key: cord-0940570-eqqsd3xl
authors: Rosa, Felipe Damascena; Burihan, Marcelo Calil; Simões, Elexandra Aparecida; Abdala, João Paulo de Souza; Barros, Orlando da Costa; Nasser, Felipe
title: Acute upper limb arterial ischemia in patients diagnosed with COVID-19: case series
date: 2021-06-16
journal: J. vasc. bras
DOI: 10.1590/1677-5449.200234
sha: e16feb9ab08e32e27728aa2e65f49eea28944003
doc_id: 940570
cord_uid: eqqsd3xl

Infection by coronavirus 2, cause of the severe acute respiratory syndrome (SARS-CoV-2) in humans, was detected for the first time in Wuhan, China, in 2019, and spread globally over the course of 2020. Its different clinical manifestations are challenging, with a wide spectrum of presentations, ranging from asymptomatic infections to severe forms that can result in death. The objective of this study is to describe a series of four cases of acute arterial ischemia involving the upper limbs in patients diagnosed with COVID-19, which were managed clinically with anticoagulation, platelet antiaggregation, and prostanoids. Two patients were discharged from hospital with regression and delimitation of the ischemic zone, without needing surgical intervention, while two patients died from pulmonary complications. Adequate understanding of the pathophysiology of this disease could support better clinical management of its complications.

The emergence of a new disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) in December 2019 in Wuhan, China, brought with it the challenge of achieving clinical and pathophysiologic characterization. The disease spread all over the world during the first half of 2020, was named the novel coronavirus disease (COVID- 19) by the World Health Organization, which declared it a pandemic in March 2020. 1 Initially presenting as a respiratory syndrome involving the lower respiratory tract, a large variety of signs, symptoms, and clinical presentations were soon observed, ranging from oligosymptomatic cases to cases that progress to respiratory insufficiency, coagulopathy, multiple organ failure, and death. 2, 3 Studies have identified a hypercoagulable state that can provoke complications in the micro and macro circulation. [4] [5] [6] Below, a series will be described of four patients who exhibited acute arterial ischemia in the upper limbs and were diagnosed with COVID-19. This project was approved by the Research Ethics Committee CAAE 37208320.5.0000.0066, ruling number: 4.303.538.

The patient was an 18-year-old, previously healthy, female who presented at the emergency room complaining of continuous pain of moderate and progressive intensity, associated with cyanosis of the fourth finger of the right hand, with onset 2 days previously. She denied fever, trauma, respiratory complaints, allergies, smoking, injected drug use, or contact with people diagnosed with COVID- 19 . She reported that she was taking a combined oral contraceptive regularly (levonorgestrel 0.15 mg and ethinylestradiol 0.03 mg). Physical examination was unremarkable, with the exception of upper limb palpation, during which pulses were present and symmetrical, but the distal phalanx of the fourth finger of the right hand had a lower temperature and had blanching cyanosis ( Figure 1 ). The results of laboratory tests ordered at admission are shown in Table 1 . Tests for rheumatoid factor and anti-DNA antibody were negative and a lupus anticoagulant test was positive. Vascular echography (VE) of the right upper limb showed patent arteries with normal caliber and triphasic flow and no abnormalities were provoked by maneuvers to identify thoracic outlet syndrome (TOS). A reverse transcriptase-polymerase chain reaction (RT-PCR) assay for SARS-CoV-2 in a nasopharyngeal sample was positive.

The patient underwent respiratory isolation and platelet antiaggregation was started with acetylsalicylic acid (ASA) at 100 mg/day, combined with full anticoagulation with enoxaparin (1 mg/kg every 12). Since the patient was still in pain, she was put on intravenous alprostadil (40 mcg every 12h) and prednisone at an anti-inflammatory dosage (0.5 mg/kg/day) for 7 days. She progressed with improvement in pain, regression of cyanosis, and resolution of the temperature gradient and was discharged from hospital on the 14th day after admission (Figure 2 ).

The patient was a 57-year-old female with systemic arterial hypertension (SAH) and type 2 diabetes mellitus (DM) who presented at the emergency room complaining of intense and continuous pain in the second finger of the left hand that was unresponsive to standard analgesics, had onset 2 days previously and was associated with paresthesia, low temperature, and non-blanching cyanosis ( Figure 3 ). She denied fever, trauma, coughing, use of injected drugs, and smoking. She stated that she was using glibenclamide, enalapril, ASA, cilostazol, and nifedipine regularly. General physical examination found nothing of note; palpation of the upper and lower extremities identified pulses present and symmetrical and a temperature drop at the level of the distal phalanx of the second finger of the left hand. The results of laboratory tests ordered at admission are shown in Table 1 . VE of the left upper limb showed patent arteries with normal caliber and triphasic flow and no significant stenosis. No abnormalities were provoked by maneuvers to identify TOS. The echocardiogram showed normal ejection fraction, with no areas of ventricular asthenia or thrombi identifiable in the cardiac chambers.

The patient was put on full anticoagulation with enoxaparin (1 mg/kg every 12), combined with intravenous alprostadil (40 mcg every 12h) and prednisone at an anti-inflammatory dosage (0.5 mg/kg/day) for 7 days. The patient recovered well, but since the non-blanching cyanosis of the finger remained, she was maintained on oral anticoagulation with warfarin, targeting an international normalized ratio (INR) between 2 and 3, in order to monitor her progress in outpatients followup. She was discharged after 7 days in hospital on oral warfarin and with an INR of 2.15. At a 14-day outpatients visit, a small area of necrosis was found on the distal phalanx ( Figure 4 ). Since a nasal swab had not been taken when she had been in hospital, a serological test for COVID-19 was ordered and the result was positive for IgG.

The patient was a 75-year-old female ex-smoker (40 pack-years) with grade III obesity, type 2 DM, SAH, and motor sequelae involving the left lower limb caused by a prior stroke. She presented at the emergency room complaining of pain in the left hand, with sudden onset 7 days previously. The pain was continuous and worsening progressively and had progressed to cyanosis of the fingers. She denied trauma, fever, coughing, dyspnea, or use of injected drugs. She was taking metformin, glibenclamide, insulin, atenolol, hydrochlorothiazide, phenytoin, and ASA. Physical examination found axillary, brachial, and ulnar pulses were present and normal, but the radial pulse was absent. The third finger had non-blanching cyanosis and a lower temperature and the remaining fingers of the left hand had blanching cyanosis ( Figure 5 ). The results of laboratory tests ordered at admission are shown in Table 1 . VE of the left upper limb showed patent arteries, with normal caliber and triphasic flow, with diffuse atherosclerosis and atherosclerotic occlusion of the proximal third of the radial artery. Maneuvers to identify TOS were negative. The echocardiogram showed a 61% ventricular ejection fraction, with no areas of ventricular asthenia or thrombi identifiable in the cardiac chambers. Computed tomography (CT) of the chest showed diffuse ground glass signs, compromising more than 50% of the pulmonary fields bilaterally ( Figure 6 ). Her RT-PCR assay for SARS-CoV-2 was positive.

She was put on full anticoagulation with enoxaparin (1 mg/kg every 12h), ASA 100 mg/day, and intravenous alprostadil (40 mcg every 12h). Her severe respiratory condition deteriorated and she died after 27 days in hospital.

The patient was an 84-year-old female who presented at the emergency room with a history of dry coughing, general malaise, lack of appetite, and recurrent episodes of dyspnea, with onset 7 days previously. She described the following personal history: SAH and dyslipidemia, taking losartan, ASA, and simvastatin. Physical examination found diffuse rales throughout the entire right hemithorax and the lower third of the left hemithorax, respiratory rate was 24 inspirations per minute, oxygen saturation was 77% in room air and 92% with an oxygen mask (4 L/min). Palpation of upper and lower extremities detected pulses present and symmetrical, with no temperature gradient. The results of laboratory tests ordered at admission are shown in Table 1 . An RT-PCR assay of a nasopharyngeal sample was positive for SARS-CoV-2. CT of the thorax showed diffuse ground-glass interstitial-alveolar opacities ( Figure 7) .

The patient's condition became critical and, on the 10th day after admission to the intensive care unit (ICU), she exhibited non-blanching cyanosis involving the right hand only, with pulses still present ( Figure 8 ). She was put on a full anticoagulation protocol with unfractionated heparin, which contained the ischemia. However, the patient died from infectious and pulmonary complications after 42 days in hospital. 

The initial presentation of COVID-19 is usually with respiratory symptoms such as dry coughing, sore throat, and general nonspecific symptoms, such as asthenia, body pains, and fever. 2, 3 The most severe cases, requiring oral endotracheal intubation and developing septic shock and coagulopathy, generally occur during a later phase, between the 7th and 12th days of the disease, provoking a need for invasive support. 2,3 Age over 60 years and presence of comorbidities such as obesity, DM, and SAH are recognized risk factors for unfavorable prognosis. 2, 3 The first three cases presented above did not develop typical clinical complaints and sought medical care because of microcirculation ischemia involving the upper limbs. Patients 1 and 2 had favorable clinical course and did not need interventions or prolonged hospital stays; anticoagulant treatment and antiplatelet drugs were started early, which could have contributed to preventing progression of the ischemic injuries. 7 Tang et al. 4 demonstrated that elevation of fibrin degeneration products, including D-dimer, and changes affecting the fibrinolytic system can be present from the initial phases of COVID-19, predisposing to pro-thrombotic states and worse prognosis. 5, 6 Anatomopathological studies have identified fibrin deposits in the alveoli and interstitial space in the lungs, with additional evidence of microcirculation thrombosis. 8 Moreover, adoption of anticoagulation protocols has been associated with reduced mortality of patients with COVID-19. 9,10 Presence of the lupus anticoagulant antibody has been observed in patients with COVID-19 and its possible relationship with the prothrombotic state is under investigation. 11 It is still unclear whether the changes to hemostasis are directly caused by SARS-COV-2 or whether they are a consequence of an exacerbated inflammatory response, the "cytokine storm". 12 As such, use of heparin may contribute both because of its anticoagulant effect and because of its anti-inflammatory effect. [13] [14] [15] [16] [17] Use of prostanoids in cases of critical ischemia without the conditions for revascularization has been described in the literature and there are previous reports of good results in terms of relief from pain and a small favorable effect on healing of wounds. There is also a case report of their use in the context of COVID-19. 18, 19 In the cases presented here, improvements in pain were observed after introduction of alprostadil, without adverse reactions.

An increase in cases of acute arterial ischemia has been reported during the pandemic. Bellosta et al. 20 described 20 cases of acute arterial ischemia of lower limbs requiring surgical revascularization. Mortality was 40% and full anticoagulation during the postoperative period was related to better prognosis and a lower rate of reinterventions during the postoperative period. 20 In this sample of patients, they did not observe major hemorrhagic events among the patients put on anticoagulation and outcomes were apparently good in relation to containment of ischemic phenomena. 8 

O surgimento de uma nova doença causada coronavírus 2 causador da síndrome respiratória aguda grave (SARS-COV-2) em dezembro de 2019 em Wuhan, na China, que se espalhou ao redor do mundo no primeiro semestre de 2020, impôs novos desafios para a caracterização clínica e fisiopatológica dessa enfermidade. Denominada doença do novo coronavírus (COVID-19) pela Organização Mundial de Saúde, a doença foi declarada pandêmica em março de 2020 1 .

Inicialmente apresentada como síndrome respiratória de vias aéreas inferiores, logo se observou uma gama de sinais, sintomas e apresentações clínicas, que vão desde casos oligossintomáticos até àqueles que evoluem com insuficiência respiratória, coagulopatia, disfunção de múltiplos órgãos e morte 2,3 . Estudos têm apontado para um estado de hipercoagulabilidade, que poderia culminar em complicações da micro e da macrocirculação [4] [5] [6] .

A seguir, será relatada uma série de quatro pacientes que apresentaram isquemia arterial aguda dos membros superiores e diagnóstico de COVID-19. Este trabalho foi aprovado pelo Comitê de Ética em Pesquisa CAAE 37208320.5.0000.0066, número do parecer: 4.303.538.

Paciente do sexo feminino, 18 anos de idade, previamente hígida, deu entrada no pronto-socorro com queixa de dor contínua, de moderada intensidade, progressiva, associada a cianose de quarto quirodáctilo direito, com início há 2 dias. Negava febre, trauma, queixas respiratórias, alergias, tabagismo, uso de drogas injetáveis ou contato com pessoas diagnosticadas com COVID-19. Referia fazer uso regular de anticoncepcional oral combinado (levonorgestrel 0,15 mg e etinilestradiol 0,03 mg). Ao exame físico, apresentava-se sem anormalidades, exceto na palpação das extremidades superiores, em que foram observados pulsos presentes, simétricos, redução da temperatura a nível de falange distal de quarto quirodáctilo direito e cianose não fixa (Figura 1). Os exames laboratoriais à admissão estão discriminados na Tabela 1. A pesquisa do fator reumatoide e do anticorpo anti-DNA foi negativa, e do anticoagulante lúpico foi positiva. A ecografia vascular (EV) do membro superior direito demonstrou artérias pérvias, de calibre preservado, com fluxo trifásico, sem alterações às manobras para identificação de síndrome do desfiladeiro torácico (SDT). O exame de reação da transcriptase reversa seguida pela reação em cadeia da polimerase (RT-PCR) para SARS-CoV-2 em amostra nasofaríngea foi positivo.

Foi realizado isolamento respiratório e iniciada antiagregação plaquetária com ácido acetilsalicílico (AAS), 100 mg/dia, associado à anticoagulação plena com enoxaparina (1 mg/kg de 12 em 12 h). Devido à manutenção de queixas álgicas, associou-se alprostadil por via intravenosa (40 mcg de 12 em 12 h) e prednisona em dose anti-inflamatória (0,5 mg/kg/dia) por 7 dias. A paciente evoluiu com melhora da dor, regressão da cianose e do gradiente térmico, recebendo alta hospitalar no 14º dia de internação (Figura 2).

Paciente do sexo feminino, 57 anos de idade, portadora de hipertensão arterial sistêmica (HAS) e diabetes melito (DM) tipo 2, deu entrada no prontosocorro com relato de dor intensa e contínua em segundo quirodáctilo esquerdo, não responsiva a analgésicos comuns, com início há 2 dias, associado à parestesia, redução de temperatura e cianose fixa (Figura 3). Negava febre, trauma, tosse, uso de drogas injetáveis ou tabagismo. Relatava fazer uso regular de glibenclamida, enalapril, AAS, cilostazol e nifedipina. Ao exame físico geral, não foram detectadas anormalidades; a palpação das extremidades superiores e inferiores identificou pulsos presentes, simétricos, com redução de temperatura a nível da falange distal de segundo quirodáctilo esquerdo. Os exames laboratoriais à admissão estão discriminados na Tabela 1. A EV do membro superior esquerdo demonstrou artérias pérvias, de calibre preservado, com fluxo trifásico, sem estenoses significativas e sem alterações às manobras para identificação de SDT. O ecocardiograma apresentou fração de ejeção preservada, sem áreas de adinamia ventricular ou trombos identificáveis em câmaras cardíacas.

Optou-se por anticoagulação plena com enoxaparina (1 mg/kg de 12 em 12 h), associado a alprostadil por via intravenosa (40 mcg de 12 em 12 h) e prednisona em dose anti-inflamatória (0,5 mg/kg/dia) por 7 dias. A paciente evoluiu bem; no entanto, devido à manutenção de cianose fixa de extremidade, optouse por manter a anticoagulação oral com varfarina, objetivando uma razão de normatização internacional (RNI) entre 2 e 3, a fim de acompanhar a delimitação do processo ambulatorialmente. A paciente recebeu alta no 7º dia de internação, com varfarina oral e RNI de 2,15. No retorno ambulatorial em 14 dias, foi observada pequena necrose seca em falange distal (Figura 4). Como não foi realizada coleta de swab nasal durante a internação, solicitou-se sorologia para COVID-19, sendo detectado IgG positivo.

Paciente do sexo feminino, 75 anos de idade, portadora de obesidade grau III, DM tipo 2, HAS, ex-tabagista (40 maços-ano), com sequela motora em membro inferior esquerdo devido a um acidente vascular encefálico isquêmico prévio. Compareceu ao pronto-socorro queixando-se de dor há 7 dias em mão esquerda, de início súbito, contínua, com piora progressiva e evolução para cianose de quirodáctilos. Negava trauma, febre, tosse, dispneia ou uso de drogas injetáveis. Relatava uso de metformina, glibenclamida, insulina, atenolol, hidroclorotiazida, fenitoína e AAS. Ao exame físico, apresentava-se com pulsos axilar, braquial e ulnar presentes e normais e pulso radial ausente, cianose fixa e redução da temperatura do terceiro quirodáctilo e cianose não fixa dos demais quirodáctilos à esquerda (Figura 5). Os exames laboratoriais à admissão estão discriminados na Tabela 1. A EV do membro superior esquerdo evidenciou artérias pérvias, de calibre preservado, com fluxo trifásico, com aterosclerose difusa e oclusão aterosclerótica da artéria radial em seu terço proximal, e as manobras para identificação de SDT foram negativas. O ecocardiograma apresentou fração de ejeção ventricular de 61%, sem áreas de adinamia ventricular ou trombos identificáveis em câmaras cardíacas. A tomografia computadorizada (TC) de tórax evidenciou imagens em vidro fosco difusamente, comprometendo mais que 50% dos campos pulmonares bilateralmente (Figura 6). O RT-PCR para SARS-CoV-2 foi positivo.

Optou-se por iniciar anticoagulação plena com enoxaparina (1 mg/kg de 12 em 12 h), AAS 100 mg/dia, associado a alprostadil por via intravenosa (40 mcg de 12 em 12h). A paciente evoluiu com quadro respiratório grave e óbito após 27 dias de internação.

Paciente do sexo feminino, 84 anos de idade, deu entrada no pronto-socorro com história de tosse seca, mal-estar geral, inapetência e episódios recorrentes de dispneia há 7 dias. A paciente relatou os seguintes antecedentes pessoais: HAS e dislipidemia, em uso de losartana, AAS e sinvastatina. Ao exame físico, apresentava crepitações difusas em todo o hemitórax direito e terço inferior de hemitórax esquerdo, frequência respiratória de 24 incursões respiratórias por minuto (irpm), saturação de oxigênio de 77% em ar ambiente e de 92% com máscara de oxigênio (4 L/min). Na palpação das extremidades superiores e inferiores, foram detectados pulsos presentes, simétricos, sem gradiente térmico. Os exames laboratoriais à admissão estão discriminados na Tabela 1. Foi realizado RT-PCR de amostra nasofaríngea, sendo positivo para SARS-CoV-2. A TC de tórax revelou opacidades interstício-alveolares em padrão vidro fosco difusamente (Figura 7) .

A paciente evoluiu com gravidade, e, no 10º dia de internação em unidade de terapia intensiva (UTI), apresentou cianose fixa somente em mão direita, com pulsos presentes (Figura 8). Foi iniciado protocolo de anticoagulação plena com heparina não fracionada, com contenção da isquemia. No entanto, a paciente foi a óbito por complicações infecciosas e pulmonares após 42 dias de internação.

A apresentação inicial da COVID-19 é usualmente com sintomas respiratórios, como tosse seca, dor de garganta, e sintomas gerais inespecíficos, como adinamia, dores no corpo e febre 2,3 . As formas mais graves, com necessidade de intubação orotraqueal, choque séptico e coagulopatia, ocorrem geralmente em uma fase mais tardia, entre o 7º e 12º dia de doença, levando à necessidade de suporte intensivo 2,3 . A idade maior que 60 anos e a presença de comorbidades, como obesidade, DM e HAS, são reconhecidos fatores de risco para prognóstico desfavorável 2,3 .

Os três primeiros casos apresentados não desenvolveram queixas clínicas típicas e procuraram assistência médica devido a quadro de isquemia de microcirculação dos membros superiores. As pacientes 1 e 2 tiveram evolução favorável, sem necessidade de intervenções e internação prolongada; o tratamento anticoagulante e antiagregante plaquetário foi iniciado precocemente, o que pode ter contribuído para impedir a progressão da lesão isquêmica 7 .

Tang et al. 4 demonstraram que elevação de produtos da degradação da fibrina, entre eles o D-dímero, e alterações do sistema fibrinolítico podem estar presentes desde as fases iniciais da COVID-19, predispondo a estados pró-trombóticos e pior prognóstico 5, 6 . Estudos anatomopatológicos identificaram deposição de fibrina nos alvéolos e espaços intersticiais dos pulmões, com evidências adicionais de trombose da microcirculação 8 . Por outro lado, a adoção de protocolos de anticoagulação foi associada à diminuição da mortalidade em pacientes com COVID-19 9,10 . A presença de anticorpo anticoagulante lúpico tem sido observada em pacientes com COVID-19, e investigase sua possível relação com estado pró-trombótico 11 . Ainda é incerto que as alterações na hemostasia sejam devido ao efeito direto do SARS-COV-2 ou se seria consequência da resposta inflamatória exacerbada, a chamada "tempestade de citoninas" 12 . Nesse sentido, o uso da heparina poderia contribuir tanto pelo seu efeito anticoagulante quanto pelo seu efeito anti-inflamatório [13] [14] [15] [16] [17] .

O uso de prostanoides em casos de isquemia crítica sem condições de revascularização é descrito na literatura, havendo relatos prévios de bons resultados na melhora da dor e pequeno efeito favorável na cicatrização de feridas. Além disso, há relato de caso de seu uso no contexto da COVID-19 18, 19 . Nos casos apresentados, foi observado melhora das queixas álgicas após a introdução de alprostadil, sem reações adversas.

O aumento de casos de isquemia arterial aguda tem sido relatado durante esta pandemia. Bellosta et al. 20 descreveram 20 casos de isquemia arterial aguda de membros inferiores, com necessidade de revascularização cirúrgica. A mortalidade foi de 40%, e a anticoagulação plena no pós-operatório foi relacionada a melhor prognóstico e menor necessidade de reintervenção no pós-operatório 20 . Nesta casuística, não se observaram eventos hemorrágicos maiores nos pacientes submetidos à anticoagulação, tendo aparentemente bom desfecho em relação à contenção dos fenômenos isquêmicos.

Coronavirus disease (COVID-19). 2020 [atualizado

Clinical features of patients infected with 2019 novel coronavirus in Wuhan

A novel coronavirus from patients with pneumonia in China

Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia

Prominent changes in blood coagulation of patients with SARS-CoV-2 infection

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Potential therapeutic effects of dipyridamole in the severely ill patients with COVID-19

COVID-19-associated coagulopathy: an exploration of mechanisms

Unfractionated heparin attenuates LPS-induced IL-8 secretion via PI3K/Akt/NF-kB signaling pathway in human endothelial cells

In-vitro suppression of IL-6 and IL-8 release from human pulmonary epithelial cells by nonanticoagulant fraction of enoxaparin

Anticoagulant and antiarrhythmic effects of heparin in the treatment of COVID-19 patients

Coronavirus disease (COVID-19). 2020 [atualizado

Clinical features of patients infected with 2019 novel coronavirus in Wuhan

A novel coronavirus from patients with pneumonia in China

Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia

Prominent changes in blood coagulation of patients with SARS-CoV-2 infection

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

Potential therapeutic effects of dipyridamole in the severely ill patients with COVID-19

Complement associated microvascular injury and thrombosis in the pathogenesis of severe COVID-19 infection: a report of five cases

Anticoagulant treatment is associated with decreased mortality in severe coronavirus disease 2019 patients with coagulopathy

Association of treatment dose anticoagulation with in-hospital survival among hospitalized patients with COVID-19

Lupus anticoagulant and abnormal coagulant tests in patients with COVID-19

COVID-19: consider cytokine storm syndromes and immunosuppression

COVID-19-associated coagulopathy: an exploration of mechanisms

Unfractionated heparin attenuates LPS-induced IL-8 secretion via PI3K/Akt/NF-kB signaling pathway in human endothelial cells

In-vitro suppression of IL-6 and IL-8 release from human pulmonary epithelial cells by nonanticoagulant fraction of enoxaparin

Anticoagulant and antiarrhythmic effects of heparin in the treatment of COVID-19 patients

COVID-19 and thrombotic or thromboembolic disease: implications for prevention, antithrombotic therapy, and follow-Up: JACC state-of-the-art review

Prostanoids for critical limb ischemia: a clinical review and consideration of current guideline recommendations

Alprostadil associated with low molecular weight heparin to treat limb ischemia caused by SARS-CoV2

PMid:32360679. Correspondência Felipe Damascena Rosa Hospital Santa Marcelina Rua Santa Marcelina

felipedcena@gmail.com Informações sobre os autores FDR -Mestre em Medicina

Hospital Santa Marcelina; Coordenador, Setor de Radiologia Vascular Intervencionista

Contribuições dos autores Concepção e desenho do estudo: FDR, MCB, FN