS AND METHODS: Thromboelastography (TEG) was used to assess blood coagulation in 48 adult patients hospitalized for COVID-19 in this prospective cohort study. Clinical risk was assessed via National Early Warning Scores (NEWS) for each day of hospitalization. RESULTS: During hospitalization, 98% of patients had one or more procoagulable TEG result. Thromboelastography results remained prothrombotic upon discharge in 80% of patients. NEWS significantly decreased by discharge compared to the peak scores. CONCLUSIONS: Overall, patients were discharged from the hospital with significant clinical improvement, but without abnormal TEG results returning to a normal range. All patients in our study survived and few had thromboembolic events, so if and for how long these patients remain at risk for future complications warrants further investigation.


Subject(s)
COVID-19 , Thromboembolism , Thrombophilia , Adult , Blood Coagulation , Humans , Prospective Studies , Thrombelastography/adverse effects , Thrombelastography/methods , Thrombophilia/etiology
2.
Acta Haematol ; 145(3): 282-296, 2022.
Article in English | MEDLINE | ID: covidwho-1832782

ABSTRACT

Coronavirus disease 2019 (COVID-19) has emerged as a pandemic at the end of 2019 and continues to exert an unfavorable worldwide health impact on a large proportion of the population. A remarkable feature of COVID-19 is the precipitation of a hypercoagulable state, mainly in severe cases, leading to micro- and macrothrombosis, respiratory failure, and death. Despite the implementation of various therapeutic regimes, including anticoagulants, a large number of patients suffer from such serious complications. This review aims to describe the current knowledge on the pathophysiology of the coagulation mechanism in COVID-19. We describe the interplay between three important mediators of the disease and how this may lead to a hyperinflammatory and prothrombotic state that affects outcome, namely, the endothelium, the immune system, and the coagulation system. In line with the hypercoagulability state during COVID-19, we further review on the rare but severe vaccine-induced thrombotic thrombocytopenia. We also summarize and comment on available anticoagulant treatment options and include suggestions for some future treatment considerations for COVID-19 anticoagulation therapy.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Thrombophilia , Anticoagulants/therapeutic use , Blood Coagulation Disorders/etiology , Blood Coagulation Disorders/therapy , COVID-19/complications , Humans , Pandemics , SARS-CoV-2 , Thrombophilia/drug therapy , Thrombophilia/etiology
3.
Anesthesiology ; 137(1): 13-14, 2022 Jul 01.
Article in English | MEDLINE | ID: covidwho-1831375
4.
BMC Nephrol ; 23(1): 175, 2022 05 06.
Article in English | MEDLINE | ID: covidwho-1822173

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is identified as the pneumonia and acute respiratory distress syndrome caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2). The intravascular thrombotic phenomena related to the COVID-19 are emerging as an important complication that contribute to significant mortality. CASE PRESENTATION: We present a 62-year-old man with severe COVID-19 and type 2 diabetes. After symptomatic and supportive treatment, the respiratory function was gradually improved. However, the patient suddenly developed abdominal pain, and the enhanced CT scan revealed renal artery thrombosis. Given the risk of surgery and the duration of the disease, clopidogrel and heparin sodium were included in the subsequent treatment. The patient recovered and remained stable upon follow-up. CONCLUSIONS: Thrombosis is at a high risk in patients with severe COVID-19 pneumonia because of hypercoagulable state, blood stasis and endothelial injury. Thrombotic events caused by hypercoagulation status secondary to vascular endothelial injury deserves our attention. Because timely anticoagulation can reduce the risk of early complications, as illustrated in this case report.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Thrombophilia , Thrombosis , COVID-19/complications , Diabetes Mellitus, Type 2/complications , Humans , Male , Middle Aged , RNA, Viral , Renal Artery/diagnostic imaging , SARS-CoV-2 , Thrombosis/diagnostic imaging , Thrombosis/etiology
5.
Am J Hematol ; 97(7): 915-923, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1813455

ABSTRACT

Sustained hypercoagulability and endotheliopathy are present in convalescent COVID-19 patients for up to 4 months from recovery. The hemostatic, endothelial, and inflammatory profiles of 39 recovered COVID-19 patients were evaluated up to 16 months after recovery from COVID-19. These values were compared with a control group of healthy volunteers (n = 124). 39 patients (71.8% males, median age 43 years) were reviewed at a mean of 12.7 ± 3.6 months following recovery. One patient without cardiovascular risk factors had post COVID-19 acute ischaemic limb. Elevated D-dimer and Factor VIII levels above normal ranges were noted in 17.9% (7/39) and 48.7% (19/39) of patients respectively, with a higher median D-dimer 0.34 FEU µg/mL (IQR 0.28, 0.46) (p < .001) and Factor VIII 150% (IQR 171, 203) (p = .004), versus controls. Thrombin generation (Thromboscreen) showed a higher median endogenous thrombin potential (ETP) of 1352 nM*min (IQR 1152, 1490) (p = .002) and a higher median peak height of 221.4 nM (IQR 170.2, 280.4) (p = 0.01) and delayed lag time 2.4 min (1.42-2.97) (p = 0.0002) versus controls. Raised vWF:Ag and ICAM-1 levels were observed in 17.9% (7/39) and 7.7% (3/39) of patients respectively, with a higher median VWF:Ag 117% (IQR 86, 154) (p = 0.02) and ICAM-1 54.1 ng/mL (IQR 43.8, 64.1) (p = .004) than controls. IL-6 was noted to be raised in 35.9% (14/39) of patients, with a higher median IL-6 of 1.5 pg/mL (IQR 0.6, 3.0) (p = 0.004) versus controls. Subgroup analysis stratifying patients by COVID-19 severity and COVID-19 vaccination preceding SARS-CoV-2 infection did not show statistically significant differences. Hypercoagulability, endothelial dysfunction, and inflammation are still detectable in some patients approximately 1 year after recovery from COVID-19.


Subject(s)
COVID-19 , Thrombophilia , Adult , COVID-19/complications , COVID-19 Vaccines , Factor VIII , Female , Humans , Inflammation , Intercellular Adhesion Molecule-1 , Male , SARS-CoV-2 , Thrombin , Thrombophilia/etiology , von Willebrand Factor
6.
Front Immunol ; 13: 862522, 2022.
Article in English | MEDLINE | ID: covidwho-1809404

ABSTRACT

Lung injury may persist during the recovery period of COVID-19 as shown through imaging, six-minute walk, and lung function tests. The pathophysiological mechanisms leading to long COVID have not been adequately explained. Our aim is to investigate the basis of pulmonary susceptibility during sequelae and the possibility that prothrombotic states may influence long-term pulmonary symptoms of COVID-19. The patient's lungs remain vulnerable during the recovery stage due to persistent shedding of the virus, the inflammatory environment, the prothrombotic state, and injury and subsequent repair of the blood-air barrier. The transformation of inflammation to proliferation and fibrosis, hypoxia-involved vascular remodeling, vascular endothelial cell damage, phosphatidylserine-involved hypercoagulability, and continuous changes in serological markers all contribute to post-discharge lung injury. Considering the important role of microthrombus and arteriovenous thrombus in the process of pulmonary functional lesions to organic lesions, we further study the possibility that prothrombotic states, including pulmonary vascular endothelial cell activation and hypercoagulability, may affect long-term pulmonary symptoms in long COVID. Early use of combined anticoagulant and antiplatelet therapy is a promising approach to reduce the incidence of pulmonary sequelae. Essentially, early treatment can block the occurrence of thrombotic events. Because impeded pulmonary circulation causes large pressure imbalances over the alveolar membrane leading to the infiltration of plasma into the alveolar cavity, inhibition of thrombotic events can prevent pulmonary hypertension, formation of lung hyaline membranes, and lung consolidation.


Subject(s)
COVID-19 , Lung Injury , Thrombophilia , Thrombosis , Aftercare , COVID-19/complications , Humans , Lung Injury/etiology , Patient Discharge , SARS-CoV-2 , Thrombophilia/etiology , Thrombosis/etiology
7.
Anesthesiology ; 137(1): 67-78, 2022 Jul 01.
Article in English | MEDLINE | ID: covidwho-1784403

ABSTRACT

BACKGROUND: COVID-19 causes hypercoagulability, but the association between coagulopathy and hypoxemia in critically ill patients has not been thoroughly explored. This study hypothesized that severity of coagulopathy would be associated with acute respiratory distress syndrome severity, major thrombotic events, and mortality in patients requiring intensive care unit-level care. METHODS: Viscoelastic testing by rotational thromboelastometry and coagulation factor biomarker analyses were performed in this prospective observational cohort study of critically ill COVID-19 patients from April 2020 to October 2020. Statistical analyses were performed to identify significant coagulopathic biomarkers such as fibrinolysis-inhibiting plasminogen activator inhibitor 1 and their associations with clinical outcomes such as mortality, extracorporeal membrane oxygenation requirement, occurrence of major thrombotic events, and severity of hypoxemia (arterial partial pressure of oxygen/fraction of inspired oxygen categorized into mild, moderate, and severe per the Berlin criteria). RESULTS: In total, 53 of 55 (96%) of the cohort required mechanical ventilation and 9 of 55 (16%) required extracorporeal membrane oxygenation. Extracorporeal membrane oxygenation-naïve patients demonstrated lysis indices at 30 min indicative of fibrinolytic suppression on rotational thromboelastometry. Survivors demonstrated fewer procoagulate acute phase reactants, such as microparticle-bound tissue factor levels (odds ratio, 0.14 [0.02, 0.99]; P = 0.049). Those who did not experience significant bleeding events had smaller changes in ADAMTS13 levels compared to those who did (odds ratio, 0.05 [0, 0.7]; P = 0.026). Elevations in plasminogen activator inhibitor 1 (odds ratio, 1.95 [1.21, 3.14]; P = 0.006), d-dimer (odds ratio, 3.52 [0.99, 12.48]; P = 0.05), and factor VIII (no clot, 1.15 ± 0.28 vs. clot, 1.42 ± 0.31; P = 0.003) were also demonstrated in extracorporeal membrane oxygenation-naïve patients who experienced major thrombotic events. Plasminogen activator inhibitor 1 levels were significantly elevated during periods of severe compared to mild and moderate acute respiratory distress syndrome (severe, 44.2 ± 14.9 ng/ml vs. mild, 31.8 ± 14.7 ng/ml and moderate, 33.1 ± 15.9 ng/ml; P = 0.029 and 0.039, respectively). CONCLUSIONS: Increased inflammatory and procoagulant markers such as plasminogen activator inhibitor 1, microparticle-bound tissue factor, and von Willebrand factor levels are associated with severe hypoxemia and major thrombotic events, implicating fibrinolytic suppression in the microcirculatory system and subsequent micro- and macrovascular thrombosis in severe COVID-19.


Subject(s)
Blood Coagulation Disorders , COVID-19 , Respiratory Distress Syndrome , Thrombophilia , Thrombosis , Blood Coagulation Disorders/complications , COVID-19/complications , Critical Illness , Fibrinolysis , Humans , Hypoxia/complications , Microcirculation , Oxygen , Plasminogen Activator Inhibitor 1 , Prospective Studies , Retrospective Studies , Thrombophilia/complications , Thromboplastin
8.
Ultrasound Obstet Gynecol ; 59(6): 813-822, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1763301

ABSTRACT

OBJECTIVES: To describe the placental pathology, fetal autopsy findings and clinical characteristics of pregnancies that resulted in stillbirth owing to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) placentitis, and to identify potential risk factors. METHODS: This was a prospective multicenter study of non-vaccinated pregnant women affected by coronavirus disease 2019 (COVID-19) in Greece from April 2020 to August 2021. A total of 165 placentas were examined histologically and six cases of stillbirth associated with SARS-CoV-2 placentitis were retrieved. Complete fetal autopsy was performed in three of these cases. Gross, histopathological, immunohistochemical, molecular and electron microscopy examinations were carried out in the stillbirth placentas and fetal organs. The histological findings of cases with SARS-CoV-2 placentitis were compared with those in 159 cases with maternal COVID-19 which resulted in a live birth. Regression analysis was used to identify predisposing risk factors for SARS-CoV-2 placentitis. RESULTS: The placentas of all six stillborn cases showed severe and extensive histological changes typical of SARS-CoV-2 placentitis, characterized by a combination of marked intervillositis with a mixed inflammatory infiltrate and massive perivillous fibrinoid deposition with trophoblast damage, associated with intensely positive immunostaining for SARS-CoV-2 spike protein, the presence of virions on electron microscopy and positive reverse-transcription polymerase chain reaction test of placental tissues. The histological lesions obliterated over 75% of the maternal intervillous space, accounting for intrauterine fetal death. Similar histological lesions affecting less than 25% of the placenta were observed in seven liveborn neonates, while the remaining 152 placentas of COVID-19-affected pregnancies with a live birth did not show these findings. Complete fetal autopsy showed evidence of an asphyctic mode of death without evidence of viral transmission to the fetus. The mothers had mild clinical symptoms or were asymptomatic, and the interval between maternal COVID-19 diagnosis and fetal death ranged from 3 to 15 days. Statistically significant predisposing factors for SARS-CoV-2 placentitis included thrombophilia and prenatally diagnosed fetal growth restriction (FGR). Multiple sclerosis was seen in one case. CONCLUSIONS: SARS-CoV-2 placentitis occurred uncommonly in COVID-19-affected pregnancies of non-vaccinated mothers and, when extensive, caused fetal demise, with no evidence of transplacental fetal infection. Thrombophilia and prenatally detected FGR emerged as independent predisposing factors for the potentially lethal SARS-CoV-2 placentitis. © 2022 International Society of Ultrasound in Obstetrics and Gynecology.


Subject(s)
COVID-19 , Chorioamnionitis , Pregnancy Complications, Infectious , Thrombophilia , COVID-19 Testing , Female , Fetal Death/etiology , Fetus/pathology , Humans , Infant, Newborn , Infectious Disease Transmission, Vertical , Placenta/pathology , Pregnancy , Pregnancy Complications, Infectious/diagnosis , Prospective Studies , Risk Factors , SARS-CoV-2 , Spike Glycoprotein, Coronavirus , Stillbirth/epidemiology , Thrombophilia/complications , Thrombophilia/pathology
9.
J Vasc Surg Venous Lymphat Disord ; 10(4): 811-817, 2022 Jul.
Article in English | MEDLINE | ID: covidwho-1757625

ABSTRACT

OBJECTIVE: The incidence of deep vein thrombosis (DVT) is increased in patients with coronavirus disease 2019 (COVID-19) and its presence is associated with worse outcomes. Ultrasound examination of patients with COVID-19 with a suspected DVT is challenging owing to concerns with disease transmission; the timely initiation of therapeutic anticoagulation is essential. This study aimed to identify patient factors associated with positive thrombus findings at ultrasound examination in patients with COVID-19 who underwent imaging for suspected DVT. METHODS: Patients who did not require intensive care unit treatment and who underwent ultrasound imaging for suspected DVT between March and December 2020 were included retrospectively. Patient demographics, comorbidities, modified Well's score, and d-dimer results on the day of ultrasound examination were recorded. Parameters for a higher likelihood of a positive DVT result were determined by comparing patients with confirmed DVT on ultrasound examination and patients with negative ultrasound findings. To determine a cut-off for d-dimer levels, a receiver operating characteristic curve was constructed. The sensitivity and specificity of the determined high-risk factors in the prediction of positive ultrasound results were calculated. RESULTS: A positive history for DVT (25% vs 4%; P < .001), thrombophilia (9% vs 2%; P = .048), immobilization (53% vs 23%; P = .001), and a Well's score ≥ 2 (50% vs 21%; P = .001) were more frequent in patients with DVT. The mean d-dimer levels were higher in patients with DVT (3871 ± 1805 vs 2075 ± 1543; P < .001). The presence of either thrombophilia or a d-dimer level of >2020 had a sensitivity of 93% and a specificity of 64%. The presence of either thrombophilia, a d-dimer level of >2020, or a Well's score of ≥2 had a sensitivity of 100% and a specificity of 51%. CONCLUSIONS: Patients with COVID-19 with a d-dimer of >2020, a positive history for thrombophilia, and a Well's score of ≥2 should undergo a timely ultrasound examination. The high risk of DVT should be remembered for all hospitalized patients with COVID-19.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Venous Thrombosis , Anticoagulants/therapeutic use , COVID-19/complications , Humans , Retrospective Studies , Thrombophilia/complications , Ultrasonography , Venous Thrombosis/diagnostic imaging , Venous Thrombosis/etiology
11.
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
13.
J Thromb Haemost ; 20(4): 1008-1014, 2022 04.
Article in English | MEDLINE | ID: covidwho-1662290

ABSTRACT

BACKGROUND: Hypercoagulability and endothelial dysfunction are hallmarks of coronavirus disease 2019 (COVID-19) and appear to predict disease severity. A high incidence of thrombosis despite thromboprophylaxis is reported in patients with moderate to severe COVID-19. Recent randomized clinical trials suggest that therapeutic-intensity heparin confers a survival benefit in moderate-severity COVID-19 compared to standard-intensity heparin, potentially by harnessing heparin-mediated endothelial-stabilizing and anti-inflammatory effects. OBJECTIVE: We hypothesized that patients with moderate-severity COVID-19 exhibit enhanced hypercoagulability despite standard-intensity thromboprophylaxis with low molecular weight heparin (LMWH) compared to non-COVID-19 hospitalized patients. METHODS: Patients with moderate COVID-19 and a control group (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]-negative hospitalized patients) receiving LMWH thromboprophylaxis were recruited. Markers of endothelial damage and plasma thrombin generation parameters were assessed. RESULTS: Tissue plasminogen activator levels were significantly increased in the COVID-19 group (8.3 ± 4.4 vs. 4.9 ± 2.4 ng/ml; P = .02) compared to non-COVID-19-hospitalized patients. Despite thromboprophylaxis, mean endogenous thrombin potential was significantly increased among COVID-19 patients (1929 ± 448 vs. 1528 ± 460.8 nM*min; P = .04) but lag time to thrombin generation was significantly prolonged (8.1 ± 1.8 vs. 6.2 ± 1.8 mins; P = .02). While tissue factor pathway inhibitor (TFPI) levels were similar in both groups, in the presence of an inhibitory anti-TFPI antibody, the difference in lag time between the groups was abrogated. CONCLUSIONS: Collectively, these data demonstrate that COVID-19 of moderate severity is associated with increased plasma thrombin generation and endothelial damage, and that hypercoagulability persists despite standard LMWH thromboprophylaxis. These findings may be of clinical interest given recent clinical trial data which suggest escalated heparin dosing in non-severe COVID-19 may be associated with improved clinical outcomes.


Subject(s)
COVID-19 , Thrombophilia , Venous Thromboembolism , Anticoagulants/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Humans , SARS-CoV-2 , Thrombophilia/diagnosis , Thrombophilia/drug therapy , Tissue Plasminogen Activator , Venous Thromboembolism/epidemiology
14.
Viruses ; 14(2)2022 01 24.
Article in English | MEDLINE | ID: covidwho-1648620

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as COVID-19, is currently developing into a rapidly disseminating and an overwhelming worldwide pandemic. In severe COVID-19 cases, hypercoagulability and inflammation are two crucial complications responsible for poor prognosis and mortality. In addition, coagulation system activation and inflammation overlap and produce life-threatening complications, including coagulopathy and cytokine storm, which are associated with overproduction of cytokines and activation of the immune system; they might be a lead cause of organ damage. However, patients with severe COVID-19 who received anticoagulant therapy had lower mortality, especially with elevated D-dimer or fibrin degradation products (FDP). In this regard, the discovery of natural products with anticoagulant potential may help mitigate the numerous side effects of the available synthetic drugs. This review sheds light on blood coagulation and its impact on the complication associated with COVID-19. Furthermore, the sources of natural anticoagulants, the role of nanoparticle formulation in this outbreak, and the prevalence of thrombosis with thrombocytopenia syndrome (TTS) after COVID-19 vaccines are also reviewed. These combined data provide many research ideas related to the possibility of using these anticoagulant agents as a treatment to relieve acute symptoms of COVID-19 infection.


Subject(s)
Anticoagulants/therapeutic use , Blood Coagulation Disorders/etiology , COVID-19 Vaccines/chemistry , COVID-19/complications , COVID-19/prevention & control , Nanoparticles/therapeutic use , Anticoagulants/administration & dosage , Anticoagulants/isolation & purification , Blood Coagulation , Blood Coagulation Disorders/classification , Blood Coagulation Disorders/prevention & control , Blood Coagulation Disorders/virology , COVID-19 Vaccines/administration & dosage , Cytokine Release Syndrome/prevention & control , Cytokine Release Syndrome/virology , Humans , Inflammation/etiology , Inflammation/prevention & control , Nanoparticles/chemistry , SARS-CoV-2/pathogenicity , Thrombophilia/etiology
15.
PLoS One ; 17(1): e0262600, 2022.
Article in English | MEDLINE | ID: covidwho-1622369

ABSTRACT

In patients with severe forms of COVID-19, thromboelastometry has been reported to display a hypercoagulant pattern. However, an algorithm to differentiate severe COVID-19 patients from nonsevere patients and healthy controls based on thromboelastometry parameters has not been developed. Forty-one patients over 18 years of age with positive qRT-PCR for SARS-CoV-2 were classified according to the severity of the disease: nonsevere (NS, n = 20) or severe (S, n = 21). A healthy control (HC, n = 9) group was also examined. Blood samples from all participants were tested by extrinsic (EXTEM), intrinsic (INTEM), non-activated (NATEM) and functional assessment of fibrinogen (FIBTEM) assays of thromboelastometry. The thrombodynamic potential index (TPI) was also calculated. Severe COVID-19 patients exhibited a thromboelastometry profile with clear hypercoagulability, which was significantly different from the NS and HC groups. Nonsevere COVID-19 cases showed a trend to thrombotic pole. The NATEM test suggested that nonsevere and severe COVID-19 patients presented endogenous coagulation activation (reduced clotting time and clot formation time). TPI data were significantly different between the NS and S groups. The maximum clot firmness profile obtained by FIBTEM showed moderate/elevated accuracy to differentiate severe patients from NS and HC. A decision tree algorithm based on the FIBTEM-MCF profile was proposed to differentiate S from HC and NS. Thromboelastometric parameters are a useful tool to differentiate the coagulation profile of nonsevere and severe COVID-19 patients for therapeutic intervention purposes.


Subject(s)
Blood Coagulation , COVID-19/blood , Thrombelastography , Thrombophilia/blood , Adult , Aged , Algorithms , COVID-19/complications , COVID-19/diagnosis , Female , Humans , Longitudinal Studies , Male , Middle Aged , SARS-CoV-2/isolation & purification , Severity of Illness Index , Thrombophilia/diagnosis , Thrombophilia/etiology , Young Adult
17.
Microvasc Res ; 140: 104310, 2022 03.
Article in English | MEDLINE | ID: covidwho-1586954

ABSTRACT

Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute endothelial injury, hypercoagulation and increased capillary permeability. Diabetes, which is also characterised by vascular injury in itself, confers an increased risk of adverse COVID-19 outcomes. It has been suggested that pre-existing endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated with COVID-19 and thus lead to increased severity of COVID-19 infection. In this article, we evaluate the current evidence exploring the impact of microvascular complications, in the form of diabetic retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring the microvascular injury patterns and clinical outcomes may come to influence care delivery algorithms for either of these conditions.


Subject(s)
COVID-19/physiopathology , Diabetic Angiopathies/physiopathology , Endothelium, Vascular/pathology , Microcirculation , Pandemics , SARS-CoV-2 , Thrombophilia/etiology , Albuminuria/etiology , COVID-19/complications , Capillary Permeability , Delivery of Health Care , Diabetic Angiopathies/complications , Diabetic Nephropathies/complications , Diabetic Nephropathies/physiopathology , Diabetic Neuropathies/complications , Diabetic Neuropathies/physiopathology , Diabetic Retinopathy/complications , Diabetic Retinopathy/physiopathology , Endothelium, Vascular/injuries , Humans , Obesity/complications , Obesity/physiopathology , Pulmonary Circulation , Pulmonary Edema/etiology , Pulmonary Edema/physiopathology , Severity of Illness Index , Thrombophilia/physiopathology , Treatment Outcome
18.
Asian Cardiovasc Thorac Ann ; 30(5): 515-523, 2022 Jun.
Article in English | MEDLINE | ID: covidwho-1582716

ABSTRACT

Coronavirus disease 2019 is the disease produced by severe acute respiratory syndrome-coronavirus-2, which is introduced into the host's cell thanks to the angiotensin-converting enzyme 2 receptor. Once there, it uses the cell's machinery to multiply itself. In this process, it generates an immune response that stimulates the lymphocytes to produce cytokines and reactive oxygen species that begin to deteriorate the endothelial cell. Complement activation, through the complement attack complex and C5a, contributes to this endothelial damage. The different mediators further promote the expression of adhesion molecules on the endothelial surface, which encourages all blood cells to adhere to the endothelial surface to form small conglomerates, called clots, which obstruct the lumen of the small blood vessels. Furthermore, the mediators of clot lysis are inhibited. All this promotes a prothrombotic environment within the pulmonary capillaries that is reflected in the elevation of D-dimer. The only solution for this cascade of events seems to be the implementation of an effective anticoagulation protocol that early counteracts the changes induced by thrombi in the pulmonary circulation and reflected in the functioning of the right ventricle.


Subject(s)
COVID-19 , Thrombophilia , Thrombosis , Blood Coagulation , Humans , SARS-CoV-2 , Thrombophilia/diagnosis , Thrombophilia/drug therapy , Thrombophilia/etiology , Thrombosis/etiology , Treatment Outcome
19.
Clin Appl Thromb Hemost ; 27: 10760296211010973, 2021.
Article in English | MEDLINE | ID: covidwho-1582642

ABSTRACT

SARS-CoV-2 in COVID-19 triggers abnormalities in coagulation parameters that can contribute to thrombosis. The goals of this research were to determine the levels of fibrinogen, D-dimer and FDP in COVID-19 patients. Following a systematic study, among 1198 articles, 35 studies were included in the meta-analysis of fibrinogen levels in both severe and non-severe groups. The funnel plot, Egger's regression asymmetry test, and Begg's test used to measure the bias of publications. All meta-analysis performed by comprehensive meta-analysis version 2 (CMA2). The pooled findings of fibrinogen levels revealed a significant rise in fibrinogen levels in severe COVID-19 than non-severe patients with COVID-19. The D-dimer and FDP levels were significantly higher in severe patients than non-severe patients with COVID-19 were. The levels of fibrinogen, D-dimer, and FDP have increased significantly in ICU patients compared to non-ICU patients. Although, levels of clotting parameters do not always correlate with the severity of disease, these findings showed the diagnostic importance for fibrinogen, D-dimer, and FDP in COVID-19. The presence of a continuous rise in serial measurements of fibrinogen, D-dimer, and FDP may predict that patients with COVID-19 may become critically ill.


Subject(s)
COVID-19/blood , Fibrin Fibrinogen Degradation Products/analysis , Fibrinogen/analysis , Hemostasis , SARS-CoV-2 , Biomarkers , COVID-19/complications , Critical Illness , Humans , Prognosis , Severity of Illness Index , Thrombophilia/blood , Thrombophilia/etiology
20.
Ann Med ; 53(1): 295-301, 2021 12.
Article in English | MEDLINE | ID: covidwho-1575822

ABSTRACT

INTRODUCTION: Critically ill patients with COVID-19 are at increased risk of developing a hypercoagulable state due to haemostatic changes directly related to the SARS-CoV-2 infection or to the consequence of the cytokine storm. Anticoagulation is now recommended to reduce the thrombotic risk. Ilio-psoas haematoma (IPH) is a potentially lethal condition that can arise during the hospitalization, especially in intensive care units (ICUs) and frequently reported as a complication of anticoagulation treatment. MATERIALS AND METHODS: We report a case series of seven subjects with SARS-CoV-2 pneumonia complicated by Ilio-psoas haematomas (IPHs) at our COVID-Hospital in Rome, Italy. RESULTS: Over the observation period, 925 subjects with confirmed SARS-CoV-2 infection were admitted to our COVID-hospital. Among them, we found seven spontaneous IPHs with an incidence of 7.6 cases per 1000 hospitalization. All the reported cases had a severe manifestation of COVID-19 pneumonia, with at least one comorbidity and 5/7 were on treatment with low weight molecular heparin for micro or macro pulmonary thrombosis. CONCLUSIONS: Given the indications to prescribe anticoagulant therapy in COVID-19 and the lack of solid evidences on the optimal dose and duration, it is important to be aware of the iliopsoas haematoma as a potentially serious complication in COVID-19 inpatients. KEY MESSAGE Critically ill patients with COVID-19 are at increased risk of hypercoagulability state and anticoagulation therapy is recommended. Ilio-psoas haematoma (IPH) is found to be a complication of anticoagulation regimen especially in severe COVID-19 cases. An incidence of 7.6 cases per 1000 admission of IPHs was reported. Hypoesthesia of the lower limbs, pain triggered by femoral rotation, hypovolaemia and anaemia are the most common symptoms and signs of IPHs that should alert physician.


Subject(s)
Anticoagulants/adverse effects , COVID-19/complications , Hematoma/epidemiology , Psoas Muscles/diagnostic imaging , Thrombophilia/drug therapy , Aged , Aged, 80 and over , COVID-19/diagnosis , COVID-19/drug therapy , COVID-19/virology , Critical Illness/mortality , Critical Illness/therapy , Female , Glucocorticoids/therapeutic use , Hematoma/chemically induced , Hematoma/diagnosis , Hematoma/drug therapy , Heparin, Low-Molecular-Weight , Hospital Mortality , Humans , Incidence , Intensive Care Units , Italy/epidemiology , Magnetic Resonance Imaging , Male , Middle Aged , Muscular Diseases , SARS-CoV-2/isolation & purification , SARS-CoV-2/pathogenicity , Severity of Illness Index , Thrombophilia/etiology , Tomography, X-Ray Computed , Treatment Outcome
SELECTION OF CITATIONS
SEARCH DETAIL