ABSTRACT
Abstract Background: Pericardial effusion is a relatively common finding and can progress to cardiac tamponade; etiological diagnosis is important for guiding treatment decisions. With advances in medicine and improvement in the social context, the most frequent etiological causes have changed. Objectives: To evaluate the clinical and laboratory characteristics, etiology, and clinical course of patients with pericardial effusion and cardiac tamponade. Materials and methods: Patients with pericardial effusion classified as small (< 10 mm), moderate (between 10-20 mm), or severe (> 20 mm) were included. Data from the clinical history, physical examination, laboratory tests, and complementary tests were evaluated in patients with pericardial effusion and cardiac tamponade. The significance level was set at 5%. Results: A total of 254 patients with a mean age of 53.09 ± 17.9 years were evaluated, 51.2% of whom were female. A total of 40.4% had significant pericardial effusion (> 20 mm). Pericardial tamponade occurred in 44.1% of patients. Among pericardial effusion patients without tamponade, the most frequent etiologies were: idiopathic (44.4%) and postsurgical (17.6%), while among those with tamponade, the most frequent etiologies were postsurgical (21.4%) and postprocedural (19.6%). The mean follow-up time was 2.2 years. Mortality was 42% and 23.2 in those with and without tamponade, respectively (p=0.001). Conclusions: There is an etiological difference between pericardial effusion patients with and without cardiac tamponade. An idiopathic etiology is more common among those without tamponade, while postinterventional/postsurgical is more common among those with tamponade. The tamponade group had a higher mortality rate.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Pericardial Effusion/etiology , Pericardial Effusion/therapy , Cardiac Tamponade/etiology , Cardiac Tamponade/therapy , Pericardial Effusion/complications , Pericardial Effusion/mortality , Pericarditis , Cardiac Tamponade/mortality , Retrospective StudiesABSTRACT
Background: Galectin-3 is the designation given to the protein that binds to ß-galactosides, expressed by activated macrophages and described as a cardiac fibrosis mediator. In hypertrophic cardiomyopathy (HCM), myocardial fibrosis is an independent predictor of adverse outcome; however, the association between Galectin-3 and myocardial fibrosis has not been studied in this cardiopathy. Objective: To evaluate the association of Galectin-3 and the presence of myocardial fibrosis in a patient with hypertrophic cardiomyopathy. Methods: Galectin-3 was measured in automated equipment using the Elisa technique in 100 participants divided into two groups: 50 patients with hypertrophic cardiomyopathy and 50 healthy control subjects. All patients with hypertrophic cardiomyopathy underwent magnetic nuclear resonance with the late enhancement technique to investigate myocardial fibrosis. For the statistical analysis, p values < 0.05 were considered statistically significant. Results: Galectin-3 levels were low and did not show significant differences between patients with hypertrophic cardiomyopathy and the control group,10.3 ± 3.1 ng/dL and 11.3 ± 2.6 ng/dL (p = 0.12) respectively. Myocardial fibrosis was a common finding and was identified in 84% (42/50) of patients with HCM, but no differences were observed between Galectin-3 levels when comparing patients with and without fibrosis, 10.3 ± 2.4 ng/dL and 10.1 ± 2.1 ng/dL (p = 0.59). Conclusion: The results did not show an association between Galectin-3 and myocardial fibrosis in patients with hypertrophic cardiomyopathy, suggesting that non-inflammatory mechanisms of myocardial fibrosis formation and cardiac remodeling are involved in this cardiopathy
Subject(s)
Humans , Male , Female , Middle Aged , Cardiomyopathy, Hypertrophic/diagnostic imaging , Galectin 3 , Endomyocardial Fibrosis , Arrhythmias, Cardiac/diagnosis , Diagnostic Imaging/methods , Magnetic Resonance Spectroscopy/methods , Biomarkers , Cardiovascular Diseases/diagnosis , Echocardiography, Doppler/methods , Data Interpretation, StatisticalABSTRACT
Chagas disease is a cause of dilated cardiomyopathy, and information about left atrial (LA) function in this disease still lacks. To assess the different LA functions (reservoir, conduit and pump functions) and their correlation with the echocardiographic parameters of left ventricular (LV) systolic and diastolic functions. 10 control subjects (CG), and patients with Chagas disease as follows: 26 with the indeterminate form (GI); 30 with ECG alterations (GII); and 19 with LV dysfunction (GIII). All patients underwent M-mode and two-dimensional echocardiography, pulsed-wave Doppler and tissue Doppler imaging. Reservoir function (Total Emptying Fraction: TEF): (p <0.0001), lower in GIII as compared to CG (p = 0.003), GI (p <0.001) and GII (p <0.001). Conduit function (Passive Emptying Fraction: PEF): (p = 0.004), lower in GIII (GIII and CG, p = 0.06; GI and GII, p = 0.06; and GII and GIII, p = 0.07). Pump function (Active Emptying Fraction: AEF): (p = 0.0001), lower in GIII as compared to CG (p = 0.05), GI (p<0.0001) and GII (p = 0.002). There was a negative correlation of E/e’ An impairment of LA functions in Chagas cardiomyopathy was observed.
A doença de Chagas é uma causa de miocardiopatia dilatada, sendo ainda pouco conhecida a função do átrio esquerdo (AE) nessa doença. Avaliar as diferenças nas funções do AE (reservatório, conduto e bomba) e sua correlação com os parâmetros ecocardiográficos das funções sistólica e diastólica do ventrículo esquerdo (VE). 10 controles (GC) e os seguintes pacientes com doença de Chagas: 26 com a forma indeterminada (GI); 30 com alterações eletrocardiográficas (GII); e 19 com disfunção de VE (GIII). Todos os pacientes foram submetidos a ecocardiografia bidimensional e em modo M, Doppler pulsado e Doppler tecidual. Função de reservatório (fração de esvaziamento total: FET) (p < 0,0001), mais baixa no GIII do que no GC (p = 0,003), GI (p < 0,001) e GII (p < 0,001). Função de conduto (fração de esvaziamento passivo: FEP) (p = 0,004), mais baixa no GIII (GIII e GC, p = 0.06; GI e GII, p = 0.06; e GII e GIII, p = 0,07). Função de bomba (fração de esvaziamento ativo: FEA) (p = 0,0001), mais baixa no GIII do que no CG (p = 0,05), GI (p<0,0001) e GII (p = 0,002). Observou-se uma correlação negativa entre E/e’média e as funções de reservatório e de bomba (FET e FEA), e uma correlação positiva entre as ondas e’média e s’ (paredes septal e lateral) e as funções de reservatório, conduto e bomba. Observou-se comprometimento das funções do AE na miocardiopatia chagásica.
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Atrial Function, Left/physiology , Chagas Cardiomyopathy/physiopathology , Ventricular Dysfunction, Left/physiopathology , Cardiomyopathy, Dilated/physiopathology , Case-Control Studies , Chagas Cardiomyopathy , Echocardiography, Doppler , Myocardial Contraction/physiology , Reference Values , Statistics, Nonparametric , Stroke Volume/physiology , Ventricular Dysfunction, LeftABSTRACT
FUNDAMENTO: O NT pro-BNP é marcador de disfunção sistólica e diastólica. OBJETIVO: Determinar os níveis de NT pro-BNP em pacientes com cardiopatia chagásica, hipertrófica, restritiva e afecções pericárdicas, e sua relação com medidas ecocardiográficas de disfunção sistólica e diastólica. MÉTODOS: Cento e quarenta e cinco pacientes foram divididos nos respectivos grupos: 1) cardiopatia chagásica (CCh) - 14 pacientes; 2) miocardiopatia hipertrófica (CMH) - 71 pacientes; 3) endomiocardiofibrose (EMF) - 26 pacientes; 4) derrame pericárdico (DP) - 18 pacientes; 5) e pericardite constritiva (PC) - 16 pacientes. Foi constituído um grupo-controle de 40 indivíduos sem doença cardíaca. O grau de acometimento miocárdico e o derrame pericárdico foram avaliados pelo ecocardiograma bidimensional e a restrição pelo Doppler pulsátil do fluxo mitral. O diagnóstico de PC foi confirmado por meio da ressonância magnética. Os níveis de NT pro-BNP foram medidos por imunoensaio com detecção por eletroquimioluminescência. RESULTADOS: O NT pro-BNP esteve aumentado (p < 0,001) na CCh (mediana 513,8 pg/ml), CMH (mediana 848 pg/ml), EMF (mediana 633 pg/ml), PC (mediana 568 pg/ml), DP (mediana 124 pg/ml), quando comparados ao grupo-controle (mediana 28 pg/ml). Não foram observadas diferenças estatisticamente significativas entre PC e EMF (p = 0,14). No grupo hipertrófico, o NT pro-BNP correlacionou-se com tamanho de átrio esquerdo (r = 0,40; p < 0,001) e relação E/Ea (p < 0,01). No grupo restritivo, houve uma tendência de correlação com pico de velocidade de onda E (r = 0,439; p = 0,06). CONCLUSÃO: O NT pro-BNP encontra-se aumentado nas diversas miocardiopatias e afecções pericárdicas, e apresenta relação com o grau de disfunção sistólica e diastólica.
BACKGROUND: NT pro-BNP is a marker of systolic and diastolic dysfunction. OBJECTIVE: To determine NT pro-BNP levels in patients with chagasic, hypertrophic, and restrictive heart diseases, as well as with pericardial diseases, and their relation to echocardiographic measurements of systolic and diastolic dysfunction. METHODS: A total of 145 patients were divided into the following groups: 1) Chagas' heart disease (CHD) - 14 patients; 2) hypertrophic cardiomyopathy (HCM) - 71 patients; 3) endomyocardial fibrosis (EMF) - 26 patients; 4) pericardial effusion (PE) - 18 patients; and 5) constrictive pericarditis (CP) - 16 patients. The control group was comprised of 40 individuals with no heart disease. The degree of myocardial impairment and pericardial effusion were assessed by two-dimensional echocardiography and the degree of restriction by pulsed Doppler transmitral flow. The diagnosis of CP was confirmed through magnetic resonance imaging. NT pro-BNP levels were determined through electrochemiluminescence immunoassay. RESULTS: NT pro-BNP was increased (p < 0.001) in CHD (median = 513.8 pg/ml), HCM (median = 848 pg/ml), EMF (median = 633 pg/ml), CP (median = 568 pg/ml), and PE (median = 124 pg/ml), when compared with the control group (median = 28 pg/ml). No statistically significant differences were found between CP and EMF (p = 0.14). In the hypertrophic group, NT pro-BNP was correlated with left atrial size (r = 0.40; p < 0.001) and with E/Ea ratio (p < 0.01). In the restrictive group, there was a trend of correlation with E-wave peak velocity (r = 0.439; p = 0.06). CONCLUSION: NT pro-BNP is increased in the different cardiomyopathies and pericardial diseases and is correlated with the degree of systolic and diastolic dysfunction.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Cardiomyopathies/diagnosis , Natriuretic Peptide, Brain/blood , Peptide Fragments/blood , Pericarditis, Constrictive/diagnosis , Ventricular Dysfunction/diagnosis , Biomarkers/blood , Case-Control Studies , Cardiomyopathies/blood , Cardiomyopathy, Hypertrophic/diagnosis , Cardiomyopathy, Hypertrophic/physiopathology , Cardiomyopathy, Restrictive/diagnosis , Cardiomyopathy, Restrictive/physiopathology , Chagas Cardiomyopathy/diagnosis , Chagas Cardiomyopathy/physiopathology , Diastole/physiology , Magnetic Resonance Imaging , Natriuretic Peptide, Brain/physiology , Prospective Studies , Peptide Fragments/physiology , Pericardial Effusion/diagnosis , Pericardial Effusion/physiopathology , Pericarditis, Constrictive/blood , Pericardium , Systole , Ventricular Dysfunction/physiopathologyABSTRACT
FUNDAMENTOS: O polimorfismo e a atividade da enzima conversora da angiotensina (ECA) contribuem, de forma significante, na expressão fenotípica e no prognóstico de pacientes com cardiomiopatia. OBJETIVOS: Determinar o polimorfismo da ECA, realizar a sua dosagem sérica e correlacioná-los com o grau de hipertrofia miocárdica e o índice de massa do ventrículo esquerdo em pacientes com cardiomiopatia hipertrófica (CMH) nas formas familiar e não familiar. CASUÍSTICA E MÉTODO: Foram estudados 136 pacientes consecutivos com CMH (69 da forma familiar e 67 da forma não familiar) com média de idade de 40,53±17,45 anos, sendo 76 do sexo masculino. Os indivíduos foram submetidos ao ecocardiograma para obtenção das medidas do septo interventricular, parede posterior e massa do ventrículo esquerdo e coleta de sangue para determinação do polimorfismo e dosagem sérica da atividade da ECA. RESULTADOS: Quanto ao genótipo do polimorfismo do gene da ECA, encontramos DD 47(35%), ID 71(52%) e II 18 (13%), sendo que do genótipo DD 34% na forma familiar e 36% na forma não familiar. A média da atividade da ECA foi de 56.414±19.236 para os pacientes com CMH na forma familiar e de 55.085±22.634 para a forma não familiar (p = 0,714). A média do índice de massa do ventrículo esquerdo na forma familiar foi 154±63 g/m2 e na forma não familiar foi 174±57 g/m2 (p = 0,008). A média do septo interventricular nas formas familiar e não familiar foi, respectivamente, 19±5 mm e 21±5 mm (p = 0,020). A média da parede posterior do ventrículo esquerdo nas formas familiar e não familiar foi, respectivamente, 10±2 mm e 12±3 mm (p = 0,0001). Não observamos correlação entre o polimorfismo e o grau de hipertrofia miocárdica (p = 0,651). Houve correlação positiva entre a atividade da ECA e o índice de massa do ventrículo esquerdo (p = 0,038)...
CKGROUND: The polymorphism and the activity of the angiotensin converting enzyme (ACE) contributes of significant form in the phenotypic expression and the prognostic of patients with cardiomyopathy. OBJECTIVES: To determine the ACE polymorphism and ACE plasma levels in patients with hypertrophic cardiomyopathy (HCM) in the familial and nonfamilial forms and to correlate it with the degree of myocardium hypertrophy and with the left ventricular mass index. PATIENTS AND METHODS: 136 consecutive patients with HCM (69 of familial and 67 of nonfamilial forms) were studied. The mean age was 40.53±17.45 years, 76 were male. The individuals were submitted to the Echo-Doppler for the measurement of interventricular septum, wall thickness and the left ventricular mass index. The blood samples were taken for extraction of the DNA for the polymerase reaction and measurement of ACE plasma levels. RESULTS: Regarding the genotype of the ACE gene polymorphism, we found DD 47 (35%), ID 71 (52%) and II 18 (13%), being that of genotype DD 34% in the familial and 36% in the nonfamilial forms. The mean of the activity of the ACE was 56.414±19.236 for the patients with HCM in the familial form and 55.085±22.634 in the non familial form (p = 0.714). The mean of the left ventricular mass index in the familial form was 154±63 g/m2 and in the nonfamilial form was 174±57 g/m2 (p = 0.0080). The mean of interventricular septum in the familial and nonfamilial forms was 19±5 mm and 21±5 mm (p = 0.0200), respectively. The mean of the wall thickness in the familial and nonfamilial forms was 10±2 mm and 12±3 mm (p = 0.0001), respectively. We did not observe correlation between the polymorphism and the degree of myocardium hypertrophy (p = 0.651)...
Subject(s)
Humans , Cardiomyopathy, Hypertrophic , Gene Frequency , Genetics , Genotype , Hypertrophy, Left Ventricular , Peptidyl-Dipeptidase A , Polymorphism, GeneticABSTRACT
OBJETIVO: Estudar os marcadores moleculares para os genes da cadeia pesada da beta-miosina cardíaca e da proteína-C de ligacão à miosina em familiares de portadores de cardiomiopatia hipertrófica. MÉTODOS: Foram estudadas 12 famílias que realizaram anamnese, exame físico, eletrocardiograma, ecocardiograma e coleta de sangue para o estudo genético através da reacão em cadeia da polimerasse. RESULTADOS: Dos 227 familiares 25 por cento eram acometidos, sendo 51 por cento do sexo masculino com idade média de 35n19 (2 a 95) anos. A análise genética mostrou ligacão com o gene da b-miosina cardíaca em uma família e, em outra, ligacão com o gene da proteína C de ligacão à miosina. Em cinco famílias foram excluídas ligacões com os dois genes; em duas, a ligacão com o gene da proteína C de ligacão à miosina, porém para o gene da b-miosina os resultados foram inconclusivos; em duas famílias os resultados foram inconclusivos para os dois genes e em uma foi excluída ligacão para o gene da b-miosina mas ficou inconclusivo para o gene da proteína C de ligacão à miosina. CONCLUSAO: Em nosso meio, talvez predominem outros genes que não aqueles descritos na literatura, ou que existam outras diferencas genéticas relacionadas com a origem de nossa populacão e/ou fatores ambientais.