RESUMO
Background: Infection caused by SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) exhibits a strong infectivity but less virulence compared to severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS). In terms of cardiovascular morbidity, susceptible population include elderly and patients with certain cardiovascular conditions. This infection has been associated with cardiac injury, cardiovascular complications and higher mortality. Objectives: The main objective of the CARDIO COVID 19-20 Registry is to determine the presence of cardiovascular comorbidities and cardiovascular complications in COVID-19 infected patients that required in-hospital treatment in different Latin American institutions. Methods: The CARDIO COVID 19-20 Registry is an observational, multicenter, ambispective, and hospital-based registry of patients with confirmed COVID-19 infection who required in-hospital treatment in Latin America. Enrollment of patients started on May 01, 2020 and was initially planned to last three months; based on the progression of pandemic in Latin America, enrollment was extended until December 2020, and could be extended once again based on the pandemic course in our continent at that moment. Conclusions: The CARDIO COVID 19-20 Registry will characterize the in-hospital population diagnosed with COVID-19 in Latin America in order to identify risk factors for worsening of cardiovascular comorbidities or for the appearance of cardiovascular complications during hospitalization and during the 30-day follow up period.
Assuntos
COVID-19/epidemiologia , Doenças Cardiovasculares/epidemiologia , Sistema de Registros , Arritmias Cardíacas/epidemiologia , Arritmias Cardíacas/etiologia , Arritmias Cardíacas/fisiopatologia , COVID-19/complicações , COVID-19/fisiopatologia , Doenças Cardiovasculares/etiologia , Doenças Cardiovasculares/fisiopatologia , Comorbidade , Doença das Coronárias/epidemiologia , Doença das Coronárias/etiologia , Doença das Coronárias/fisiopatologia , Insuficiência Cardíaca/epidemiologia , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/fisiopatologia , Humanos , América Latina , Miocardite/epidemiologia , Miocardite/etiologia , Miocardite/fisiopatologia , SARS-CoV-2 , Trombose/epidemiologia , Trombose/etiologia , Trombose/fisiopatologiaAssuntos
Humanos , Feminino , Adulto , Função Ventricular Esquerda , Disfunção Ventricular Esquerda/diagnóstico por imagem , Cardiomiopatia de Takotsubo/diagnóstico por imagem , Miocardite/fisiopatologia , Ecocardiografia/métodos , Espectroscopia de Ressonância Magnética/métodos , Eletrocardiografia/métodos , Serviços Médicos de Emergência , Unidades de Terapia IntensivaRESUMO
The association between hypertension, diabetes, cardio and cerebrovascular disease and severe and fatal COVID-19, described in different countries, is remarkable. Myocardial damage and myocardial dysfunction are postulated as a possible causal nexus. Frequent findings of elevated troponin levels and electrocardiographic anomalies support this concept. On the other hand, hypotheses in favour and against a deleterious effect of angiotensin converting enzyme inhibitors and angiotensin receptor blockers, a usual treatment for cardiovascular disease, have been raised. There is currently no solid evidence and thus properly designed studies on this subject are urgently needed. In this context, patients with cardiovascular disease should especially avoid being exposed to the virus, should not self-medicate and rapidly seek medical advice should they show symptoms of infection.
Assuntos
Betacoronavirus , Doenças Cardiovasculares/fisiopatologia , Infecções por Coronavirus/fisiopatologia , Pandemias , Pneumonia Viral/fisiopatologia , Fatores Etários , Idoso , Bloqueadores do Receptor Tipo 1 de Angiotensina II/efeitos adversos , Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico , Enzima de Conversão de Angiotensina 2 , Inibidores da Enzima Conversora de Angiotensina/efeitos adversos , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Inibidores da Enzima Conversora de Angiotensina/uso terapêutico , Anti-Hipertensivos/efeitos adversos , Anti-Hipertensivos/farmacologia , Anti-Hipertensivos/uso terapêutico , Betacoronavirus/efeitos dos fármacos , COVID-19 , Doenças Cardiovasculares/complicações , Infecções por Coronavirus/complicações , Diagnóstico Precoce , Coração/fisiopatologia , Humanos , Hipertensão/complicações , Hipertensão/tratamento farmacológico , Hipertensão/fisiopatologia , Pessoa de Meia-Idade , Miocardite/etiologia , Miocardite/fisiopatologia , Peptidil Dipeptidase A/efeitos dos fármacos , Peptidil Dipeptidase A/fisiologia , Pneumonia Viral/complicações , Receptores Virais/efeitos dos fármacos , Receptores Virais/fisiologia , Sistema Renina-Angiotensina/efeitos dos fármacos , Sistema Renina-Angiotensina/fisiologia , Fatores de Risco , SARS-CoV-2 , AutomedicaçãoRESUMO
CCL3, a member of the CC-chemokine family, has been associated with macrophage recruitment to heart tissue and parasite control in the acute infection of mouse with Trypanosoma cruzi, the causative agent of Chagas disease. Here, we approached the participation of CCL3 in chronic chagasic cardiomyopathy (CCC), the main clinical form of Chagas disease. We induced CCC in C57BL/6 (ccl3+/+) and CCL3-deficient (ccl3-/-) mice by infection with the Colombian Type I strain. In ccl3+/+ mice, high levels of CCL3 mRNA and protein were detected in the heart tissue during the acute and chronic infection. Survival was not affected by CCL3 deficiency. In comparison with ccl3+/+, chronically infected ccl3-/- mice presented reduced cardiac parasitism and inflammation due to CD8+ cells and macrophages. Leukocytosis was decreased in infected ccl3-/- mice, paralleling the accumulation of CD8+ T cells devoid of activated CCR5+ LFA-1+ cells in the spleen. Further, T. cruzi-infected ccl3-/-mice presented reduced frequency of interferon-gamma (IFNγ)+ cells and numbers of parasite-specific IFNγ-producing cells, while the T. cruzi antigen-specific cytotoxic activity was increased. Stimulation of CCL3-deficient macrophages with IFNγ improved parasite control, in a milieu with reduced nitric oxide (NOx) and tumor necrosis factor (TNF), but similar interleukin-10 (IL-10), concentrations. In comparison with chronically T. cruzi-infected ccl3+/+ counterparts, ccl3-/- mice did not show enlarged heart, loss of left ventricular ejection fraction, QTc prolongation and elevated CK-MB activity. Compared with ccl3+/+, infected ccl3-/- mice showed reduced concentrations of TNF, while IL-10 levels were not affected, in the heart milieu. In spleen of ccl3+/+ NI controls, most of the CD8+ T-cells expressing the CCL3 receptors CCR1 or CCR5 were IL-10+, while in infected mice these cells were mainly TNF+. Lastly, selective blockage of CCR1/CCR5 (Met-RANTES therapy) in chronically infected ccl3+/+ mice reversed pivotal electrical abnormalities (bradycardia, prolonged PR, and QTc interval), in correlation with reduced TNF and, mainly, CCL3 levels in the heart tissue. Therefore, in the chronic T. cruzi infection CCL3 takes part in parasite persistence and contributes to form a CD8+ T-cell and macrophage-enriched cardiac inflammation. Further, increased levels of CCL3 create a scenario with abundant IFNγ and TNF, associated with cardiomyocyte injury, heart dysfunction and QTc prolongation, biomarkers of severity of Chagas' heart disease.
Assuntos
Cardiomiopatia Chagásica/fisiopatologia , Quimiocina CCL3/fisiologia , Interferon gama/fisiologia , Macrófagos Peritoneais/parasitologia , Parasitemia/fisiopatologia , Trypanosoma cruzi/fisiologia , Fator de Necrose Tumoral alfa/fisiologia , Animais , Linfócitos T CD8-Positivos/efeitos dos fármacos , Linfócitos T CD8-Positivos/imunologia , Células Cultivadas , Cardiomiopatia Chagásica/parasitologia , Cardiomiopatia Chagásica/patologia , Quimiocina CCL3/deficiência , Quimiocina CCL3/farmacologia , Quimiocina CCL5/farmacologia , Quimiocina CCL5/uso terapêutico , Quimiotaxia de Leucócito/efeitos dos fármacos , Citocinas/biossíntese , Citocinas/genética , Citocinas/farmacologia , Eletrocardiografia/efeitos dos fármacos , Feminino , Interferon gama/farmacologia , Macrófagos Peritoneais/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Miocardite/etiologia , Miocardite/patologia , Miocardite/fisiopatologia , RNA Mensageiro/biossíntese , Receptores de Quimiocinas/antagonistas & inibidores , Receptores de Quimiocinas/biossíntese , Receptores de Quimiocinas/genética , Organismos Livres de Patógenos Específicos , Baço/imunologia , Baço/metabolismo , Volume Sistólico , Trypanosoma cruzi/isolamento & purificação , Fator de Necrose Tumoral alfa/análiseRESUMO
Background: Rheumatic carditis is a challenge for treatment and secondary prophylaxis, due to severe valve sequelae. Objective: To evaluate the cases of rheumatic carditis in patients under 18 years old treated with corticosteroids.Methods: An observational, longitudinal and retrospective study was carried out on the profile of patients, in the period of 2000-2015. We selected those who received corticosteroid therapy at immunosuppressive doses, for the treatment of carditis and were aged 5 to 18 years. Data were extracted from medical records. Calculations of: averages, standard deviations, medians and interquartile ranges, ratios and 95% confidence intervals were obtained. Chi-square and Wilcoxon tests were applied for comparisons. The level of significance was 5%. Results: Of the 93 cases, 93.53% developed moderate or severe carditis. Mitral regurgitation was detected in 100% of the sample. Pulse therapy was administered in 11.83%. Surgery was performed in 23.69% of patients: mitral, aortic and/or tricuspid valve repair or replacement. The evolution of the cases was favorable in 70.96%. There was a good response among those who received only clinical treatment and those who belonged to the surgical group. The comparison of the initial and posterior valve lesions to the corticoid use was statistically significant (p < 0.001). A difference between the ejection fraction medians was observed (p = 0.048). Hospitalization was required twice or more for 45.16% of the patients. The mortality rate was 5.38%.Conclusions: The patients showed significant clinical improvement. The treatment was effective, reducing trivalvular impairment
Assuntos
Humanos , Masculino , Feminino , Criança , Adolescente , Febre Reumática/terapia , Corticosteroides/uso terapêutico , Hospitais Públicos , Miocardite/complicações , Miocardite/fisiopatologia , Valva Aórtica , Penicilinas/uso terapêutico , Próteses e Implantes , Atenção Terciária à Saúde/métodos , Prednisona/administração & dosagem , Interpretação Estatística de Dados , Resultado do Tratamento , Estudo Observacional , Antibacterianos/administração & dosagem , Valva Mitral , Insuficiência da Valva MitralRESUMO
Chagas disease is caused by the trypanosomatid Trypanosoma cruzi, which chronically causes heart problems in up to 30% of infected patients. Chagas disease was initially restricted to Latin America. However, due to migratory events, this disease may become a serious worldwide health problem. During Chagas disease, many patients die of cardiac arrhythmia despite the apparent benefits of anti-arrhythmic therapy (e.g., amiodarone). Here, we assimilate the cardiac form of Chagas disease to an inflammatory cardiac disease. Evidence from the literature, mostly provided using experimental models, supports this view and argues in favor of new strategies for treating cardiac arrhythmias in Chagas disease by modulating cytokine production and/or action. But the complex nature of myocardial inflammation underlies the need to better understand the molecular mechanisms of the inflammatory response during Chagas disease. Here, particular attention has been paid to tumor necrosis factor alpha (TNF) and transforming growth factor beta (TGF-ß) although other cytokines may be involved in the chagasic cardiomyopathy.
Assuntos
Cardiomiopatia Chagásica/metabolismo , Sistema de Condução Cardíaco/metabolismo , Mediadores da Inflamação/metabolismo , Miocardite/metabolismo , Miócitos Cardíacos/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Trypanosoma cruzi/patogenicidade , Fator de Necrose Tumoral alfa/metabolismo , Potenciais de Ação , Animais , Anti-Inflamatórios/uso terapêutico , Remodelamento Atrial , Cardiomiopatia Chagásica/tratamento farmacológico , Cardiomiopatia Chagásica/parasitologia , Cardiomiopatia Chagásica/fisiopatologia , Sistema de Condução Cardíaco/efeitos dos fármacos , Sistema de Condução Cardíaco/parasitologia , Sistema de Condução Cardíaco/fisiopatologia , Frequência Cardíaca , Interações Hospedeiro-Patógeno , Humanos , Mediadores da Inflamação/antagonistas & inibidores , Contração Miocárdica , Miocardite/tratamento farmacológico , Miocardite/parasitologia , Miocardite/fisiopatologia , Miócitos Cardíacos/efeitos dos fármacos , Miócitos Cardíacos/parasitologia , Transdução de Sinais , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Remodelação VentricularRESUMO
Chest pain is a common complaint in the emergency department (ED). Besides a careful history and physical exam; electrocardiogram, laboratory tests and imaging studies are widely available diagnostic tests that are used for patient assessment. When ST elevation and elevated cardiac enzymes are present the most likely diagnosis are ST elevation myocardial infarction (STEMI) or myocarditis. In this case report we present two low risk patients for major adverse cardiac event with ST elevation and elevated cardiac enzymes and how a careful risk assessment and detailed electrocardiogram evaluation could help differentiating between these two diagnoses.
Assuntos
Dor no Peito/etiologia , Miocardite/diagnóstico , Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico , Adulto , Diagnóstico Diferencial , Eletrocardiografia , Humanos , Masculino , Miocardite/fisiopatologia , Medição de Risco/métodos , Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia , Adulto JovemRESUMO
BACKGROUND AND AIM OF THE STUDY: International records indicate that only 2.6% of patients with heart transplants have valvular heart disease. The study aim was to evaluate the epidemiological and clinical profile of patients with valvular heart disease undergoing heart transplantation. METHODS: Between 1985 and 2013, a total of 569 heart transplants was performed at the authors' institution. Twenty patients (13 men, seven women; mean age 39.5 +/- 15.2 years) underwent heart transplant due to structural (primary) valvular disease. Analyses were made of the patients' clinical profile, laboratory data, echocardiographic and histopathological data, and mortality and rejection. RESULTS: Of the patients, 18 (90%) had a rheumatic etiology, with 85% having undergone previous valve surgery (45% had one or more operations), and 95% with a normal functioning valve prosthesis at the time of transplantation. Atrial fibrillation was present in seven patients (35%), while nine (45%) were in NYHA functional class IV and eight (40%) in class III. The indication for cardiac transplantation was refractory heart failure in seven patients (35%) and persistent NYHA class III/IV in ten (50%). The mean left ventricular ejection fraction (LVEF) was 26.6 +/- 7.9%. The one-year mortality was 20%. Histological examination of the recipients' hearts showed five (27.7%) to have reactivated rheumatic myocarditis without prior diagnosis at the time of transplantation. Univariate analysis showed that age, gender, LVEF, rheumatic activity and rejection were not associated with mortality at one year. CONCLUSION: Among the present patient cohort, rheumatic heart disease was the leading cause of heart transplantation, and a significant proportion of these patients had reactivated myocarditis diagnosed in the histological analyses. Thus, it appears valid to investigate the existence of rheumatic activity, especially in valvular cardiomyopathy with severe systolic dysfunction before transplantation.
Assuntos
Insuficiência Cardíaca/cirurgia , Transplante de Coração , Doenças das Valvas Cardíacas/cirurgia , Cardiopatia Reumática/cirurgia , Adulto , Brasil , Bases de Dados Factuais , Progressão da Doença , Feminino , Rejeição de Enxerto/mortalidade , Insuficiência Cardíaca/diagnóstico , Insuficiência Cardíaca/mortalidade , Insuficiência Cardíaca/fisiopatologia , Transplante de Coração/efeitos adversos , Transplante de Coração/mortalidade , Doenças das Valvas Cardíacas/diagnóstico , Doenças das Valvas Cardíacas/mortalidade , Doenças das Valvas Cardíacas/fisiopatologia , Humanos , Masculino , Pessoa de Meia-Idade , Miocardite/mortalidade , Miocardite/fisiopatologia , Miocardite/cirurgia , Estudos Retrospectivos , Cardiopatia Reumática/diagnóstico , Cardiopatia Reumática/mortalidade , Cardiopatia Reumática/fisiopatologia , Fatores de Risco , Volume Sistólico , Sístole , Fatores de Tempo , Resultado do Tratamento , Disfunção Ventricular Esquerda/mortalidade , Disfunção Ventricular Esquerda/fisiopatologia , Disfunção Ventricular Esquerda/cirurgia , Função Ventricular Esquerda , Adulto JovemRESUMO
OBJECTIVE: To evaluate the clinical associations between rheumatic fever and antiphospholipid syndrome and the impact of coexistence of these two diseases in an individual. METHODS: Systematic review in electronics databases, regarding the period from 1983 to 2012. The keywords: "Rheumatic Fever," "Antiphospholipid Syndrome," and "Antiphospholipid Antibody Syndrome" are used. RESULTS: were identified 11 cases described in the literature about the association of rheumatic fever and antiphospholipid syndrome. Clinical presentation of rheumatic fever was characterized by the predominance of carditis (11/11) and chorea (7/11). Regarding the manifestations of APS, the stroke was observed in 7/11 (63.6%), with one of them having probable embolic origin. CONCLUSION: The present study brings the information that the association between APS and RF is quite rare, however, is of great clinical importance. Doctors who deal with the RF should include in their differential diagnosis the APS, especially in the presence of stroke in patients with RF and whose echocardiogram does not show intracavitary thrombi.
Assuntos
Síndrome Antifosfolipídica/diagnóstico , Febre Reumática/diagnóstico , Anticorpos Antifosfolipídeos/sangue , Síndrome Antifosfolipídica/complicações , Síndrome Antifosfolipídica/imunologia , Síndrome Antifosfolipídica/fisiopatologia , Coreia/fisiopatologia , Diagnóstico Diferencial , Humanos , Miocardite/fisiopatologia , Febre Reumática/complicações , Febre Reumática/imunologia , Febre Reumática/fisiopatologia , Acidente Vascular Cerebral/fisiopatologiaRESUMO
BACKGROUND: After brain death (BD) donors usually experience cardiac dysfunction, which is responsible for a considerable number of unused organs. Causes of this cardiac dysfunction are not fully understood. Some authors argue that autonomic storm with severe hemodynamic instability leads to inflammatory activation and myocardial dysfunction. OBJECTIVES: To investigate the hypothesis that thoracic epidural anesthesia blocks autonomic storm and improves graft condition by reducing the inflammatory response. METHODS: Twenty-eight male Wistar rats (250-350 g) allocated to four groups received saline or bupivacaine via an epidural catheter at various times in relation to brain-death induction. Brain death was induced by a sudden increase in intracranial pressure by rapid inflation of a ballon catheter in the extradural space. Blood gases, electrolytes, and lactate analyses were performed at time zero, and 3 and 6 hours. Blood leukocytes were counted at 0 and 6 hours. After 6 hours of BD, we performed euthanasia to measure vascular adhesion molecule (VCAM)-1, intracellular adhesion molecule (ICAM)-1, interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, Bcl-2 and caspase-3 on cardiac tissue. RESULTS: Thoracic epidural anesthesia was effective to block the autonomic storm with a significant difference in mean arterial pressure between the untreated (saline) and the bupivacaine group before BD (P < .05). However, no significant difference was observed for the expressions of VCAM-1, ICAM-1, TNF-α, IL-1ß, Bcl-2, and caspase-3 (P > .05). CONCLUSION: Autonomic storm did not seem to be responsible for the inflammatory changes associated with BD; thoracic epidural anesthesia did not modify the expression of inflammatory mediators although it effectively blocked the autonomic storm.