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1.
Crit Care ; 25(1): 95, 2021 03 08.
Artigo em Inglês | MEDLINE | ID: mdl-33685461

RESUMO

Endothelial cells play a key role in maintaining intravascular patency through their anticoagulant properties. They provide a favorable environment for plasma anticoagulant proteins, including antithrombin, tissue factor pathway inhibitor, and protein C. Under septic conditions, however, the anticoagulant properties of endothelial cells are compromised. Rather, activated/injured endothelial cells can provide a scaffold for intravascular coagulation. For example, the expression of tissue factor, an important initiator of the coagulation pathway, is induced on the surface of activated endothelial cells. Phosphatidylserine, a high-affinity scaffold for gamma-carboxyglutamate domain containing coagulation factors, including FII, FVII, FIX, and FX, is externalized to the outer leaflet of the plasma membrane of injured endothelial cells. Hemodilution decreases not only coagulation factors but also plasma anticoagulant proteins, resulting in unleashed activation of coagulation on the surface of activated/injured endothelial cells. The aberrant activation of coagulation can be suppressed in part by the supplementation of recombinant antithrombin and recombinant thrombomodulin. This review aims to overview the physiological and pathological functions of endothelial cells along with proof-of-concept in vitro studies. The pathophysiology of COVID-19-associated thrombosis is also discussed.


Assuntos
/complicações , Coagulação Intravascular Disseminada/fisiopatologia , Células Endoteliais/patologia , Sepse/fisiopatologia , /fisiopatologia , Ensaios Clínicos Fase III como Assunto , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Trombose/fisiopatologia , Trombose/virologia
2.
J Med Case Rep ; 15(1): 112, 2021 Mar 02.
Artigo em Inglês | MEDLINE | ID: mdl-33653414

RESUMO

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 infection can lead to a constellation of viral and immune symptoms called coronavirus disease 2019. Emerging literature increasingly supports the premise that severe acute respiratory syndrome coronavirus 2 promotes a prothrombotic milieu. However, to date there have been no reports of acute aortic occlusion, itself a rare phenomenon. We report a case of fatal acute aortic occlusion in a patient with coronavirus disease 2019. CASE REPORT: A 59-year-old Caucasian male with past medical history of peripheral vascular disease presented to the emergency department for evaluation of shortness of breath, fevers, and dry cough. His symptoms started 5-7 days prior to the emergency department visit, and he received antibiotics in the outpatient setting without any effect. He was found to be febrile, tachypneic, and hypoxemic. He was placed on supplemental oxygen via a non-rebreather mask. Chest X-ray showed multifocal opacifications. Intravenous antibiotics for possible pneumonia were initiated. Hydroxychloroquine was initiated to cover possible coronavirus disease 2019 pneumonia. During the hospitalization, the patient became progressively hypoxemic, for which he was placed on bilevel positive airway pressure. D-dimer, ferritin, lactate dehydrogenase, and C-reactive protein were all elevated. Severe acute respiratory syndrome coronavirus 2 reverse transcription polymerase chain reaction was positive. On day 3, the patient was upgraded to the intensive care unit. Soon after he was intubated, he developed a mottled appearance of skin, which extended from his bilateral feet up to the level of the subumbilical plane. Bedside ultrasound revealed an absence of flow from the mid-aorta to both common iliac arteries. The patient was evaluated emergently by vascular surgery. After a discussion with the family, it was decided to proceed with comfort-directed care, and the patient died later that day. DISCUSSION: Viral infections have been identified as a source of prothrombotic states due to direct injury of vascular tissue and inflammatory cascades. Severe acute respiratory syndrome coronavirus 2 appears to follow a similar pattern, with numerous institutions identifying elevated levels of thrombotic complications. We believe that healthcare providers should be aware of both venous and arterial thrombotic complications associated with coronavirus disease 2019, including possible fatal outcome.


Assuntos
Doenças da Aorta , Arteriopatias Oclusivas , Trombose , Ultrassonografia/métodos , Aorta Abdominal/diagnóstico por imagem , Doenças da Aorta/diagnóstico , Doenças da Aorta/etiologia , Doenças da Aorta/fisiopatologia , Arteriopatias Oclusivas/diagnóstico , Arteriopatias Oclusivas/etiologia , Arteriopatias Oclusivas/fisiopatologia , Coagulação Sanguínea , /complicações , /terapia , Deterioração Clínica , Evolução Fatal , Humanos , Masculino , Pessoa de Meia-Idade , Conforto do Paciente , Testes Imediatos , /patogenicidade , Trombose/diagnóstico por imagem , Trombose/etiologia , Trombose/fisiopatologia
3.
ACS Chem Neurosci ; 12(4): 573-580, 2021 02 17.
Artigo em Inglês | MEDLINE | ID: mdl-33538586

RESUMO

Long-COVID is a postviral illness that can affect survivors of COVID-19, regardless of initial disease severity or age. Symptoms of long-COVID include fatigue, dyspnea, gastrointestinal and cardiac problems, cognitive impairments, myalgia, and others. While the possible causes of long-COVID include long-term tissue damage, viral persistence, and chronic inflammation, the review proposes, perhaps for the first time, that persistent brainstem dysfunction may also be involved. This hypothesis can be split into two parts. The first is the brainstem tropism and damage in COVID-19. As the brainstem has a relatively high expression of ACE2 receptor compared with other brain regions, SARS-CoV-2 may exhibit tropism therein. Evidence also exists that neuropilin-1, a co-receptor of SARS-CoV-2, may be expressed in the brainstem. Indeed, autopsy studies have found SARS-CoV-2 RNA and proteins in the brainstem. The brainstem is also highly prone to damage from pathological immune or vascular activation, which has also been observed in autopsy of COVID-19 cases. The second part concerns functions of the brainstem that overlap with symptoms of long-COVID. The brainstem contains numerous distinct nuclei and subparts that regulate the respiratory, cardiovascular, gastrointestinal, and neurological processes, which can be linked to long-COVID. As neurons do not readily regenerate, brainstem dysfunction may be long-lasting and, thus, is long-COVID. Indeed, brainstem dysfunction has been implicated in other similar disorders, such as chronic pain and migraine and myalgic encephalomyelitis or chronic fatigue syndrome.


Assuntos
Encefalopatias/fisiopatologia , Tronco Encefálico/fisiopatologia , Inflamação/fisiopatologia , Trombose/fisiopatologia , /metabolismo , Encefalopatias/metabolismo , Encefalopatias/virologia , Tronco Encefálico/irrigação sanguínea , Tronco Encefálico/metabolismo , Tronco Encefálico/virologia , /fisiopatologia , Humanos , Inflamação/metabolismo , Inflamação/virologia , Neuropilina-1/metabolismo , RNA Viral/isolamento & purificação , RNA Viral/metabolismo , /genética , Trombose/metabolismo , Trombose/virologia , Tropismo Viral
4.
Vasc Endovascular Surg ; 55(3): 239-244, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33342395

RESUMO

PURPOSE: The incidence of type II endoleaks (ELII) after endovascular aneurysm repair (EVAR) ranges from 10-44%. Aneurysm thrombus density after EVAR could predict successful aneurysm exclusion. MATERIALS AND METHODS: Twenty-seven patients with an abdominal aortic aneurysm (AAA) who had a CT scan within the first 45 days (early group) post-surgery or after 7 months (late group) were included. Thrombus density was analyzed on non-contrast enhanced CT scans. RESULTS: A total of 5/13 (38%) patients in the early group had an ELII and 9/14 (64.3%) in the late group had a persistent ELII since surgery. In the early group, thrombus density was similar in patients with or without an ELII (mean: 39.9 ± 4.8 vs. 41.9 ± 3.4, p = 0.7; median: 38.7 ± 4.8 vs. 39.7 ± 3.1, p = 0.8). In patients with an ELII, there was no difference in thrombus density at 45 days and after 7 months (mean: 39.9 ± 4.8 vs. 40.2 ± 2.1, p = 0.9; median: 38.7 ± 4.8 vs. 38 ± 2.6, p = 0.9). In patients without an ELII, thrombus density was significantly higher at 45 days than after 7 months (mean: 41.9 ± 3.44 vs. 25.7 ± 2.0, p = 0.005; median: 39.7 ± 3.11 vs. 24.4 ± 1.5, p = 0.004). In patients with an ELII, thrombus density was significantly higher after 7 months than in patients without an ELII (mean: 40.2 ± 2.1 vs. 25.7 ± 2.0. p = 0.001; median: 38 ± 2.6 vs. 24.4 ± 1.5, p = 0.003). CONCLUSION: Low thrombus density after EVAR on late unenhanced CT scans predicts aneurysm exclusion.


Assuntos
Aneurisma da Aorta Abdominal/cirurgia , Aortografia , Angiografia por Tomografia Computadorizada , Endoleak/diagnóstico por imagem , Procedimentos Endovasculares , Trombose/diagnóstico por imagem , Idoso , Idoso de 80 Anos ou mais , Aneurisma da Aorta Abdominal/diagnóstico por imagem , Aneurisma da Aorta Abdominal/fisiopatologia , Endoleak/etiologia , Endoleak/fisiopatologia , Procedimentos Endovasculares/efeitos adversos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Trombose/fisiopatologia , Fatores de Tempo , Resultado do Tratamento
5.
Eur Rev Med Pharmacol Sci ; 24(23): 12609-12622, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33336781

RESUMO

OBJECTIVE: In human pathology, SARS-CoV-2 utilizes multiple molecular pathways to determine structural and biochemical changes within the different organs and cell types. The clinical picture of patients with COVID-19 is characterized by a very large spectrum. The reason for this variability has not been clarified yet, causing the inability to make a prognosis on the evolution of the disease. MATERIALS AND METHODS: PubMed search was performed focusing on the role of ACE 2 receptors in allowing the viral entry into cells, the role of ACE 2 downregulation in triggering the tissue pathology or in accelerating previous disease states, the role of increased levels of Angiotensin II in determining endothelial dysfunction and the enhanced vascular permeability, the role of the dysregulation of the renin angiotensin system in COVID-19 and the role of cytokine storm. RESULTS: The pathological changes induced by SARS-CoV-2 infection in the different organs, the correlations between the single cell types targeted by the virus in the different human organs and the clinical consequences, COVID-19 chronic pathologies in liver fibrosis, cardiac fibrosis and atrial arrhythmias, glomerulosclerosis and pulmonary fibrosis, due to the systemic fibroblast activation induced by angiotensin II are discussed. CONCLUSIONS: The main pathways involved showed different pathological changes in multiple tissues and the different clinical presentations. Even if ACE2 is the main receptor of SARS-CoV-2 and the main entry point into cells for the virus, ACE2 expression does not always explain the observed marked inter-individual variability in clinical presentation and outcome, evidencing the complexity of this disorder. The proper interpretation of the growing data available might allow to better classifying COVID-19 in human pathology.


Assuntos
Angiotensina II/metabolismo , /metabolismo , Cardiomiopatias/metabolismo , Síndrome da Liberação de Citocina/metabolismo , Endotélio Vascular/fisiopatologia , Cirrose Hepática/metabolismo , Síndrome de Resposta Inflamatória Sistêmica/metabolismo , Trombose/metabolismo , Angiotensina I/metabolismo , Fibrilação Atrial/metabolismo , Fibrilação Atrial/fisiopatologia , Coagulação Sanguínea , /fisiopatologia , Permeabilidade Capilar , Cardiomiopatias/patologia , Cardiomiopatias/fisiopatologia , Síndrome da Liberação de Citocina/fisiopatologia , Citocinas/metabolismo , Fibroblastos/metabolismo , Fibroblastos/patologia , Fibrose , Humanos , Cirrose Hepática/patologia , Cirrose Hepática/fisiopatologia , Miocardite/metabolismo , Miocardite/patologia , Miocardite/fisiopatologia , Sistema Renina-Angiotensina , Síndrome de Resposta Inflamatória Sistêmica/fisiopatologia , Trombose/fisiopatologia , Internalização do Vírus
7.
PLoS One ; 15(10): e0239222, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33001983

RESUMO

BACKGROUND: To prevent bio-accumulation of low molecular weight heparins (LMWHs) in patients with decreased kidney function, dosage reduction and anti-Xa monitoring has been suggested. The aim of this study was to investigate the effect of pre-emptive dosage reduction of LMWH on anti-Xa levels. Furthermore, we investigated the association between anti-Xa levels and bleeding, thrombotic events and mortality. METHODS: In this single center study, we followed 499 patients with decreased renal function in whom anti-Xa levels were measured. We observed how many patients had anti-Xa levels that fell within the reference range, with a standard protocol of a pre-emptive dosage reduction of LMWH (25% reduction in patients with an estimated glomerular filtration rate (eGFR) between 30 and 60 ml/min/1.73m2 and a reduction of 50% in patients with an eGFR below the 30 ml/min/1.73m2). Furthermore, Cox proportional hazard analyses were used to estimate hazard ratios to investigate the association between anti-Xa levels and major bleeding, thrombotic events and mortality within three months of follow-up. RESULTS: In a cohort of 499 patients (445 dalteparin and 54 nadroparin users), a pre-emptive dosage reduction of LMWH led to adequate levels of anti-Xa in only 19% of the patients (12% for the dalteparin users and 50% for nadroparin users). We did not find an association between anti-Xa levels and bleeding, thrombosis or mortality. CONCLUSION: Pre-emptive dosage reduction of LMWH leads to low anti-Xa levels in a large proportion, but this was not associated with bleeding, thrombosis or mortality.


Assuntos
Inibidores do Fator Xa/metabolismo , Heparina de Baixo Peso Molecular/efeitos adversos , Rim/efeitos dos fármacos , Rim/fisiopatologia , Idoso , Estudos de Coortes , Relação Dose-Resposta a Droga , Feminino , Hemorragia/fisiopatologia , Heparina de Baixo Peso Molecular/metabolismo , Humanos , Masculino , Pessoa de Meia-Idade , Trombose/fisiopatologia
8.
Eur Heart J ; 41(32): 3038-3044, 2020 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-32882706

RESUMO

The vascular endothelium provides the crucial interface between the blood compartment and tissues, and displays a series of remarkable properties that normally maintain homeostasis. This tightly regulated palette of functions includes control of haemostasis, fibrinolysis, vasomotion, inflammation, oxidative stress, vascular permeability, and structure. While these functions participate in the moment-to-moment regulation of the circulation and coordinate many host defence mechanisms, they can also contribute to disease when their usually homeostatic and defensive functions over-reach and turn against the host. SARS-CoV-2, the aetiological agent of COVID-19, causes the current pandemic. It produces protean manifestations ranging from head to toe, wreaking seemingly indiscriminate havoc on multiple organ systems including the lungs, heart, brain, kidney, and vasculature. This essay explores the hypothesis that COVID-19, particularly in the later complicated stages, represents an endothelial disease. Cytokines, protein pro-inflammatory mediators, serve as key danger signals that shift endothelial functions from the homeostatic into the defensive mode. The endgame of COVID-19 usually involves a cytokine storm, a phlogistic phenomenon fed by well-understood positive feedback loops that govern cytokine production and overwhelm counter-regulatory mechanisms. The concept of COVID-19 as an endothelial disease provides a unifying pathophysiological picture of this raging infection, and also provides a framework for a rational treatment strategy at a time when we possess an indeed modest evidence base to guide our therapeutic attempts to confront this novel pandemic.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Endotélio Vascular/fisiopatologia , Estresse Oxidativo , Pneumonia Viral/complicações , Trombose/etiologia , Infecções por Coronavirus/epidemiologia , Citocinas/metabolismo , Humanos , Pandemias , Pneumonia Viral/epidemiologia , Trombose/metabolismo , Trombose/fisiopatologia
9.
J Vasc Interv Radiol ; 31(11): 1831-1835, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32958378

RESUMO

PURPOSE: To review the immediate flow response and incidence of steal syndrome after taper reduction of tapered dialysis grafts. MATERIAL AND METHODS: This was a retrospective review of a quality assurance database of all hemodialysis access interventions performed between 2005 and 2017. It identified 77 patients who underwent a taper reduction procedure, involving angioplasty of the arterial limb of the graft and the arterial anastomosis for graft thrombosis/poor flow. A subset of patients underwent 5-, 6-, or 7-mm balloon taper reduction angioplasty coupled with intravascular direct flow measurement (n = 15 with 16 dialysis grafts). A two-tailed Wilcoxon matched-pairs signed-rank test was used to compare pre- and post-taper reduction flows. Mean duration of follow-up was 3.5 years (range, 0-12.5 years). RESULTS: Mean access survival after taper reduction was 20.2 months (range, 0.10-94.4 months). Pre- and post-taper reduction access flows (mean Qb ± standard deviation) were 574 ± 315 ml/min and 929 ± 352 ml/min, respectively (P < .0001). The mean ratio of post- to pre-taper reduction flows was 1.6 (range, 1.1-10.2). No patients developed steal syndrome within 6 months after taper reduction. CONCLUSIONS: Dialysis graft arterial anastomotic taper reduction did not result in the development of steal syndrome within 6 months. In the subset of patients who underwent flow measurements, taper reduction was associated with nearly a 2-fold improvement in access flow, which is a key predictor of access function.


Assuntos
Angioplastia com Balão , Derivação Arteriovenosa Cirúrgica/instrumentação , Implante de Prótese Vascular/instrumentação , Prótese Vascular , Oclusão de Enxerto Vascular/terapia , Diálise Renal , Trombose/terapia , Adulto , Idoso , Idoso de 80 Anos ou mais , Angioplastia com Balão/efeitos adversos , Derivação Arteriovenosa Cirúrgica/efeitos adversos , Velocidade do Fluxo Sanguíneo , Implante de Prótese Vascular/efeitos adversos , Bases de Dados Factuais , Feminino , Oclusão de Enxerto Vascular/diagnóstico por imagem , Oclusão de Enxerto Vascular/etiologia , Oclusão de Enxerto Vascular/fisiopatologia , Humanos , Isquemia/etiologia , Isquemia/fisiopatologia , Masculino , Pessoa de Meia-Idade , Desenho de Prótese , Estudos Retrospectivos , Fatores de Risco , Trombose/diagnóstico por imagem , Trombose/etiologia , Trombose/fisiopatologia , Fatores de Tempo , Resultado do Tratamento , Adulto Jovem
10.
J Thromb Thrombolysis ; 50(4): 790-794, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32789730

RESUMO

Several autopsy studies showed microthrombi in pulmonary circulation of severe COVID-19 patients. The major limitation of these investigations is that the autopsy provided static information. Some of these alterations could be secondary to the disseminated intravascular coagulation (DIC) observed as the final standard route to the multisystem organ failure exhibited in critically ill patients. We report preliminary results of an in vivo evaluation of sublingual microcirculation in thirteen patients with severe COVID-19 requiring mechanical ventilation. We observed multiple filling defects moving within the microvessels indicative of thrombi in most of the cases 11/13 (85%). This is the first imaging documentation of microvascular thrombosis in living severe COVID-19 patients since the beginning of the hospitalization. The clinical relevance of microvascular thrombosis in this disease requires further research.


Assuntos
Coagulação Sanguínea , Infecções por Coronavirus/complicações , Microcirculação , Soalho Bucal/irrigação sanguínea , Pneumonia Viral/complicações , Trombose/fisiopatologia , Idoso , Betacoronavirus/patogenicidade , Infecções por Coronavirus/terapia , Infecções por Coronavirus/virologia , Feminino , Interações Hospedeiro-Patógeno , Humanos , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/terapia , Pneumonia Viral/virologia , Fluxo Sanguíneo Regional , Respiração Artificial , Índice de Gravidade de Doença , Trombose/sangue , Trombose/diagnóstico por imagem , Trombose/virologia
12.
Radiología (Madr., Ed. impr.) ; 62(4): 327-329, jul.-ago. 2020. ilus
Artigo em Espanhol | IBECS | ID: ibc-194251

RESUMO

Varón de 57 años con antecedente de infarto de miocardio anterior. En una tomografía axial computarizada (TAC) cardíaca realizada 3 años más tarde, se objetiva una imagen hipodensa en el ápex del ventrículo izquierdo. Ante la sospecha de trombo, se completa el estudio mediante resonancia magnética cardíaca (RMC) con gadolinio, ecocardiografía transtorácica (ETT) 2D con ecopotenciador y ETT tridimensional. A través de la imagen multimodalidad se comprueba la ausencia de trombo


Cardiac computed tomography showed a hypodense area in the apex of the left ventricle in a 57-year-old man with a history of anterior myocardial infarction three years earlier. To confirm or rule out a suspected thrombus, he underwent gadolinium-enhanced cardiac magnetic resonance imaging, contrast-enhanced two-dimensional transthoracic echocardiography, and three-dimensional transthoracic echocardiography. Multimodality imaging ruled out the presence of a thrombus


Assuntos
Humanos , Masculino , Pessoa de Meia-Idade , Trombose/diagnóstico por imagem , Imagem Multimodal/métodos , Tomografia Computadorizada por Raios X/métodos , Cardiopatias/diagnóstico por imagem , Trombose/fisiopatologia , Processamento de Imagem Assistida por Computador , Gadolínio/administração & dosagem , Ecocardiografia/instrumentação
13.
PLoS One ; 15(7): e0235392, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32726315

RESUMO

Platelets upregulate the generation of thrombin and reinforce the fibrin clot which increases the incidence risk of venous thromboembolism (VTE). However, the role of platelets in the pathogenesis of venous cardiovascular diseases remains hard to quantify. An experimentally validated model of thrombin generation dynamics is formulated. The model predicts that a high platelet count increases the peak value of generated thrombin as well as the endogenous thrombin potential (ETP) as reported in experimental data. To investigate the effects of platelets density, shear rate, and wound size on the initiation of blood coagulation, we calibrate a previously developed model of venous thrombus formation and implement it in 3D using a novel cell-centered finite-volume solver. We conduct numerical simulations to reproduce in vitro experiments of blood coagulation in microfluidic capillaries. Then, we derive a reduced one-equation model of thrombin distribution from the previous model under simplifying hypotheses and we use it to determine the conditions of clotting initiation on the platelet count, the shear rate, and the plasma composition. The initiation of clotting also exhibits a threshold response to the size of the wounded region in good agreement with the reported experimental findings.


Assuntos
Coagulação Sanguínea/fisiologia , Plaquetas/fisiologia , Modelos Teóricos , Contagem de Plaquetas/métodos , Testes de Coagulação Sanguínea , Plaquetas/metabolismo , Fibrina/metabolismo , Humanos , Agregação Plaquetária/fisiologia , Fluxo Sanguíneo Regional/fisiologia , Resistência ao Cisalhamento/fisiologia , Trombina/metabolismo , Tromboplastina/metabolismo , Trombose/metabolismo , Trombose/fisiopatologia , Veias/metabolismo , Veias/fisiologia
14.
Arterioscler Thromb Vasc Biol ; 40(9): 2114-2126, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32640902

RESUMO

OBJECTIVE: Quantitative relationships between the extent of injury and thrombus formation in vivo are not well understood. Moreover, it has not been investigated how increased injury severity translates to blood-flow modulation. Here, we investigated interconnections between injury length, clot growth, and blood flow in a mouse model of laser-induced thrombosis. Approach and Results: Using intravital microscopy, we analyzed 59 clotting events collected from the cremaster arteriole of 14 adult mice. We regarded injury length as a measure of injury severity. The injury caused transient constriction upstream and downstream of the injury site resulting in a 50% reduction in arteriole diameter. The amount of platelet accumulation and fibrin formation did not depend on arteriole diameter or deformation but displayed an exponentially increasing dependence on injury length. The height of the platelet clot depended linearly on injury length and the arteriole diameter. Upstream arteriolar constriction correlated with delayed upstream velocity increase, which, in turn, determined downstream velocity. Before clot formation, flow velocity positively correlated with the arteriole diameter. After the onset of thrombus growth, flow velocity at the injury site negatively correlated with the arteriole diameter and with the size of the above-clot lumen. CONCLUSIONS: Injury severity increased platelet accumulation and fibrin formation in a persistently steep fashion and, together with arteriole diameter, defined clot height. Arterial constriction and clot formation were characterized by a dynamic change in the blood flow, associated with increased flow velocity.


Assuntos
Músculos Abdominais/irrigação sanguínea , Arteríolas/patologia , Coagulação Sanguínea , Trombose/patologia , Lesões do Sistema Vascular/patologia , Animais , Arteríolas/lesões , Arteríolas/fisiopatologia , Velocidade do Fluxo Sanguíneo , Plaquetas/metabolismo , Constrição Patológica , Modelos Animais de Doenças , Fibrina/metabolismo , Microscopia Intravital , Masculino , Camundongos , Microscopia de Fluorescência , Índice de Gravidade de Doença , Trombose/sangue , Trombose/fisiopatologia , Fatores de Tempo , Lesões do Sistema Vascular/sangue , Lesões do Sistema Vascular/fisiopatologia
15.
Arch Cardiovasc Dis ; 113(10): 642-651, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32712202

RESUMO

Major thromboembolic complications in patients with atrial fibrillation, secondary to thromboembolism from the left atrium or the left atrial appendage, are a major concern because of their burden of disabling stroke and mortality. To date, non-vitamin K antagonist oral anticoagulants (NOACs) are considered the first-line strategy in most patients with atrial fibrillation receiving chronic anticoagulation, as they have major advantages compared with vitamin K antagonists, including minimization of intracranial bleeding risk. Although several studies and post-hoc analyses have provided initial data on the use of NOACs in patients with documented atrial and/or left atrial appendage thrombosis, the benefit of NOACs in these patients has not been fully elucidated. In this review, we reappraise current evidence supporting the use of NOACs in patients with established atrial and/or left atrial appendage thrombosis, discussing potential mechanisms favouring the use of a NOAC-based strategy in this special setting.


Assuntos
Antitrombinas/administração & dosagem , Fibrilação Atrial/tratamento farmacológico , Inibidores do Fator Xa/administração & dosagem , Acidente Vascular Cerebral/prevenção & controle , Tromboembolia/prevenção & controle , Trombose/tratamento farmacológico , Administração Oral , Antitrombinas/efeitos adversos , Fibrilação Atrial/epidemiologia , Fibrilação Atrial/fisiopatologia , Medicina Baseada em Evidências , Inibidores do Fator Xa/efeitos adversos , Hemorragia/induzido quimicamente , Humanos , Fatores de Risco , Acidente Vascular Cerebral/epidemiologia , Acidente Vascular Cerebral/fisiopatologia , Tromboembolia/epidemiologia , Tromboembolia/fisiopatologia , Trombose/epidemiologia , Trombose/fisiopatologia , Resultado do Tratamento
17.
Vasc Endovascular Surg ; 54(8): 670-675, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32720863

RESUMO

OBJECTIVES: Surgical thrombectomy for acute arteriovenous fistula (AVF) thrombosis is one of the primary salvage intervention. The independent risk factors affecting the patency of AVF after a successful thrombectomy are yet unknown. Here, the author aimed to report the results of surgically corrected AVFs and the independent risk factors which may cause early failure following the surgical salvage. METHODS: The study cohort comprised 24 patients who had acute AVF thrombosis and underwent successful surgical thrombectomy in the first 24 to 48 hours between January 2016 and April 2020 in our center. The study group was divided into patients with recurrent AVF thrombosis (n = 11, 45.8%) and without recurrent AVF thrombosis (n = 13, 54.1%) following surgical thrombectomy with a follow-up of 22.4 ± 6.8 months. Postthrombectomy primary and secondary patency of AVF were also evaluated. RESULTS: The mean age of the cohort was 58.1 ± 15.2 years. A simple thrombectomy was performed for all cases. Only 2 cases have required a revision at the anastomosis due to severe intimal hyperplasia. Postthrombectomy primary patency rate was 45.5% for 18 months. Receiver operating characteristic analysis was performed with a resulting area under the curve value of 0.81 (95% CI: 0.35-0.94, P = .006) for flow (mL)/d-dimer (ng/mL) <0.63 in predicting recurrent AVF thrombosis following surgical thrombectomy. CONCLUSIONS: Flow (mL)/d-dimer (ng/mL) <0.63 was independent predictor of recurrent thrombosis (RT) of a surgically salvaged AVF. The patients at risk for RT or who may benefit from further intervention should be identified with predictive parameters.


Assuntos
Derivação Arteriovenosa Cirúrgica/efeitos adversos , Produtos de Degradação da Fibrina e do Fibrinogênio/análise , Oclusão de Enxerto Vascular/cirurgia , Diálise Renal , Trombectomia , Trombose/cirurgia , Grau de Desobstrução Vascular , Adulto , Idoso , Biomarcadores/sangue , Velocidade do Fluxo Sanguíneo , Feminino , Oclusão de Enxerto Vascular/sangue , Oclusão de Enxerto Vascular/diagnóstico , Oclusão de Enxerto Vascular/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Recidiva , Estudos Retrospectivos , Fatores de Risco , Trombectomia/efeitos adversos , Trombose/sangue , Trombose/diagnóstico , Trombose/fisiopatologia , Fatores de Tempo , Resultado do Tratamento
18.
Paediatr Respir Rev ; 35: 20-24, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32653469

RESUMO

Since the initial description in 2019, the novel coronavirus SARS-Cov-2 infection (COVID-19) pandemic has swept the globe. The most severe form of the disease presents with fever and shortness of breath, which rapidly deteriorates to respiratory failure and acute lung injury (ALI). COVID-19 also presents with a severe coagulopathy with a high rate of venous thromboembiolism. In addition, autopsy studies have revealed co-localized thrombosis and inflammation, which is the signature of thromboinflammation, within the pulmonary capillary vasculature. While the majority of published data is on adult patients, there are parallels to pediatric patients. In our experience as a COVID-19 epicenter, children and young adults do develop both the coagulopathy and the ALI of COVID-19. This review will discuss COVID-19 ALI from a hematological perspective with discussion of the distinct aspects of coagulation that are apparent in COVID-19. Current and potential interventions targeting the multiple thromboinflammatory mechanisms will be discussed.


Assuntos
Lesão Pulmonar Aguda/sangue , Infecções por Coronavirus/sangue , Inflamação/sangue , Pneumonia Viral/sangue , Trombose/sangue , Lesão Pulmonar Aguda/tratamento farmacológico , Lesão Pulmonar Aguda/imunologia , Lesão Pulmonar Aguda/fisiopatologia , Anticoagulantes/uso terapêutico , Antitrombinas/uso terapêutico , Betacoronavirus , Transtornos da Coagulação Sanguínea/sangue , Transtornos da Coagulação Sanguínea/imunologia , Transtornos da Coagulação Sanguínea/fisiopatologia , Capilares/imunologia , Capilares/fisiopatologia , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/fisiopatologia , Endotélio Vascular/imunologia , Endotélio Vascular/fisiopatologia , Inibidores do Fator Xa/uso terapêutico , Humanos , Inflamação/tratamento farmacológico , Inflamação/imunologia , Inflamação/fisiopatologia , Pandemias , Ativação Plaquetária , Inibidores da Agregação de Plaquetas/uso terapêutico , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/imunologia , Pneumonia Viral/fisiopatologia , Embolia Pulmonar/sangue , Embolia Pulmonar/imunologia , Embolia Pulmonar/fisiopatologia , Trombina/imunologia , Trombina/metabolismo , Trombose/tratamento farmacológico , Trombose/imunologia , Trombose/fisiopatologia
19.
ACS Chem Neurosci ; 11(14): 2048-2050, 2020 07 15.
Artigo em Inglês | MEDLINE | ID: mdl-32614178

RESUMO

In COVID-19, lung manifestations present as a slowly evolving pneumonia with insidious early onset interstitial pulmonary edema that undergoes acute exacerbation in the late stages and microvascular thrombosis. Currently, these manifestations are considered to be only consequences of pulmonary SARS-CoV-2 virus infection. We are proposing a new hypothesis that neurogenic insult may also play a major role in the pathogenesis of these manifestations. SARS-CoV-2 mediated inflammation of the nucleus tractus solitarius (NTS) may play a role in the acute exacerbation of pulmonary edema and microvascular clotting in COVID-19 patients.


Assuntos
Infecções por Coronavirus/fisiopatologia , Hipotensão/fisiopatologia , Pulmão/irrigação sanguínea , Microvasos/fisiopatologia , Pneumonia Viral/fisiopatologia , Edema Pulmonar/fisiopatologia , Núcleo Solitário/fisiopatologia , Trombose/fisiopatologia , Betacoronavirus , Permeabilidade Capilar/fisiologia , Infecções por Coronavirus/imunologia , Síndrome da Liberação de Citocina/imunologia , Síndrome da Liberação de Citocina/fisiopatologia , Nervo Facial , Nervo Glossofaríngeo , Humanos , Inflamação , Pulmão/imunologia , Microvasos/imunologia , Pandemias , Sistema Nervoso Parassimpático/fisiopatologia , Pneumonia Viral/imunologia , Edema Pulmonar/imunologia , Núcleo Solitário/imunologia , Nervo Vago , Vasoconstrição
20.
J Vis Exp ; (159)2020 05 24.
Artigo em Inglês | MEDLINE | ID: mdl-32510519

RESUMO

The formation of blood clots involves complex interactions between endothelial cells, their underlying matrix, various blood cells, and proteins. The endothelium is the primary source of many of the major hemostatic molecules that control platelet aggregation, coagulation, and fibrinolysis. Although the mechanism of thrombosis has been investigated for decades, in vitro studies mainly focus on situations of vascular damage where the subendothelial matrix gets exposed, or on interactions between cells with single blood components. Our method allows studying interactions between whole blood and an intact, confluent vascular cell network. By utilizing primary human endothelial cells, this protocol provides the unique opportunity to study the influence of endothelial cells on thrombus dynamics and gives valuable insights into the pathophysiology of thrombotic disease. The use of custom-made microfluidic flow channels allows application of disease-specific vascular geometries and model specific morphological vascular changes. The development of a thrombus is recorded in real-time and quantitatively characterized by platelet adhesion and fibrin deposition. The effect of endothelial function in altered thrombus dynamics is determined by postanalysis through immunofluorescence staining of specific molecules. The representative results describe the experimental setup, data collection, and data analysis. Depending on the research question, parameters for every section can be adjusted including cell type, shear rates, channel geometry, drug therapy, and postanalysis procedures. The protocol is validated by quantifying thrombus formation on the pulmonary artery endothelium of patients with chronic thromboembolic disease.


Assuntos
Coagulação Sanguínea , Plaquetas/metabolismo , Células Endoteliais/metabolismo , Microfluídica/métodos , Adesividade Plaquetária , Agregação Plaquetária , Trombose/fisiopatologia , Células Endoteliais/citologia , Fibrinólise , Hemostasia , Humanos , Microfluídica/instrumentação
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