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1.
Front Cardiovasc Med ; 11: 1446992, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-39011495
2.
J Hepatol ; 81(5): 872-885, 2024 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-38908437

RESUMO

BACKGROUND & AIMS: The underlying mechanisms and clinical impact of portal microthrombosis in severe COVID-19 are unknown. Intrapulmonary vascular dilation (IPVD)-related hypoxia has been described in severe liver diseases. We hypothesised that portal microthrombosis is associated with IPVD and fatal respiratory failure in COVID-19. METHODS: Ninety-three patients who died from COVID-19 were analysed for portal microvascular damage (histology), IPVD (histology and chest-computed tomography, CT), and hypoxemia (arterial blood gas). Seventeen patients who died from COVID-19-unrelated pneumonia served as controls. Vascular lesions and microthrombi were phenotyped for endothelial (vWF) and pericyte (αSMA/PDGFR-ß) markers, tissue factor (TF), viral spike protein and nucleoprotein (SP, NP), fibrinogen, and platelets (CD41a). Viral particles in vascular cells were assessed by transmission electron microscopy. Cultured pericytes were infected with SARS-CoV-2 to measure TF expression and tubulisation of human pulmonary microvascular endothelial cells was assessed upon vWF treatment. RESULTS: IPVD was present in 16/66 patients with COVID-19, with available liver and lung histology, and was associated with younger age (62 vs. 78 years-old), longer illness (25 vs. 14 days), worsening hypoxemia (PaO2/FiO2 from 209 to 89), and an increased requirement for ventilatory support (63% vs. 22%) compared to COVID-19/Non-IPVD. IPVD, absent in controls, was confirmed by chest CT. COVID-19/IPVD liver histology showed portal microthrombosis in >82.5% of portal areas, with a thicker wall of αSMA/PDGFR-ß+/SP+/NP+ pericytes compared with COVID-19/Non-IPVD. Thrombosed portal venules correlated with αSMA+ area, whereas infected SP+/NP+ pericytes expressed TF. SARS-CoV-2 viral particles were observed in portal pericytes. In vitro SARS-CoV-2 infection of pericytes upregulated TF and induced endothelial cells to overexpress vWF, which expanded human pulmonary microvascular endothelial cell tubules. CONCLUSIONS: SARS-CoV-2 infection of liver pericytes elicits a local procoagulant response associated with extensive portal microthrombosis, IPVD and worsening respiratory failure in fatal COVID-19. IMPACT AND IMPLICATIONS: Vascular involvement of the liver represents a serious complication of COVID-19 infection that must be considered in the work-up of patients with long-lasting and progressively worsening respiratory failure, as it may associate with the development of intrapulmonary vascular dilations. This clinical picture is associated with a procoagulant phenotype of portal venule pericytes, which is induced by SARS-CoV-2 infection of pericytes. Both observations provide a model that may apply, at least in part, to other vascular disorders of the liver, featuring obliterative portal venopathy, similarly characterised at the clinical level by development of hypoxemia and at the histological level by phlebosclerosis and reduced calibre of the portal vein branches in the absence of cirrhosis. Moreover, our findings shed light on an overlooked player in the pathophysiology of thrombosis, i.e. pericytes, which may present a novel therapeutic target.


Assuntos
COVID-19 , Pulmão , Pericitos , SARS-CoV-2 , Humanos , COVID-19/complicações , COVID-19/mortalidade , Pericitos/patologia , Pericitos/metabolismo , Pericitos/virologia , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Pulmão/patologia , Tromboplastina/metabolismo , Tromboplastina/análise , Fenótipo , Células Endoteliais/patologia , Células Endoteliais/metabolismo , Células Endoteliais/virologia , Pneumonia Viral/complicações , Pneumonia Viral/mortalidade , Pneumonia Viral/virologia , Pneumonia Viral/patologia , Veia Porta/patologia , Betacoronavirus , Trombose Venosa/virologia , Trombose Venosa/patologia , Trombose Venosa/etiologia , Hipóxia
3.
Dig Liver Dis ; 2024 Jun 03.
Artigo em Inglês | MEDLINE | ID: mdl-38834381

RESUMO

INTRODUCTION: Factor XI (FXI) is associated with thrombosis in patients without liver disease, but it alterations and prognostic value in cirrhosis are uncertain. PATIENTS AND METHODS: We studied a prospective cohort of cirrhosis patients determining FXI and its association with portal vein thrombosis (PVT), bleeding, and hepatic decompensation/ACLF during 1-year follow-up. Odds ratios (OR) and 95 % CIs were calculated using logistic regression. RESULTS: We included 183 patients (Child-Pugh [CP] A/B/C 57/59/57). FXI was reduced in cirrhosis, decreasing with CP stage (78 % [66-94] vs. 58 % [44-78] vs. 41 % [30-52] in CP A, B, and C, respectively; p < 0.001). FXI was correlated with MELD score (rho: -0.6, p < 0.001), INR (rho: -0.6, p < 0.001), and platelet count (rho: 0.4, p < 0.001). Sixteen patients (8.7 %) experienced PVT, which only predictor was baseline platelet count (OR: 0.94; CI95 %: 0.91-0.97, p < 0.001). Bleeding occurred in 7 patients (3.8 %). Cirrhosis severity, platelet count, fibrinogen, and FXI (60% vs. 78 %; p = 0.2) were comparable between bleeding and non-bleeding individuals. Finally, no association was found between FXI and hepatic decompensation/ACLF, which were predicted by lower albumin and platelet count, respectively. CONCLUSION: FXI seems not to be responsible for thrombosis and cirrhosis progression. The lack of association between low FXI and bleeding events, however, indirectly opens to future studies evaluating FXI inhibitors in cirrhosis.

4.
Front Cardiovasc Med ; 11: 1386733, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38803660

RESUMO

Cardiac amyloidosis is a group of diseases characterized by the deposition of amyloid fibers in cardiac tissue. Two forms are mainly reported: light chain (AL) and transthyretin (ATTR) amyloidosis. Among the complications of transthyretin amyloidosis there are thrombotic events and, to a lesser extent, hemorrhagic events. The latter are likely caused by perivascular amyloid deposition resulting in capillary fragility, in addition to INR lability during anticoagulant therapy. The onset of thrombotic events may be caused by the high prevalence of atrial fibrillation (AF), mechanical cardiac dysfunction and atrial myopathy observed in patients with transthyretin amyloidosis. It remains unclear why thromboembolic events occur even in patients with sinus rhythm or adequate anticoagulation, though a hypercoagulable state or underlying inflammation may be involved. We report a case of cryptogenic ischemic stroke in an 86-year-old woman with transthyretin amyloidosis and sinus rhythm. Traditional coagulation tests, whole blood rotational thromboelastometry and impedance aggregometry did not show a hypercoagulable state. The thrombin generation assay did not reveal a prothrombotic state. However, the study of extracellular vesicles highlighted underlying immune-mediated endothelial damage likely responsible for the thrombotic diathesis. It could be hypothesized that inflammation plays a role in the hypercoagulability of patients with transthyretin amyloidosis. Larger prospective studies are needed to validate our hypothesis.

5.
Semin Thromb Hemost ; 50(6): 866-872, 2024 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-38181816

RESUMO

The incidence of venous thromboembolism (VTE) in the pediatric population has increased more than 10-fold in the last 20 years, as a consequence of the advancement of resuscitation and surgical techniques and the global increase in life expectancy of children suffering from chronic pathologies. Monitoring anticoagulant therapy to achieve outcomes within the target range in childhood VTE, parenteral administration of medications, and frequent blood tests in children are often cumbersome. Availability of safe and effective oral agents with pediatric data to support use would be of clear benefit. A physiologically based pharmacokinetic model was developed to estimate the appropriate dosing schedule for rivaroxaban in children. This incorporated growth/maturation and variability in anthropometrics (e.g., body height, weight, and body mass index), anatomy (e.g., organ weight), physiology (e.g., blood flow rates), metabolism and excretion. Rivaroxaban use in pediatric population underwent a complete investigational program, consisting mainly of one phase I pharmacokinetics/pharmacodynamics trial, three phase II trials, one phase III trial. The phase III trial enrolled 500 patients from birth to <18 years and documented the efficacy and safety of rivaroxaban regimens at dose equivalent to the adult 20 mg dose for the prevention of fatal or symptomatic nonfatal recurrent VTE and major bleeding versus heparin or vitamin K antagonists. Results were similar to those in rivaroxaban studies in adults. The efficacy and safety of rivaroxaban in children reported in the EINSTEIN JUNIOR trial provide further support to previous trials in adults (EINSTEIN Program), which demonstrate a favorable profile for the use of rivaroxaban for the management of VTE in challenging patient populations. Other clinical evidence contributing to the use of rivaroxaban among different risk groups in pediatric VTE population confirms the consistency with principal trial. Our review aims to describe the rationale for using rivaroxaban oral suspension in clinical practice and to summarize its multiple indications in each vascular bed (e.g., cerebral venous thrombosis, symptomatic or asymptomatic central venous catheter-associated thrombosis), etiology, and patients setting.


Assuntos
Rivaroxabana , Tromboembolia Venosa , Humanos , Rivaroxabana/uso terapêutico , Rivaroxabana/farmacocinética , Rivaroxabana/efeitos adversos , Tromboembolia Venosa/tratamento farmacológico , Criança , Adolescente , Pré-Escolar , Lactente , Inibidores do Fator Xa/uso terapêutico , Inibidores do Fator Xa/farmacocinética , Inibidores do Fator Xa/efeitos adversos , Ensaios Clínicos como Assunto
6.
Thromb Res ; 234: 21-31, 2024 02.
Artigo em Inglês | MEDLINE | ID: mdl-38142487

RESUMO

BACKGROUND: Several studies have evaluated the possible association between whole blood viscoelastic testing (VET) parameters in patients hospitalized for acute Coronavirus disease 2019 (COVID-19) pneumonia and mortality. A few studies found no significant differences between survivors and non-survivors, though other studies identified potential predictors of COVID-19-related mortality. We conducted a systematic review and meta-analysis of the literature to evaluate the possible association between standard thromboelastometry/graphy parameters and mortality in patients hospitalized for acute COVID-19 pneumonia. METHODS: Relevant studies were searched through MEDLINE, EMBASE, and Google Scholar from their inception until 15th June 2023. We aimed to identify any study including: i) adults admitted to intensive care units (ICU) or medicine wards (MW) for acute COVID-19 pneumonia; ii) viscoelastic testing; iii) mortality. RESULTS: We included 13 studies: nine prospective and four retrospective, 231 (30.4 %) non-survivors and 528 (69.6 %) survivors. Mortality rates ranged from 12.8 % to 67.5 %. The studies using the TEG apparatus found a significant difference in K time in the Kaolin test among survivors vs. non-survivors (mean difference [MD] 0.20, 95 % confidence interval [CI] 0.12, 0.28, I2 0%). The studies using the rotational thromboelastometry apparatus found a significant difference in CT-INTEM (MD -17.14, 95 % CI -29.23, -5.06, I2 0%) and LI60-EXTEM (MD -1.00, 95 % CI -1.00, -1.00, I2 0%) assays among survivors vs. non-survivors. CONCLUSION: We identified no specific hypercoagulable or hypocoagulable profile associated with mortality in patients with COVID-19-related pneumonia. Large prospective studies are needed to explore the possible prognostic role of VET in this subset of patients.


Assuntos
COVID-19 , Pneumonia , Trombofilia , Adulto , Humanos , Estudos Retrospectivos , Estudos Prospectivos
7.
J Clin Med ; 12(20)2023 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-37892778

RESUMO

Transthyretin amyloidosis (ATTR) is a group of diseases caused by the deposition of insoluble fibrils derived from misfolded transthyretin, which compromises the structure and function of various organs, including the heart. Thromboembolic events and increased bleeding risk are among the most important complications of ATTR, though the underlying mechanisms are not yet fully understood. Transthyretin plays a complex role in the coagulation cascade, contributing to the activation and regulation of the coagulation and fibrinolytic systems. The prevalence of atrial fibrillation, cardiac mechanical dysfunction, and atrial myopathy in patients with ATTR may contribute to thrombosis, though such events may also occur in patients with a normal sinus rhythm and rarely in properly anticoagulated patients. Haemorrhagic events are modest and mainly linked to perivascular amyloid deposits with consequent capillary fragility and coagulation anomalies, such as labile international-normalised ratio during anticoagulant therapy. Therefore, it is paramount to carefully stratify the thrombotic and haemorrhagic risks, especially when initiating anticoagulant therapy. Our review aims to ascertain the prevalence of thromboembolic and haemorrhagic events in ATTR and identify potential risk factors and predictors and their impact on antithrombotic therapy.

8.
Pharmaceuticals (Basel) ; 16(10)2023 Oct 18.
Artigo em Inglês | MEDLINE | ID: mdl-37895957

RESUMO

In the last decades, studies on the inflammatory signaling pathways in multiple pathological contexts have revealed new targets for novel therapies. Among the family of G-protein-coupled Proteases Activated Receptors, PAR2 was identified as a driver of the inflammatory cascade in many pathologies, ranging from autoimmune disease to cancer metastasis. For this reason, many efforts have been focused on the development of potential antagonists of PAR2 activity. This work focuses on a small molecule, 1-Piperidine Propionic Acid (1-PPA), previously described to be active against inflammatory processes, but whose target is still unknown. Stabilization effects observed by cellular thermal shift assay coupled to in-silico investigations, including molecular docking and molecular dynamics simulations, suggested that 1-PPA binds PAR2 in an allosteric pocket of the receptor inactive conformation. Functional studies revealed the antagonist effects on MAPKs signaling and on platelet aggregation, processes mediated by PAR family members, including PAR2. Since the allosteric pocket binding 1-PPA is highly conserved in all the members of the PAR family, the evidence reported here suggests that 1-PPA could represent a promising new small molecule targeting PARs with antagonistic activity.

9.
J Clin Med ; 12(15)2023 Jul 25.
Artigo em Inglês | MEDLINE | ID: mdl-37568292

RESUMO

Coagulation factor XI (FXI) promotes fibrin formation and inhibits fibrinolysis. Elevated plasma FXI levels, limited to a single measurement, are associated with a higher thrombotic risk. Our case-control study aimed to identify the effect of persistently increased plasma FXI levels on the risk of deep vein thrombosis (DVT). All patients evaluated between January 2016 and January 2018 for a first episode of proximal DVT of the lower extremity were considered for enrolment. Plasma FXI levels were measured at least 1 month after the discontinuation of anticoagulant treatment (T1). The patients with increased plasma FXI levels (>90th percentile of controls) were tested again 3 months later (T2). Among the 200 enrolled patients (M/F 114/86, age range 26-87 years), 47 patients had increased plasma FXI levels at T1 and16 patients had persistently increased plasma FXI levels at T2. The adjusted odds ratio for DVT was 2.4 (95% CI, 1.3 to 5.5, p < 0.001) for patients with increased FXI levels at T1 and 5.2 (95% CI, 2.3 to 13.2, p < 0.001) for patients with persistently high FXI levels at T2. Elevated FXI levels constitute a risk factor for deep vein thrombosis, and this risk nearly doubled in patients with persistently increased plasma FXI levels. Larger prospective studies are needed to confirm our findings.

11.
Front Cardiovasc Med ; 10: 1219274, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37283587
13.
Front Cardiovasc Med ; 10: 1335296, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-38259312

RESUMO

The most frequent haematological malignancy associated with acquired hypo/dysfibrinogenemia is multiple myeloma. We present an unusual case of severe haemorrhagic diathesis due to acquired hypofibrinogenemia in a patient with early T-cell precursor acute lymphoblastic leukaemia/lymphoma (ETP-ALL/LBL). A 57-year-old male was admitted to the General Internal Medicine Department of Padova University Hospital for acute massive haematomas of the left lower extremity associated with macrohaematuria. Coagulation tests showed prolonged prothrombin time, activated partial thromboplastin time and thrombin time due to isolated severe hypofibrinogenemia (antigen 0.70 g/L and activity 26%). The radiological workup showed a bulky lesion located in the anterior mediastinum, and a biopsy led to the diagnosis of ETP-ALL/LBL. Fibrinogen replacement therapy failed to correct the bleeding diathesis and we were able to exclude other frequent causes of acquired hypofibrinogenemia (i.e., liver dysfunction, fibrinogen-specific antibody or drug toxicity); therefore, we hypothesised that hypofibrinogenemia might stem either from enhanced removal of fibrinogen from the circulation or consumptive coagulopathy. Notably, only after initiating a specific chemotherapy treatment did the patient start showing improvement in bleeding symptoms and achieve normal fibrinogen levels.

14.
Best Pract Res Clin Haematol ; 35(1): 101346, 2022 03.
Artigo em Inglês | MEDLINE | ID: mdl-36030065

RESUMO

Patients with pancreatic cancer have a very high risk of both venous and arterial thrombosis compared with other cancers, caused by a tumour-driven hypercoagulable state. Better understanding of pancreatic cancer-associated prothrombotic and proinflammatory mechanisms opens the door to controlling prothrombotic states, ideally, without affecting the overall haemostasis. This narrative review brings together currently available evidence on epidemiology and pathogenesis of thrombotic complications in pancreatic adenocarcinoma. We describe risk factors for thrombosis and established and novel mechanisms of hypercoagulability. Among novel pathways of hypercoagulability, the release of neutrophils extracellular traps (NETs) by activated neutrophils and the crucial role of extracellular vesicles (EV) in participating in platelet and coagulation activation were described. We also reported recent evidence on EV role in thrombin generation amplification through the activation of the intrinsic pathway, discussing potential molecules implicated in this process.


Assuntos
Adenocarcinoma , Neoplasias Pancreáticas , Trombofilia , Trombose , Humanos , Neoplasias Pancreáticas
16.
Viruses ; 14(4)2022 03 31.
Artigo em Inglês | MEDLINE | ID: mdl-35458467

RESUMO

Background: Therapeutic/intermediate-dose heparin reduces the risk of thromboembolic events but increases the risk of major bleeding in patients hospitalized for acute COVID-19 pneumonia. Objectives: To prospectively assess the incidence of objectively proven venous thromboembolism (VTE) and identify predisposing risk factors in a cohort of hospitalized patients with acute COVID-19 pneumonia undergoing prophylactic-dose heparin. Patients and methods: All consecutive patients admitted for acute COVID-19 pneumonia to the General Internal Medicine Unit of Padova University Hospital, Italy between November 2020 and April 2021, and undergoing prophylactic-dose heparin, were enrolled. Demographic and clinical characteristics and laboratory and radiological findings were recorded on admission. Cases were patients who developed VTE during their hospital stay. Univariable and multivariable logistic regression analyses were used to ascertain the risk factors associated with developing in-hospital VTE. Results: 208 patients (median age: 77 years; M/F 98/110) were included; 37 (18%) developed in-hospital VTE during a median follow-up of 10 days (IQR, 4−18). VTE patients were significantly younger (p = 0.004), more obese (p = 0.002), and had a lower Padua prediction score (p < 0.03) and reduced PaO2/FIO2 ratio (p < 0.03) vs. controls. Radiological findings of bilateral pulmonary infiltrates were significantly more frequent in VTE patients than controls (p = 0.003). Multivariable regression showed that obesity (1.75, 95% CI 1.02−3.36; p = 0.04) and bilateral pulmonary infiltrates on X-rays (2.39, 95% CI 1.22−5.69; p = 0.04) were correlated with increased risk of in-hospital VTE. Conclusions: Obesity and bilateral pulmonary infiltrates on imaging may help clinicians to identify patients admitted to medical wards for acute COVID-19 pneumonia at risk of developing VTE despite prophylactic-dose heparin. Further studies are needed to evaluate whether the administration of therapeutic/intermediate-dose heparin may help prevent VTE episodes without further increasing the bleeding risk.


Assuntos
COVID-19 , Tromboembolia Venosa , Idoso , Anticoagulantes/uso terapêutico , COVID-19/epidemiologia , Heparina/efeitos adversos , Humanos , Obesidade/complicações , Estudos Retrospectivos , Fatores de Risco , Tromboembolia Venosa/tratamento farmacológico , Tromboembolia Venosa/epidemiologia , Tromboembolia Venosa/prevenção & controle
17.
Thromb Haemost ; 122(8): 1352-1360, 2022 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-35253140

RESUMO

A large number of daily requests to exclude possible prothrombotic risk factors for coronavirus disease 2019 (COVID-19) vaccines were received. Our aim was to longitudinally evaluate coagulation profiles in a series of healthy subjects who received COVID-19 vaccination and assess hypercoagulability thereafter. Volunteers awaiting a first or second dose of either the ChAdOx1 or BNT162b2 vaccine were enrolled. Venous samples were obtained at baseline (before the vaccine) and longitudinally 3 ± 2 days (T1) and 10 ± 2 days after the vaccine (T2). Global coagulation monitoring was assessed via platelet count, whole blood thromboelastometry and impedance aggregometry, plasma thrombin generation, and anti-platelet factor 4 (PF4)/heparin immunoglobulin G antibodies. One hundred and twenty-two subjects were enrolled (61 [50%] ChAdOx1 and 61 BNT162b2). The ChAdOx1 cohort showed a slight but transient increase in thrombin generation (mainly endogenous thrombin potential [ETP] with thrombomodulin and ETP ratio) at T1, which promptly decreased at T2. In addition, the second dose of either vaccine was associated with increased thrombin peak, ETP with thrombomodulin, and ETP ratio. At baseline, 3.2% of the ChAdOx1 cohort and 1.6% BNT162b2 cohort were positive for PF4/heparin antibodies with a stable titer through T1 and T2. No relevant differences were detected in platelet count and aggregation, or thromboelastometry parameters. No thrombotic or hemorrhagic events occurred. We can confirm that no clinically meaningful hypercoagulability occurred after either vaccine, albeit keeping in mind that thrombin generation may increase in the first days after the second dose of either vaccine and after the first dose of the ChAdOx1 vaccine.


Assuntos
Vacinas contra COVID-19 , COVID-19 , Trombofilia , Vacina BNT162 , COVID-19/prevenção & controle , Vacinas contra COVID-19/efeitos adversos , Heparina/efeitos adversos , Humanos , Estudos Longitudinais , Trombina , Trombomodulina , Trombofilia/diagnóstico , Trombofilia/etiologia , Vacinação
18.
Res Pract Thromb Haemost ; 6(2): e12678, 2022 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-35284776

RESUMO

Background: Low plasma levels of protein C or protein S are associated with venous thromboembolism rather than myocardial infarction. The high coagulant activity in patients with thrombophilia with a (familial) defect in protein C or S is explained by defective protein C activation, involving thrombomodulin and protein S. This causes increased plasmatic thrombin generation. Objective: Assess the role of platelets in the thrombus- and fibrin-forming potential in patients with familial protein C or protein S deficiency under high-shear flow conditions. Patients/Methods: Whole blood from 23 patients and 15 control subjects was perfused over six glycoprotein VI-dependent microspot surfaces. By real-time multicolor microscopic imaging, kinetics of platelet thrombus and fibrin formation were characterized in 49 parameters. Results and Conclusion: Whole-blood flow perfusion over collagen, collagen-like peptide, and fibrin surfaces with low or high GPVI dependency indicated an unexpected impairment of platelet activation, thrombus phenotype, and fibrin formation but unchanged platelet adhesion, observed in patients with protein C deficiency and to a lesser extent protein S deficiency, when compared to controls. The defect extended from diminished phosphatidylserine exposure and thrombus contraction to delayed and suppressed fibrin formation. The mechanism was thrombomodulin independent, and may involve negative platelet priming by plasma components.

20.
Angiology ; 73(7): 649-654, 2022 08.
Artigo em Inglês | MEDLINE | ID: mdl-34989625

RESUMO

The incidence of post-thrombotic syndrome (PTS) in patients with deep vein thrombosis (DVT) treated with direct oral anticoagulants (DOACs) remains a matter of debate. Hence, our endeavor to investigate a large cohort of patients with a first episode of proximal DVT treated with DOACs to ascertain the incidence and predisposing risk factors for PTS. All consecutive patients referred to the Thrombotic and Haemorrhagic Diseases Unit of Padova University Hospital (Italy) between January 2014 and January 2018 for a first episode of proximal DVT were considered for enrollment. Participants received DOACs for a minimum period of 3 months. PTS was assessed using the Villalta score up to 36 months after DVT diagnosis. Among 769 enrolled patients (M/F 353/416, age range 26-87 years), 152 (19.8%) developed PTS and 30 (3.9%) developed severe PTS. The adjusted hazard ratio was significant for obesity (1.64, 95% CI 1.28-2.39) and DVT site (femoral and/or iliac veins vs popliteal vein) (1.23, 95% CI 1.15-3.00). The incidence of PTS is not negligible in patients with proximal DVT despite the use of DOACs. We identified obesity and iliofemoral DVT as possible risk factors for PTS. Larger prospective studies are needed to confirm our findings and optimize therapeutic strategies.


Assuntos
Síndrome Pós-Trombótica , Trombose Venosa , Adulto , Idoso , Idoso de 80 Anos ou mais , Anticoagulantes/efeitos adversos , Humanos , Pessoa de Meia-Idade , Obesidade/complicações , Síndrome Pós-Trombótica/epidemiologia , Síndrome Pós-Trombótica/etiologia , Síndrome Pós-Trombótica/prevenção & controle , Fatores de Risco , Trombose Venosa/tratamento farmacológico , Trombose Venosa/epidemiologia
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