RESUMEN
Introducción y objetivos: La insuficiencia pulmonar (IP) es una complicación frecuente tras la intervención de cardiopatías congénitas. La expresión en leucocitos mononucleares circulantes (LMC) de los adrenoceptores (ß1 y ß2) y de las cinasas (GRK2, GRK3 y GRK5) refleja los cambios neurohumorales que se producen en la insuficiencia cardiaca (IC). El objetivo principal es describir la expresión génica de dichas moléculas en LMC de pacientes con IP grave. Métodos: Estudio prospectivo que analizó la expresión de las moléculas descritas en LMC de pacientes con IP grave en comparación con controles sanos y pacientes con IC avanzada. Resultados: Se estudió a 35 pacientes con IP grave, 22 controles y 13 pacientes con IC. El análisis de comparaciones múltiples mostró que en los controles la cantidad de ARN mensajero de adrenoceptor ß2 era mayor que el que presentaban los pacientes con IP y con IC, con similar expresión en estos 2 grupos: 748,49 (intervalo, 1.703,87) frente a 402,80 (1.210,81) frente a 287,46 (685,69) (p = 0,001). Estos mismos hallazgos se obtuvieron en la expresión génica de GRK2: 760,89 (1.169,46) frente a 445,17 (1.190,69) frente a 284,09 (585,27) (p < 0,001). No hubo diferencias en la expresión de estas moléculas según las variables clínicas de los pacientes con IP. Conclusiones: El patrón de expresión génica de GRK2 y del adrenoceptor ß2 de los pacientes con IP grave, como marcadores moleculares de disfunción cardiaca, se encuentra alterado respecto a los controles y es similar al de los pacientes con IC avanzada
Introduction and objectives: Pulmonary regurgitation (PR) is a frequent complication after repair of congenital heart disease. Lymphocyte expression of adrenoceptors (ß1 and ß2) and kinases (GRK2, GRK3, and GRK5) reflects the neurohumoral changes that occur in heart failure (HF). The main objective of this study was to describe the gene expression of these molecules in circulating lymphocytes in patients with severe PR. Methods: A prospective study was conducted to analyze lymphocyte expression of these molecules in patients with severe PR and compare it with expression in healthy controls and patients with advanced HF. Results: We studied 35 patients with severe PR, 22 healthy controls, and 13 patients with HF. Multiple comparisons analysis showed that ß2-adrenoceptor gene expression levels were higher in the control group than in patients in the PR and HF groups and that expression in the latter 2 groups was similar (748.49 [rank 1703.87] vs 402.80 [rank 1210.81] vs 287.46 [rank 685.69] P = .001). Similar findings were obtained in gene expression of GRK2 (760.89 [rank 1169.46] vs 445.17 [rank 1190.69] vs 284.09 [rank 585.27] P < .001). There were no differences in expression levels of these molecules according to clinical variables in patients with PR. Conclusions: The gene expression pattern of GRK2 and ß2-adrenoceptor as molecular markers of cardiac dysfunction was altered in patients with severe PR compared with controls and was similar to expression in patients with advanced HF
Asunto(s)
Humanos , Masculino , Femenino , Adulto Joven , Adulto , Persona de Mediana Edad , Insuficiencia de la Válvula Pulmonar/fisiopatología , Insuficiencia Cardíaca/fisiopatología , Receptores Adrenérgicos beta/genética , Leucocitos Mononucleares , Quinasas de Receptores Adrenérgicos beta/análisis , Biomarcadores/análisis , Marcadores Genéticos , Estudios Prospectivos , Estudios de Casos y Controles , ARN Mensajero/genética , Cardiopatías Congénitas/cirugía , Complicaciones Posoperatorias/epidemiologíaRESUMEN
INTRODUCTION AND OBJECTIVES: Pulmonary regurgitation (PR) is a frequent complication after repair of congenital heart disease. Lymphocyte expression of adrenoceptors (ß1 and ß2) and kinases (GRK2, GRK3, and GRK5) reflects the neurohumoral changes that occur in heart failure (HF). The main objective of this study was to describe the gene expression of these molecules in circulating lymphocytes in patients with severe PR. METHODS: A prospective study was conducted to analyze lymphocyte expression of these molecules in patients with severe PR and compare it with expression in healthy controls and patients with advanced HF. RESULTS: We studied 35 patients with severe PR, 22 healthy controls, and 13 patients with HF. Multiple comparisons analysis showed that ß2-adrenoceptor gene expression levels were higher in the control group than in patients in the PR and HF groups and that expression in the latter 2 groups was similar (748.49 [rank 1703.87] vs 402.80 [rank 1210.81] vs 287.46 [rank 685.69] P = .001). Similar findings were obtained in gene expression of GRK2 (760.89 [rank 1169.46] vs 445.17 [rank 1190.69] vs 284.09 [rank 585.27] P < .001). There were no differences in expression levels of these molecules according to clinical variables in patients with PR. CONCLUSIONS: The gene expression pattern of GRK2 and ß2-adrenoceptor as molecular markers of cardiac dysfunction was altered in patients with severe PR compared with controls and was similar to expression in patients with advanced HF.