Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 35
Filtrar
2.
Med Sci Monit ; 26: e922167, 2020 May 18.
Artigo em Inglês | MEDLINE | ID: mdl-32418983

RESUMO

BACKGROUND Inflammation plays an important part in the pathogenesis of cardiogenic shock (CGS). Whether the neutrophil-lymphocyte ratio (NLR), an integrated biomarker of inflammation, is associated with the outcome of CGS patients remains unknown. This retrospective cohort study was performed to identify the utility of using NLR among patients with CGS. MATERIAL AND METHODS Data were extracted from the MIMIC database. We applied smooth curve fitting to define the NLR cutoff values. The primary outcome was 30-day mortality. Cox proportional hazards models, subgroup analysis, and receiver operator characteristic (ROC) curve analysis were performed. RESULTS A total of 1470 CGS patients were extracted, among which 801 (54.5%) were men. The mean age of the population was 70.37 years. An inverse U-shaped relationship was observed between NLR and mortality in CGS patients, with the highest risk being at values ranging from 9.4 to 15. For the primary outcome of 30-day mortality, the adjusted HR (95% CI) values of the middle tertile (NLR 9.4-15) and the upper tertile (NLR >15) were 1.47 (1.14, 1.88) and 1.22 (0.94, 1.57) compared with the reference of lower tertile (NLR <9.4). ROC curve analysis showed that NLR had a more sensitive prognostic value in predicting 30-day mortality of CGS than the neutrophil or lymphocyte percentage alone (0.660 vs. 0.540, 0.549). CONCLUSIONS An inverse U-shaped curve was presented between NLR and the mortality of CGS. NLR seemed to be a readily available and independent prognostic biomarker for patients with CGS. The prognostic value of NLR was more sensitive than the neutrophil or lymphocyte percentage alone, but not as good as SOFA or SAPSII score.


Assuntos
Contagem de Leucócitos/métodos , Choque Cardiogênico/imunologia , Choque Cardiogênico/patologia , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Estudos de Coortes , Bases de Dados Factuais , Feminino , Humanos , Inflamação/patologia , Estimativa de Kaplan-Meier , Contagem de Linfócitos/métodos , Linfócitos/patologia , Masculino , Pessoa de Meia-Idade , Neutrófilos/patologia , Prognóstico , Modelos de Riscos Proporcionais , Curva ROC , Estudos Retrospectivos , Choque Cardiogênico/mortalidade
3.
Front Immunol ; 11: 600684, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33488595

RESUMO

A plethora of leukocyte modulations have been reported in critically ill patients. Critical illnesses such as acute respiratory distress syndrome and cardiogenic shock, which potentially require extracorporeal membrane oxygenation (ECMO) support, are associated with changes in leukocyte numbers, phenotype, and functions. The changes observed in these illnesses could be compounded by exposure of blood to the non-endothelialized surfaces and non-physiological conditions of ECMO. This can result in further leukocyte activation, increased platelet-leukocyte interplay, pro-inflammatory and pro-coagulant state, alongside features of immunosuppression. However, the effects of ECMO on leukocytes, in particular their phenotypic and functional signatures, remain largely overlooked, including whether these changes have attributable mortality and morbidity. The aim of our narrative review is to highlight the importance of studying leukocyte signatures to better understand the development of complications associated with ECMO. Increased knowledge and appreciation of their probable role in ECMO-related adverse events may assist in guiding the design and establishment of targeted preventative actions.


Assuntos
Oxigenação por Membrana Extracorpórea , Leucócitos/imunologia , Síndrome do Desconforto Respiratório/imunologia , Choque Cardiogênico/imunologia , Humanos , Leucócitos/patologia , Síndrome do Desconforto Respiratório/patologia , Síndrome do Desconforto Respiratório/terapia , Choque Cardiogênico/patologia , Choque Cardiogênico/terapia
4.
J Cardiovasc Med (Hagerstown) ; 20(4): 264-266, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30720635

RESUMO

: Heart transplantation is a life-saving therapy for some patients admitted for acute myocarditis. However, controversial exists about the major risk of rejection following heart transplantation in specific types of myocarditis. Because of relatively few data on the post heart transplant outcomes, we report the long-term follow-up of a 39-year-old patient with a previous history of ulcerative colitis, which rapidly worsened heart failure until an emergency heart transplant in 2004.The clinical course was complicated by many episodes of rejection; lastly, after the development of severe cardiac allograft vasculopathy, re-heart transplantation was needed. The main findings of this case are: 1) inflammatory aetiology should always be suspected in patients with concomitant autoimmune disease that developing rapidly progressing heart failure; 2) patients with inflammatory myocardial disease undergoing heart transplantation should also undergo strict immunological surveillance; 3) the option of performing the re-heart transplant in a patient with a so complex management in the first one could be uncertain, but in this case the young age and lack of noncardiac comorbidities were effective to favour the survivor after two immunologically so challenging heart transplantation.


Assuntos
Autoimunidade , Colite Ulcerativa/imunologia , Rejeição de Enxerto/imunologia , Transplante de Coração/efeitos adversos , Miocardite/cirurgia , Sarcoidose/cirurgia , Adulto , Biópsia , Colite Ulcerativa/diagnóstico , Colite Ulcerativa/terapia , Angiografia Coronária , Diagnóstico Diferencial , Ecocardiografia , Rejeição de Enxerto/diagnóstico , Rejeição de Enxerto/terapia , Humanos , Imunossupressores/administração & dosagem , Masculino , Miocardite/diagnóstico , Miocardite/imunologia , Plasmaferese , Valor Preditivo dos Testes , Reoperação , Sarcoidose/diagnóstico , Sarcoidose/imunologia , Choque Cardiogênico/imunologia , Fatores de Tempo , Resultado do Tratamento
5.
Can J Cardiol ; 34(1): 92.e1-92.e3, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-29275889

RESUMO

The ever-increasing use of immune checkpoint inhibitors in cancer is leading to a high incidence of autoimmune side effects. This report discusses an autoimmune fulminant myocarditis in an elderly patient with metastatic pulmonary adenocarcinoma in whom the most advanced invasive heart failure therapies were used successfully. She was treated with nivolumab. This case illustrates a severe cardiovascular complication of immunotherapy and highlights to cardiologists the importance of aggressive treatments in patients with metastatic cancers whose prognosis has improved dramatically.


Assuntos
Antineoplásicos/efeitos adversos , Miocardite/etiologia , Nivolumabe/efeitos adversos , Adenocarcinoma de Pulmão/tratamento farmacológico , Idoso , Antineoplásicos/administração & dosagem , Edema/etiologia , Feminino , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/imunologia , Humanos , Miocardite/imunologia , Peptídeo Natriurético Encefálico/sangue , Nivolumabe/administração & dosagem , Fragmentos de Peptídeos/sangue , Choque Cardiogênico/etiologia , Choque Cardiogênico/imunologia , Troponina/sangue
6.
Shock ; 47(2): 165-174, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-27749762

RESUMO

INTRODUCTION: Patients with cardiogenic shock (CS) are at a high risk of developing infectious complications; however, their early detection is difficult, mainly due to a frequently occurring noninfectious inflammatory response, which accompanies an extensive myocardial infarction (MI) or a postcardiac arrest syndrome. The goal of our prospective study was to describe infectious complications in CS and the immune/inflammatory response based on a serial measurement of several blood-based inflammatory biomarkers. METHODS: Eighty patients with CS were evaluated and their infections were monitored. Inflammatory markers (C-reactive protein, procalcitonin, pentraxin 3, presepsin) were measured seven times per week. The control groups consisted of 11 patients with ST segment elevation myocardial infarction without CS and without infection, and 22 patients in septic shock. RESULTS: Infection was diagnosed in 46.3% of patients with CS; 16 patients developed an infection within 48 h. Respiratory infection was most common, occurring in 33 out of 37 patients. Infection was a significant or even the main reason of death only in 3.8% of all patients with CS, and we did not find statistically significant difference in 3-month mortality between group of patients with CS with and without infection. There was no statistically significant prolongation of the duration of mechanical ventilation associated with infection. Strong inflammatory response is often in patients with CS due to MI, but we found no significant difference in the course of the inflammatory response expressed by evaluated biomarkers in patients with CS with and without infection. We found a strong relationship between the elevated inflammatory markers (sampled at 12 h) and the 3-month mortality: the area under the curve of receiver operating characteristic ranged between 0.683 and 0.875. CONCLUSION: The prevalence of infection in patients with CS was 46.3%, and respiratory tract infections were the most common type. Infections did not prolong statistically significantly the duration of mechanical ventilation and did not increase the prevalence of hospital mortality in this high-risk CS population. CS due to acute myocardial infarction was accompanied by a strong and highly variable inflammatory response, but it did not reach the intensity of the inflammatory response observed in patients with septic shock. An extensive immune/inflammatory response in patients with CS is linked to a poor prognosis.


Assuntos
Biomarcadores/metabolismo , Choque Cardiogênico/imunologia , Choque Cardiogênico/metabolismo , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Proteína C-Reativa/genética , Proteína C-Reativa/metabolismo , Calcitonina/metabolismo , Feminino , Mortalidade Hospitalar , Humanos , Receptores de Lipopolissacarídeos/metabolismo , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/sangue , Infarto do Miocárdio/imunologia , Infarto do Miocárdio/metabolismo , Fragmentos de Peptídeos/metabolismo , Prognóstico , Estudos Prospectivos , Curva ROC , Fatores de Risco , Componente Amiloide P Sérico/genética , Componente Amiloide P Sérico/metabolismo , Choque Cardiogênico/sangue , Choque Séptico/sangue , Choque Séptico/imunologia , Choque Séptico/metabolismo
7.
J Cardiovasc Med (Hagerstown) ; 17 Suppl 2: e151-e153, 2016 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-25643196

RESUMO

: A 31-year-old man presenting with cardiogenic shock and left ventricular ejection fraction of 10% received the diagnosis of giant cell myocarditis by endomyocardial biopsy. The patient was successfully treated with high-dose inotropes, intra-aortic balloon pump and venoarterial extracorporeal membrane oxygenation for 21 days associated with combined immunosuppression (thymoglobulin, steroids, cyclosporine). Immunosuppression including thymoglobulin is the regimen associated with the highest probability of recovery in case of giant cell myocarditis. Immunosuppression needs time to be effective; thus, hemodynamic support must be guaranteed. In the present case, we observed that full recovery can be obtained up to 21 days of support with extracorporeal membrane oxygenation and adequate immunosuppression.


Assuntos
Soro Antilinfocitário/administração & dosagem , Oxigenação por Membrana Extracorpórea , Células Gigantes/efeitos dos fármacos , Imunossupressores/administração & dosagem , Miocardite/terapia , Choque Cardiogênico/terapia , Adulto , Biópsia , Cardiotônicos/uso terapêutico , Terapia Combinada , Células Gigantes/imunologia , Células Gigantes/patologia , Humanos , Balão Intra-Aórtico , Imageamento por Ressonância Magnética , Masculino , Miocardite/diagnóstico , Miocardite/imunologia , Miocardite/fisiopatologia , Recuperação de Função Fisiológica , Choque Cardiogênico/diagnóstico , Choque Cardiogênico/imunologia , Fatores de Tempo , Resultado do Tratamento
9.
Int J Artif Organs ; 38(2): 113-6, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-25656010

RESUMO

PURPOSE: A new hemoadsorption device intended as adjunctive treatment for patients with elevated cytokine levels in the setting of SIRS and sepsis has shown promising results. We report on the beneficial application of the device in a patient with cardiogenic septic shock receiving combined extracorporeal life support with rECMO, LVAD, and CVVH despite his highly septic condition. METHODS: A 39-year-old patient presented with fulminant ARDS and cardiogenic septic shock. A veno-arterial ECMO was implanted for circulatory support. During the course of illness, the patient developed acute renal failure in addition to his chronic renal insufficiency, making initiation of CVVH necessary. Due to a complete cardiac arrest in both ventricles, a left ventricular assist device (LVAD) in combination with right ECMO (rECMO) was implanted despite manifest septic conditions. In the post-operative course IL-6 levels and vasopressor dosages increased drastically. A CytoSorb hemoadsorption device was therefore installed in the CVVH circuit and 3 sessions were run during the following 4 days. RESULTS: During CytoSorb treatment, inflammatory markers IL-6, procalcitonin, and C-reactive protein decreased concomitant with significantly reduced vasopressor support. No adverse device-related side effects were documented during or after the treatment sessions. CONCLUSIONS: This is the first clinical case report of a highly septic patient treated with the combined use of LVAD, rECMO, CVVH, and CytoSorb. The combination was practical, technically feasible, and beneficial for the patient. This combination represents a reasonable approach to improve survival in patients with multiple organ dysfunction necessitating several organ supportive techniques.


Assuntos
Citocinas/sangue , Oxigenação por Membrana Extracorpórea , Hemofiltração/métodos , Mediadores da Inflamação/sangue , Choque Cardiogênico/terapia , Choque Séptico/terapia , Injúria Renal Aguda/diagnóstico , Injúria Renal Aguda/terapia , Adulto , Biomarcadores/sangue , Terapia Combinada , Desenho de Equipamento , Hemofiltração/instrumentação , Humanos , Masculino , Insuficiência Renal Crônica/diagnóstico , Insuficiência Renal Crônica/terapia , Síndrome do Desconforto Respiratório/diagnóstico , Síndrome do Desconforto Respiratório/terapia , Choque Cardiogênico/sangue , Choque Cardiogênico/diagnóstico , Choque Cardiogênico/imunologia , Choque Séptico/sangue , Choque Séptico/diagnóstico , Choque Séptico/imunologia , Fatores de Tempo , Resultado do Tratamento
10.
J Intensive Care Med ; 30(2): 115-8, 2015 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-24371250

RESUMO

Cardiomyopathy secondary to toxic shock syndrome (TSS) is an uncommon but potentially life-threatening problem. We report the case of a 51-year-old male who presented with profound cardiogenic shock and multiorgan failure that could not be managed by conventional therapy with intravenous fluids, vasopressors and inotropes. Venoarterial extracorporeal membrane oxygenation (VA ECMO) was instituted as a bridge to recovery. After administration of antibiotics and intravenous immunoglobulin, the patient's condition improved and he was successfully weaned off ECMO after 6 days. The patient recovered from multiorgan failure, and left ventricular ejection fraction improved from <10% pre-ECMO to 65% 8 months after discharge. This case supports the view that VA ECMO can be used successfully to support vital organ perfusion in patients with profound but reversible cardiomyopathy attributed to TSS.


Assuntos
Oxigenação por Membrana Extracorpórea , Úlcera da Perna/microbiologia , Insuficiência de Múltiplos Órgãos/imunologia , Choque Cardiogênico/imunologia , Choque Séptico/imunologia , Infecções Cutâneas Estafilocócicas/microbiologia , Infecções Estreptocócicas/microbiologia , Antibacterianos/administração & dosagem , Exsudatos e Transudatos/microbiologia , Hemodinâmica , Humanos , Unidades de Terapia Intensiva , Masculino , Pessoa de Meia-Idade , Insuficiência de Múltiplos Órgãos/fisiopatologia , Insuficiência de Múltiplos Órgãos/terapia , Respiração Artificial , Choque Cardiogênico/fisiopatologia , Choque Cardiogênico/terapia , Choque Séptico/fisiopatologia , Choque Séptico/terapia , Infecções Cutâneas Estafilocócicas/imunologia , Infecções Estreptocócicas/imunologia , Resultado do Tratamento
11.
Clin Res Cardiol ; 103(4): 301-13, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24374759

RESUMO

AIMS: Type 17 helper T (Th17) cells producing the proinflammatory signature cytokine interleukin (IL)-17 are conterregulated by regulatory T cells (Treg) producing anti-inflammatory cytokines like transforming growth factor (TGF)-ß and interleukin-(IL)-10. An imbalance of the Th17/Treg-ratio toward Th17 cell subset was shown to be involved in plaque destabilization and acute myocardial infarction (AMI), while no data exist in infarction-related cardiogenic shock (CS). The objective of this study was to evaluate the role of Th17/Treg and their related cytokines in uncomplicated AMI and infarction-related CS. METHODS AND RESULTS: In an observational monocentric study, blood sample from age-matched healthy controls (HC, n = 20), patients with uncomplicated AMI (n = 20), patients with CS who survived for at least 28 days (CS-survivors, n = 20) and CS-non-survivors (n = 20) were analyzed. Circulating Th17 and Treg cell subsets and their intracellular cytokine expression were measured by flow cytometry and associated with circulating proinflammatory Th17-derived cytokines IL-6, IL-17 and their anti-inflammatory Treg-derived cytokines TGF-ß and IL-10 measured by enzyme immunoassay. According to the severity of ACS, CS-non-survivors showed the highest levels of Th17 (p < 0.001) and the lowest levels of Treg cells (p < 0.001) favoring a Th17/Treg imbalance toward the proinflammatory Th17 response (p < 0.001). Changes of T cell subsets were also associated with a proinflammatory cytokine expression measured by increased IL-6 (p < 0.001) and IL-17 levels (p < 0.001) and decreased TGF-ß (p < 0.001) and IL-10 levels (p = 0.057). For the Th17/Treg-ratio at admission, a cut-off point of >0.33 had a sensitivity of 90 % and a specificity of 80 % to determine 28-day mortality in CS (confirmed by ROC analysis, area under the curve: 0.88 ± 0.06, p < 0.001). Th17/Treg-ratio >0.33 was observed to be an independent predictor for 1-year mortality in CS confirmed by Cox proportional hazard analysis (hazard ratio (HR): 4.31; 95 % confidence interval (CI) 1.44-12.93; p = 0.009). CONCLUSION: The Th17/Treg imbalance toward a Th17 shift might represent a promising candidate as therapeutic target and risk indicator in cardiogenic shock.


Assuntos
Citocinas/metabolismo , Infarto do Miocárdio/imunologia , Choque Cardiogênico/imunologia , Linfócitos T Reguladores/imunologia , Células Th17/imunologia , Ensaio de Imunoadsorção Enzimática , Citometria de Fluxo , Alemanha , Hemodinâmica , Humanos , Infarto do Miocárdio/mortalidade , Choque Cardiogênico/mortalidade , Análise de Sobrevida
12.
Acute Card Care ; 12(4): 115-8, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-21039083

RESUMO

Cardiogenic shock (CS) is the leading cause of death in patients with acute myocardial infarction (MI) and we badly need new approaches in its treatment. It has been demonstrated that a number of inflammatory cytokines (IL-1ß, IL-6, IL-8, TNF-α, CRP, soluble adhesion molecules, complement system etc) are elevated in acute MI complicated by CS. Baseline levels of pro- inflammatory cytokines have predictive value for the development of CS and subsequent mortality. The deleterious effects of pro- inflammatory cytokines may be due to excessive nitric oxide production by enzyme named NOS. However in multicenter randomized TRIUMPH study non-selective NOS inhibition was ineffective in the treatment of cardiogenic shock. A challenging subject of future studies will be treatment of CS with specific inhibitors of inducible isoform of NOS. Considering the results of treatment of patients with septic shock it would be reasonable to study the effects of small doses of corticosteroids and hemofiltration in patients with CS and signs of SIRS.


Assuntos
Choque Cardiogênico/imunologia , Síndrome de Resposta Inflamatória Sistêmica/fisiopatologia , Corticosteroides/uso terapêutico , Citocinas/fisiologia , Inibidores Enzimáticos/uso terapêutico , Hemofiltração , Humanos , Infarto do Miocárdio/complicações , Óxido Nítrico/fisiologia , Óxido Nítrico Sintase/antagonistas & inibidores , Óxido Nítrico Sintase/fisiologia , Ensaios Clínicos Controlados Aleatórios como Assunto , Choque Cardiogênico/etiologia , Choque Cardiogênico/metabolismo , Choque Cardiogênico/fisiopatologia , Choque Cardiogênico/terapia , Síndrome de Resposta Inflamatória Sistêmica/imunologia , Síndrome de Resposta Inflamatória Sistêmica/metabolismo , Síndrome de Resposta Inflamatória Sistêmica/terapia , Resultado do Tratamento
13.
Am J Physiol Heart Circ Physiol ; 297(2): H654-63, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19502556

RESUMO

Altered cGMP signaling has been implicated in myocardial depression, morbidity, and mortality associated with sepsis. Previous studies, using inhibitors of soluble guanylate cyclase (sGC), suggested that cGMP generated by sGC contributed to the cardiac dysfunction and mortality associated with sepsis. We used sGC(alpha)(1)-deficient (sGC(alpha)(1)(-/-)) mice to unequivocally determine the role of sGC(alpha)(1)beta(1) in the development of cardiac dysfunction and death associated with two models of inflammatory shock: endotoxin- and TNF-induced shock. At baseline, echocardiographic assessment and invasive hemodynamic measurements of left ventricular (LV) dimensions and function did not differ between wild-type (WT) mice and sGC(alpha)(1)(-/-) mice on the C57BL/6 background (sGC(alpha)(1)(-/-B6) mice). At 14 h after endotoxin challenge, cardiac dysfunction was more pronounced in sGC(alpha)(1)(-/-B6) than WT mice, as assessed using echocardiographic and hemodynamic indexes of LV function. Similarly, Ca(2+) handling and cell shortening were impaired to a greater extent in cardiomyocytes isolated from sGC(alpha)(1)(-/-B6) than WT mice after endotoxin challenge. Importantly, morbidity and mortality associated with inflammatory shock induced by endotoxin or TNF were increased in sGC(alpha)(1)(-/-B6) compared with WT mice. Together, these findings suggest that cGMP generated by sGC(alpha)(1)beta(1) protects against cardiac dysfunction and mortality in murine inflammatory shock models.


Assuntos
Guanilato Ciclase/genética , Guanilato Ciclase/metabolismo , Receptores Citoplasmáticos e Nucleares/genética , Receptores Citoplasmáticos e Nucleares/metabolismo , Choque Cardiogênico , Disfunção Ventricular Esquerda , Animais , Pressão Sanguínea/fisiologia , Cálcio/metabolismo , Células Cultivadas , Modelos Animais de Doenças , Ecocardiografia , Endotoxinas/toxicidade , Ativação Enzimática/fisiologia , Regulação Enzimológica da Expressão Gênica/fisiologia , Estimativa de Kaplan-Meier , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Contração Miocárdica/fisiologia , Miócitos Cardíacos/citologia , Miócitos Cardíacos/fisiologia , Óxido Nítrico/metabolismo , Sepse/imunologia , Sepse/metabolismo , Sepse/mortalidade , Choque Cardiogênico/imunologia , Choque Cardiogênico/metabolismo , Choque Cardiogênico/mortalidade , Guanilil Ciclase Solúvel , Fator de Necrose Tumoral alfa/toxicidade , Disfunção Ventricular Esquerda/diagnóstico por imagem , Disfunção Ventricular Esquerda/imunologia , Disfunção Ventricular Esquerda/mortalidade , Pressão Ventricular/fisiologia
14.
Circ J ; 73(5): 970-3, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-19088395

RESUMO

The progress of immunosuppressive therapy has made heart transplantation the standard therapy for end-stage heart failure. However, humoral rejection of the cardiac allograft is still a challenging problem associated with high incidence of graft loss and patient mortality. The present patient developed profound cardiogenic shock requiring extracorporeal life support on the 8th day after heart transplantation. Endomyocardial biopsy revealed no cellular rejection, and complement component C4d was positively stained on the capillary endothelium. The patient was successfully treated with repeated plasmapheresis and administration of anti-CD20 monoclonal antibody, rituximab, as well as with steroid pulse and increased standard immunosuppressive medication.


Assuntos
Formação de Anticorpos , Cardiomiopatia Dilatada/cirurgia , Rejeição de Enxerto/terapia , Transplante de Coração/efeitos adversos , Terapia de Imunossupressão/métodos , Imunossupressores/administração & dosagem , Plasmaferese , Choque Cardiogênico/terapia , Anticorpos Monoclonais/administração & dosagem , Anticorpos Monoclonais Murinos , Biópsia , Capilares/imunologia , Complemento C4b/metabolismo , Quimioterapia Combinada , Endocárdio/imunologia , Oxigenação por Membrana Extracorpórea , Rejeição de Enxerto/imunologia , Rejeição de Enxerto/patologia , Humanos , Balão Intra-Aórtico , Masculino , Pessoa de Meia-Idade , Miocárdio/imunologia , Fragmentos de Peptídeos/metabolismo , Pulsoterapia , Rituximab , Choque Cardiogênico/imunologia , Choque Cardiogênico/patologia , Esteroides/administração & dosagem , Fatores de Tempo , Transplante Homólogo , Resultado do Tratamento
15.
Curr Opin Infect Dis ; 21(3): 293-7, 2008 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-18448975

RESUMO

PURPOSE OF REVIEW: Despite abundant literature on hantavirus, few reports have focused on the shock in hantavirus pulmonary syndrome. This review approaches recent advances that allow us to better understand the pathogenesis of hantavirus pulmonary syndrome shock. RECENT FINDINGS: Hantavirus pulmonary syndrome has been studied in a hamster model that mimics human shock and respiratory failure. In-vitro experiments show that pathogenic hantaviruses are able to inhibit antiviral responses, and that cytotoxicity of hantavirus-specific T cells enhances the permeability of infected endothelial cells. The idea that the primary cardiac lesion of shock is mostly functional has been shaken by the report of a typical myocarditis in hearts from human hantavirus pulmonary syndrome fatal cases. The involvement of regulatory T cells on hantavirus persistence in its rodent reservoir suggests that these cells could protect from severe hantavirus pulmonary syndrome and shock. SUMMARY: Hantavirus pulmonary syndrome shock is probably related to an exacerbated immune response of CD8+ T cells producing cytotoxicity on infected endothelial cells, presence of myocarditis and myocardial depression induced by nitric oxide. The virulence elements in G1 glycoprotein could also contribute to shock. Active suppression of immune T regulatory cells is probably involved in hantavirus pulmonary syndrome pathogenesis. These are all new aspects of hantavirus pulmonary syndrome pathogenesis that stimulate further studies to elucidate mechanisms of shock and to develop effective treatment strategies.


Assuntos
Síndrome Pulmonar por Hantavirus/complicações , Choque Cardiogênico/imunologia , Choque Cardiogênico/virologia , Animais , Linfócitos T CD8-Positivos/imunologia , Cricetinae , Síndrome Pulmonar por Hantavirus/imunologia , Síndrome Pulmonar por Hantavirus/virologia , Humanos , Mesocricetus , Camundongos , Modelos Animais , Miocardite/virologia
16.
Swiss Med Wkly ; 131(3-4): 35-40, 2001 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-11219189

RESUMO

OBJECTIVES: In patients with septic shock, circulating monocytes become refractory to stimulation with microbial products. Whether this hyporesponsive state is induced by infection or is related to shock is unknown. To address this question, we measured TNF alpha production by monocytes or by whole blood obtained from healthy volunteers (controls), from patients with septic shock, from patients with severe infection (bacterial pneumonia) without shock, and from patients with cardiogenic shock without infection. MEASUREMENTS: The numbers of circulating monocytes, of CD14+ monocytes, and the expression of monocyte CD14 and the LPS receptor, were assessed by flow cytometry. Monocytes or whole blood were stimulated with lipopolysaccharide endotoxin (LPS), heat-killed Escherichia coli or Staphylococcus aureus, and TNF alpha production was measured by bioassay. RESULTS: The number of circulating monocytes, of CD14+ monocytes, and the monocyte CD14 expression were significantly lower in patients with septic shock than in controls, in patients with bacterial pneumonia or in those with cardiogenic shock (p < 0.001). Monocytes or whole blood of patients with septic shock exhibited a profound deficiency of TNF alpha production in response to all stimuli (p < 0.05 compared to controls). Whole blood of patients with cardiogenic shock also exhibited this defect (p < 0.05 compared to controls), although to a lesser extent, despite normal monocyte counts and normal CD14 expression. CONCLUSIONS: Unlike patients with bacterial pneumonia, patients with septic or cardiogenic shock display profoundly defective TNF alpha production in response to a broad range of infectious stimuli. Thus, down-regulation of cytokine production appears to occur in patients with systemic, but not localised, albeit severe, infections and also in patients with non-infectious circulatory failure. Whilst depletion of monocytes and reduced monocyte CD14 expression are likely to be critical components of the hyporesponsiveness observed in patients with septic shock, other as yet unidentified factors are at work in this group and in patients with cardiogenic shock.


Assuntos
Receptores de Lipopolissacarídeos/sangue , Linfócitos/imunologia , Monócitos/imunologia , Pneumonia Bacteriana/imunologia , Choque Cardiogênico/imunologia , Choque Séptico/imunologia , Fator de Necrose Tumoral alfa/biossíntese , Antígenos CD/sangue , Células Cultivadas , Infecções Comunitárias Adquiridas/sangue , Infecções Comunitárias Adquiridas/imunologia , Humanos , Lipopolissacarídeos/farmacologia , Linfócitos/efeitos dos fármacos , Monócitos/efeitos dos fármacos , Pneumonia Bacteriana/sangue , Valores de Referência , Choque Cardiogênico/sangue , Choque Séptico/sangue
17.
Mol Cell Biochem ; 212(1-2): 45-50, 2000 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-11108135

RESUMO

The anti-inflammatory cytokine IL-10 is up-regulated in response to TNF-alpha suggesting a control mechanism of inflammation. In addition, we recently found systemic IL-10 release in response to acute stress reactions in the absence of any systemic inflammation. In vitro and in vivo studies in experimental models suggest that catecholamines induce IL-10 release via a cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) dependent pathway. Here we studied patients for plasma IL-10 after acute myocardial infarction, a very stressful event without significant signs of systemic inflammation. In fact, the activation of the sympathetic system initiated by cardiac infarction was accompanied by a temporary systemic release of IL-10. Catecholamine induced IL-10 may be released by different cells. Recently, we demonstrated that catecholamines directly stimulate the IL-10 promoter/enhancer via a cAMP/PKA pathway in monocytic cells. A cAMP responsive element (CRE) was identified as major target. Here we show that there is no influence of catecholamines on the IL-10 promoter activity in T-cells. In contrast to monocytic cells, in T-cells cAMP-induced PKA-dependent phosphorylation of the CRE-binding protein 1 (CREB-1) seems to play a marginal role in IL-10 induction, which was reflected by a low cAMP-dependent IL-10-promoter/enhancer stimulation in reporter gene assays. Thus, catecholamines are directly involved in the regulation of IL-10 expression in monocytic but not in T-cells after acute stressful conditions.


Assuntos
Catecolaminas/fisiologia , Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico/metabolismo , Interleucina-10/genética , Monócitos/imunologia , Infarto do Miocárdio/imunologia , Regiões Promotoras Genéticas/efeitos dos fármacos , Ativação Transcricional , Doença Aguda , Idoso , Bucladesina/farmacologia , Catecolaminas/uso terapêutico , Linhagem Celular , Epinefrina/sangue , Feminino , Humanos , Interleucina-10/sangue , Células Jurkat , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/sangue , Norepinefrina/sangue , Choque Cardiogênico/sangue , Choque Cardiogênico/tratamento farmacológico , Choque Cardiogênico/imunologia , Linfócitos T/imunologia , Transfecção
19.
Int J Cardiol ; 72(1): 3-10, 1999 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-10636626

RESUMO

AIMS: Exposure to bacterial endotoxin, perhaps due to bowel congestion or ischaemia and altered gut permeability, may result in immune activation that is characteristic for patients with severe heart failure. It is known that blood procalcitonin rises in response to bacterial endotoxin exposure. METHODS: We measured procalcitonin in a group of 29 patients with acute cardiogenic shock and no sign of infection (all without bacteraemia) and 26 with septic shock. Blood was analysed for procalcitonin, interleukin-6, tumour necrosis factor-alpha (TNF-alpha), c-reactive protein (CRP) and neopterin. Patients were managed conventionally in an intensive care unit with no further experimental procedures. RESULTS: Three cardiogenic (10%) and seven septic shock patients (27%) survived. Most patients with acute heart failure surviving 12 h or more (18 of 20) developed a pyrexia (738.0 degrees C) of unknown origin in the absence of positive cultures, with a rise in procalcitonin (1.4+/-0.8 to 48.0+/-16.2 ng/ml, P<0.001), CRP (76.5+/-16.4 to 154.7+/-22.9 mg/l, P<0.001) and neopterin (20.7+/-3.5 to 41.2+/-6.7 nmol/l, P<0.001). Patients with septic shock had higher initial levels of cytokines, and higher peak levels. Those with heart failure surviving (n=3) and those dying in the first 12 h (n=9) had no rise in cytokine levels. The patients with high procalcitonin had a higher temperature (38.9+/-0.3 vs. 37.3+/-0.23 degrees C, P<0.05), TNF-alpha (43.95+/-9.64 vs. 16.43+/-4.33 pg/ml; P<0.005) and CRP (146.1+/-18.4 vs. 68.2+/-39.6 mg/ml, P<0.005). Peak procalcitonin levels correlated with peak temperature (r=0.74, P<0.001). CONCLUSION: Cardiogenic shock causes a pyrexia of unknown origin in patients surviving for 12 h and that is associated with a rise in procalcitonin levels. This lends support to the hypothesis that patients with cardiogenic shock may be being exposed to bacterial endotoxin at a time when bowel wall congestion and or ischaemia is likely to be present.


Assuntos
Translocação Bacteriana , Calcitonina/sangue , Febre de Causa Desconhecida/etiologia , Precursores de Proteínas/sangue , Choque Cardiogênico/imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Peptídeo Relacionado com Gene de Calcitonina , Citocinas/sangue , Endotoxinas/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Choque Cardiogênico/sangue , Choque Cardiogênico/complicações , Choque Cardiogênico/mortalidade , Choque Séptico/sangue , Choque Séptico/imunologia , Choque Séptico/microbiologia , Choque Séptico/mortalidade , Análise de Sobrevida
20.
Z Kardiol ; 85(11): 820-7, 1996 Nov.
Artigo em Alemão | MEDLINE | ID: mdl-9064944

RESUMO

We studied the plasma levels of TNF-alpha, IL-6, IL-8 and soluble adhesion molecules (sE-Selectin, sL-Selectin, sVCAM-1) immediately before and during mechanical circulatory support with a Biventricular Assist Device System (BVAD-"Berlin Heart") in comparison to patients with chronic heart failure (NYHA classes II/III) and patients with coronary artery disease with normal ventricular function. Additionally, the biocompatibility of the membranes used in the "Berlin Heart" was tested in vitro. IL-6 and IL-8 but not TNF-alpha could only be detected in patients with cardiogenic shock immediately before starting circulatory support. Furthermore, plasma concentrations of soluble adhesion molecules were statistically significantly elevated in patients with cardiogenic shock compared to patients with coronary artery disease. This picture of a systemic inflammatory response syndrome without significant level of TNF-alpha looks quite similar to that seen in patients following trauma and severe operations. During mechanical circulatory support plasma levels of cytokines and soluble adhesion molecules dropped to low levels in patients, who were successfully maintained on BVAD. By contrast, we have found persistently elevated levels of these mediators in patients with fatal outcome. This seems not to be the result of individual distinct response of blood cells to contact with the artificial surfaces of the device. In summary, our data suggest the development of a systemic inflammatory response syndrome may be due to hypoxia during cardiogenic shock. Persistence of systemic inflammation suggests failing of the mechanical support. Therefore, the monitoring of inflammatory mediators may be relevant as a prognostic marker in these patients (disappearance of peripheral hypoxia).


Assuntos
Doença das Coronárias/terapia , Insuficiência Cardíaca/terapia , Coração Auxiliar , Mediadores da Inflamação/sangue , Choque Cardiogênico/terapia , Adulto , Idoso , Moléculas de Adesão Celular/sangue , Doença das Coronárias/imunologia , Feminino , Insuficiência Cardíaca/imunologia , Humanos , Interleucina-6/sangue , Interleucina-8/sangue , Masculino , Teste de Materiais , Membranas Artificiais , Pessoa de Meia-Idade , Prognóstico , Choque Cardiogênico/imunologia , Síndrome de Resposta Inflamatória Sistêmica/diagnóstico , Síndrome de Resposta Inflamatória Sistêmica/imunologia , Fator de Necrose Tumoral alfa/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...