Análise de Custo-Efetividade do Monitoramento da Insuficiência Cardíaca pelo proBNP comparado ao Monitoramento Clínico

Fundamento: Inexiste atualmente um guia prático para orientar a intensidade do tratamento farmacológico de pacientes com insuficiência cardíaca (IC) crônica. Objetivo: Verificar se a farmacoterapia orientada pelas concentraçoes da fraçao amino-terminal do pro-BNP (proBNP) resulta em melhor desfecho e menor custo se comparada ao monitoramento clínico isolado, em pacientes com IC crônica. Métodos: Para a análise de custo-efetividade foi utilizada uma árvore de decisao modelada para o cenário do Sistema Suplementar de Saúde Brasileiro. Foram utilizados dados de efetividade publicados em ensaio clínico controlado e randomizado (ECCR) e dados de custos do tratamento obtidos de estudos brasileiros sobre epidemiologia e custos da IC. Foram contabilizados custos diretos com hospitalizaçoes, atendimentos de urgência, consultas, medicamentos ambulatoriais, exames complementares e valor do teste do proBNP, em um período de 12 meses. A unidade de efetividade avaliada fo

Análise de Custo-Efetividade do Monitoramento da Insuficiência Cardíaca pelo proBNP comparado ao Monitoramento Clínico

Fundamento: Inexiste atualmente um guia prático para orientar a intensidade do tratamento farmacológico de pacientes com insuficiência cardíaca (IC) crônica. Objetivo: Verificar se a farmacoterapia orientada pelas concentraçoes da fraçao amino-terminal do pro-BNP (proBNP) resulta em melhor desfecho e menor custo se comparada ao monitoramento clínico isolado, em pacientes com IC crônica. Métodos: Para a análise de custo-efetividade foi utilizada uma árvore de decisao modelada para o cenário do Sistema Suplementar de Saúde Brasileiro. Foram utilizados dados de efetividade publicados em ensaio clínico controlado e randomizado (ECCR) e dados de custos do tratamento obtidos de estudos brasileiros sobre epidemiologia e custos da IC. Foram contabilizados custos diretos com hospitalizaçoes, atendimentos de urgência, consultas, medicamentos ambulatoriais, exames complementares e valor do teste do proBNP, em um período de 12 meses. A unidade de efetividade avaliada fo

Incremental value of B-type natriuretic peptide for early risk prediction of infective endocarditis

SummaryBackgroundEarly and accurate risk prediction is an unmet clinical need in patients with infective endocarditis (IE). The aim of this study was to determine the value of B-type natriuretic peptide (BNP) levels obtained on admission for the prediction of in-hospital death in IE patients.MethodsBetween 2009 and 2011, consecutive patients with IE diagnosed using the revised Duke criteria and admitted to the emergency department were evaluated prospectively. BNP levels were measured on admission. Death during hospitalization was the primary endpoint.ResultsAmong 104 consecutive patients with IE and with available BNP levels, 34 (32.7%) died in hospital. BNP levels were significantly higher in patients who died as compared to survivors (709.0 pg/ml vs. 177.5 pg/ml, p<0.001). The accuracy of BNP to predict death as quantified by the area under the receiver operating characteristics curve was 0.826 (95% confidence interval (CI) 0.747–0.905). The value of BNP was additive to that provided by clinical, microbiological, and echocardiography assessment. On multivariate analysis, new heart failure (hazard ratio (HR) 2.02, 95% CI 1.15–3.57, p=0.015), sepsis (HR 2.10, 95% CI 1.25–3.55, p=0.005), Staphylococcus aureus endocarditis (HR 2.67, 95% CI 1.60–4.45, p<0.001), left ventricular ejection fraction ≤55% (HR 1.63, 95% CI 1.00–2.65, p=0.047), and BNP (HR 1.04, 95% CI 1.02–1.06, p<0.001) were independent predictors of in-hospital mortality.ConclusionAmong patients with IE, BNP levels obtained on admission provide incremental value for early and accurate risk prediction

Biomarkers for prediction of mortality in left-sided infective endocarditis

Background: Evidence regarding biomarkers for risk prediction in patients with infective endocarditis (IE) is limited. We aimed to investigate the value of a panel of biomarkers for the prediction of in-hospital mortality in patients with IE. Methods: Between 2016 and 2018, consecutive IE patients admitted to the emergency department were prospectively included. Blood concentrations of nine biomarkers were measured at admission (D0) and on the seventh day (D7) of antibiotic therapy: C-reactive protein (CRP), sensitive troponin I (s-cTnI), procalcitonin, B-type natriuretic peptide (BNP), neutrophil gelatinase-associated lipocalin (NGAL), interleukin 6 (IL6), tumor necrosis factor α (TNF-α), proadrenomedullin, alpha-1-acid glycoprotein, and galectin 3. The primary endpoint was in-hospital mortality. Results: Among 97 patients, 56% underwent cardiac surgery, and in-hospital mortality was 27%. At admission, six biomarkers were independent predictors of in-hospital mortality: s-cTnI (OR 3.4; 95%CI 1.8–6.4; P < 0.001), BNP (OR 2.7; 95%CI 1.4–5.1; P = 0.002), IL-6 (OR 2.06; 95%CI 1.3–3.7; P = 0.019), procalcitonin (OR 1.9; 95%CI 1.1–3.2; P = 0.018), TNF-α (OR 1.8; 95%CI 1.1–2.9; P = 0.019), and CRP (OR 1.8; 95%CI 1.0–3.3; P = 0.037). At admission, S-cTnI provided the highest accuracy for predicting mortality (area under the ROC curve: s-cTnI 0.812, BNP 0.727, IL-6 0.734, procalcitonin 0.684, TNF-α 0.675, CRP 0.670). After 7 days of antibiotic therapy, BNP and inflammatory biomarkers improved their performance (s-cTnI 0.814, BNP 0.823, IL-6 0.695, procalcitonin 0.802, TNF-α 0.554, CRP 0.759). Conclusion: S-cTnI concentration measured at admission had the highest accuracy for mortality prediction in patients with IE

Diretriz sobre Diagnóstico e Tratamento da Cardiomiopatia Hipertrófica – 2024

Hypertrophic cardiomyopathy (HCM) is a form of genetically caused heart muscle disease, characterized by the thickening of the ventricular walls. Diagnosis requires detection through imaging methods (Echocardiogram or Cardiac Magnetic Resonance) showing any segment of the left ventricular wall with a thickness &gt; 15 mm, without any other probable cause. Genetic analysis allows the identification of mutations in genes encoding different structures of the sarcomere responsible for the development of HCM in about 60% of cases, enabling screening of family members and genetic counseling, as an important part of patient and family management. Several concepts about HCM have recently been reviewed, including its prevalence of 1 in 250 individuals, hence not a rare but rather underdiagnosed disease. The vast majority of patients are asymptomatic. In symptomatic cases, obstruction of the left ventricular outflow tract (LVOT) is the primary disorder responsible for symptoms, and its presence should be investigated in all cases. In those where resting echocardiogram or Valsalva maneuver does not detect significant intraventricular gradient (&gt; 30 mmHg), they should undergo stress echocardiography to detect LVOT obstruction. Patients with limiting symptoms and severe LVOT obstruction, refractory to beta-blockers and verapamil, should receive septal reduction therapies or use new drugs inhibiting cardiac myosin. Finally, appropriately identified patients at increased risk of sudden death may receive prophylactic measure with implantable cardioverter-defibrillator (ICD) implantation.La miocardiopatía hipertrófica (MCH) es una forma de enfermedad cardíaca de origen genético, caracterizada por el engrosamiento de las paredes ventriculares. El diagnóstico requiere la detección mediante métodos de imagen (Ecocardiograma o Resonancia Magnética Cardíaca) que muestren algún segmento de la pared ventricular izquierda con un grosor &gt; 15 mm, sin otra causa probable. El análisis genético permite identificar mutaciones en genes que codifican diferentes estructuras del sarcómero responsables del desarrollo de la MCH en aproximadamente el 60% de los casos, lo que permite el tamizaje de familiares y el asesoramiento genético, como parte importante del manejo de pacientes y familiares. Varios conceptos sobre la MCH han sido revisados recientemente, incluida su prevalencia de 1 entre 250 individuos, por lo tanto, no es una enfermedad rara, sino subdiagnosticada. La gran mayoría de los pacientes son asintomáticos. En los casos sintomáticos, la obstrucción del tracto de salida ventricular izquierdo (TSVI) es el trastorno principal responsable de los síntomas, y su presencia debe investigarse en todos los casos. En aquellos en los que el ecocardiograma en reposo o la maniobra de Valsalva no detecta un gradiente intraventricular significativo (&gt; 30 mmHg), deben someterse a ecocardiografía de esfuerzo para detectar la obstrucción del TSVI. Los pacientes con síntomas limitantes y obstrucción grave del TSVI, refractarios al uso de betabloqueantes y verapamilo, deben recibir terapias de reducción septal o usar nuevos medicamentos inhibidores de la miosina cardíaca. Finalmente, los pacientes adecuadamente identificados con un riesgo aumentado de muerte súbita pueden recibir medidas profilácticas con el implante de un cardioversor-desfibrilador implantable (CDI).A cardiomiopatia hipertrófica (CMH) é uma forma de doença do músculo cardíaco de causa genética, caracterizada pela hipertrofia das paredes ventriculares. O diagnóstico requer detecção por métodos de imagem (Ecocardiograma ou Ressonância Magnética Cardíaca) de qualquer segmento da parede do ventrículo esquerdo com espessura &gt; 15 mm, sem outra causa provável. A análise genética permite identificar mutações de genes codificantes de diferentes estruturas do sarcômero responsáveis pelo desenvolvimento da CMH em cerca de 60% dos casos, permitindo o rastreio de familiares e aconselhamento genético, como parte importante do manejo dos pacientes e familiares. Vários conceitos sobre a CMH foram recentemente revistos, incluindo sua prevalência de 1 em 250 indivíduos, não sendo, portanto, uma doença rara, mas subdiagnosticada. A vasta maioria dos pacientes é assintomática. Naqueles sintomáticos, a obstrução do trato de saída do ventrículo esquerdo (OTSVE) é o principal distúrbio responsável pelos sintomas, devendo-se investigar a sua presença em todos os casos. Naqueles em que o ecocardiograma em repouso ou com Manobra de Valsalva não detecta gradiente intraventricular significativo (&gt; 30 mmHg), devem ser submetidos à ecocardiografia com esforço físico para detecção da OTSVE.&nbsp;&nbsp; Pacientes com sintomas limitantes e grave OTSVE, refratários ao uso de betabloqueadores e verapamil, devem receber terapias de redução septal ou uso de novas drogas inibidoras da miosina cardíaca. Por fim, os pacientes adequadamente identificados com risco aumentado de morta súbita podem receber medida profilática com implante de cardiodesfibrilador implantável (CDI)

ProBNP for stratifying patients with heart failure

OBJECTIVE: To verify whether the serum levels of N-Terminal ProBNP fraction (ProBNP) allow us to identify with accuracy the clinical functional status of patients with heart failure (HF), because the clinical diagnosis of this syndrome is based basically on clinical data when the complementary tests have lower specificity. METHODS: Sixty-nine patients with a history of HF were studied. Their mean age of was 53.5 years and 78.3% were males. All underwent clinical and echocardiographic evaluations and a test to determine the serum dosage of ProBNP. According to clinical manifestation, patients were in the following functional classes (FC), 14% FC I, 40.6% FC II, 28.1% FC III, and 23.4% FC IV. The mean ejection fraction (EF) was 0.28. RESULTS: ProBNP did not differ according to age, sex, and cause of cardiopathy. No correlation existed between EF and the ProBNP serum level. ProBNP levels were significantly lower in patients in FC I than those in FC II (42 vs 326.7 pmol/L; P=0.0001), and in FC II than those in FC III (P=0.01). ProBNP levels did not differ statically between FC III and IV patients (888.1 vs 1082.8 pmol/L; P=0.25). ProBNP values greater than 100 pmol/L identify patients with decompensated HF with a sensitivity of 98%. CONCLUSION: ProBNP values over 100 pmol/L were indicative of HF, and patients with advanced HF had values over 270 pmol/L. A ProBNP dosage test was an excellent auxiliary in the clinical characterization of patients with HF