46 research outputs found
Otimização do tratamento medicamentoso na doença arterial coronariana: tarefa para o subespecialista?
Análise econômica dos Stents coronarianos farmacológicos no Brasil: para todos ou para poucos pacientes? Economic analysis of drug-eluting coronary stents in Brazil: a choice for all or just for a few patients?
DIRETRIZ DA SOCIEDADE BRASILEIRA DE CARDIOLOGIA E DA SOCIEDADE BRASILEIRA DE HEMODINÂMICA E CARDIOLOGIA INTERVENCIONISTA SOBRE INTERVENÇÃO CORONÁRIA PERCUTÂNEA
Inst Dante Pazzanese Cardiol, Sao Paulo, SP, BrazilUniv Sao Paulo, Fac Med, Hosp Clin, Ribeirao Preto, SP, BrazilHosp Coracao Anis Rassi, Goiania, Go, BrazilInst Coracao Triangulo, Uberlandia, MG, BrazilEscola Paulista Med, Sao Paulo, SP, BrazilHosp Felicio Rocho, Belo Horizonte, MG, BrazilReal & Benemerita Soc Portuguesa Beneficencia, Sao Paulo, SP, BrazilUniv Sao Paulo, Fac Med, Inst Coracao, Hosp Clin, Sao Paulo, SP, BrazilFundacao Univ Cardiol, Inst Cardiol Rio Grande do Sul, Porto Alegre, RS, BrazilHosp Santa Paula, Cardioctr, Joao Pessoa, Paraiba, BrazilHosp Bandeirantes, Sao Paulo, SP, BrazilClin Sao Vicente, Rio De Janeiro, RJ, BrazilUniv Fed Sao Paulo, Escola Paulista Med, Sao Paulo, SP, BrazilWeb of Scienc
Chagas heart disease: pathophysiologic mechanisms, prognostic factors and risk stratification
Chagas heart disease (CHD) results from infection with the protozoan parasite Trypanosoma cruzi and is the leading cause of infectious myocarditis worldwide. It poses a substantial public health burden due to high morbidity and mortality. CHD is also the most serious and frequent manifestation of chronic Chagas disease and appears in 20-40% of infected individuals between 10-30 years after the original acute infection. In recent decades, numerous clinical and experimental investigations have shown that a low-grade but incessant parasitism, along with an accompanying immunological response [either parasite-driven (most likely) or autoimmune-mediated], plays an important role in producing myocardial damage in CHD. At the same time, primary neuronal damage and microvascular dysfunction have been described as ancillary pathogenic mechanisms. Conduction system disturbances, atrial and ventricular arrhythmias, congestive heart failure, systemic and pulmonary thromboembolism and sudden cardiac death are the most common clinical manifestations of chronic Chagas cardiomyopathy. Management of CHD aims to relieve symptoms, identify markers of unfavourable prognosis and treat those individuals at increased risk of disease progression or death. This article reviews the pathophysiology of myocardial damage, discusses the value of current risk stratification models and proposes an algorithm to guide mortality risk assessment and therapeutic decision-making in patients with CHD
Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial
Chagas cardiomyopathy is the most frequent and most severe manifestation of chronic Chagas disease, and is one of the leading causes of morbidity and death in Latin America. Although the pathogenesis of Chagas cardiomyopathy is incompletely understood, it may involve several mechanisms, including parasite-dependent myocardial damage, immune-mediated myocardial injury (induced by the parasite itself and by self-antigens), and microvascular and neurogenic disturbances. In the past three decades, a consensus has emerged that parasite persistence is crucial to the development and progression of Chagas cardiomyopathy. In this context, antiparasitic treatment in the chronic phase of Chagas disease could prevent complications related to the disease. However, according to the results of the BENEFIT trial, benznidazole seems to have no benefit for arresting disease progression in patients with chronic Chagas cardiomyopathy. In this review, we give an update on the main pathogenic mechanisms of Chagas disease, and re-examine and discuss the results of the BENEFIT trial, together with its limitations and implications
Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial
Chagas Heart Disease: Pathophysiologic Mechanisms, Prognostic Factors and Risk Stratification
Chagas heart disease (CHD) results from infection with the protozoan
parasite Trypanosoma cruzi and is the leading cause of infectious
myocarditis worldwide. It poses a substantial public health burden due
to high morbidity and mortality. CHD is also the most serious and
frequent manifestation of chronic Chagas disease and appears in 20-40%
of infected individuals between 10-30 years after the original acute
infection. In recent decades, numerous clinical and experimental
investigations have shown that a low-grade but incessant parasitism,
along with an accompanying immunological response [either
parasite-driven (most likely) or autoimmune-mediated], plays an
important role in producing myocardial damage in CHD. At the same time,
primary neuronal damage and microvascular dysfunction have been
described as ancillary pathogenic mechanisms. Conduction system
disturbances, atrial and ventricular arrhythmias, congestive heart
failure, systemic and pulmonary thromboembolism and sudden cardiac
death are the most common clinical manifestations of chronic Chagas
cardiomyopathy. Management of CHD aims to relieve symptoms, identify
markers of unfavourable prognosis and treat those individuals at
increased risk of disease progression or death. This article reviews
the pathophysiology of myocardial damage, discusses the value of
current risk stratification models and proposes an algorithm to guide
mortality risk assessment and therapeutic decision-making in patients
with CHD
Sertraline for the treatment of mild to moderate major depression: Brazilian multicenter study
Introduction: To evaluate the efficacy, safety, and tolerability of sertraline for the treatment of Brazilian patients with mild to moderate major depression. Patients and methods: Patients were 18 years old or older treated on an out-patient basis. Previous medications were stopped for a 2-week washout period. Afterwards, patients received sertraline, initial dose of 50 mg/day up to the 4 th week. The dose could then be increased up to 200 mg/day according to the efficacy and tolerability. Therapeutic efficacy was evaluated with the Montgomery-Asberg Depression Rating Scale (MADRS), Hamilton scale for depression (HAM-D), and Clinical Global Impression (CGI). Results: 51 patients (42 women) were evaluated regarding efficacy and safety. Treatment with sertraline significantly decreased scores of MADRS, HAM-D e ICGfrom 15.7 ± 6.1; 12.2 ± 3.9 e 3.5 ± 0.6 to 6.2 ± 6.5; 5.4 ± 4.7 e 2.3 ± 1.0 (P < 0.0001), respectively. Sertraline was well tolerated. Gastro-intestinal upset (N=14; 24.6%), headache (N=7; 12.3%), sleep alterations (H-7; 12.3%), dizziness (N-4; 7.0%), and anorexia (N=4; 7.0%) were the most common adverse events. Six patients discontinued the treatment due to adverse events. Conclusion: Sertraline is efficient and presents a favorable safety and tolerability profile for the treatment of Brazilian patients with mild to moderate major depression. © Copyright Moreira Jr. Editora.USPFaculdade de Medicina Universidade Federal de Goiás, Goiânia - GOFundação Faculdade Federal de Ciências Médicas de Porto AlegreFundação Faculdade Federal de Ciências Médicas de Porto Alegre, Porto Alegre - RSDisciplina de Medicina InternaDisciplina de Alergia e Imunopatologia Clínica Faculdade de Medicina Estadual de MaríliaEscola Paulista de Medicina UnifespFaculdade de Medicina de Botucatu UnespFaculdade de Medicina Estadual de MaríliaUSP, São PauloDepartamento de Medicina Clínica Universidade Federal de PernambucoUFPERoyal National Hospital for Rheumatic Diseases Saint Thomas'Hospital UKServiço de Reumatologia Hospital Heliópolis, São Paulo - SP, Rua T 38 No 917 - Setor Bueno, Goiânia - GOInstituição Anis Rassi Hospital, E. Av. J. Alves, 453 - esq. c/ r. 9, CEP 74110-020Faculdade de Medicina de Botucatu Unes
Chagas disease
Chagas disease is a chronic, systemic, parasitic infection caused by the protozoan Trypanosoma cruzi, and was discovered in 1909. The disease affects about 8 million people in Latin America, of whom 30-40% either have or will develop cardiomyopathy, digestive megasyndromes, or both. In the past three decades, the control and management of Chagas disease has undergone several improvements. Large-scale vector control programmes and screening of blood donors have reduced disease incidence and prevalence. Although more effective trypanocidal drugs are needed, treatment with benznidazole (or nifurtimox) is reasonably safe and effective, and is now recommended for a widened range of patients. Improved models for risk stratification are available, and certain guided treatments could halt or reverse disease progression. By contrast, some challenges remain: Chagas disease is becoming an emerging health problem in non-endemic areas because of growing population movements; early detection and treatment of asymptomatic individuals are underused; and the potential benefits of novel therapies (eg, implantable cardioverter defibrillators) need assessment in prospective randomised trials
