Objetivo: Estudar a relação entre a espessura do tecido adiposo epicárdico (TAE) e os níveis plasmáticos de adiponectina em pacientes venezuelanos. Sujeitos e métodos: Foram selecionados 31 pacientes com diagnóstico de síndrome metabólica (SM) (grupo de estudo) e 27 controles. Foram medidos a glicose, os lipídios e a adiponectina. Foram determinados a espessura do TAE, a fração de ejeção, a função diastólica, a massa ventricular esquerda (MVE) e o volume atrial esquerdo (VAI) pela ecocardiografia transtorácica. Resultados: A espessura do TAE foi maior em pacientes com SM (5,69 ± 1,12 contra 3,52 ± 0,80 mm; p = 0,0001) com uma correlação positiva com o índice de massa corporal (IMC) (r = 0,661; p = 0,0001), circunferência da cintura (CC) (r = 0,664; p = 0,0001), pressão arterial sistólica (PAS) (r = 0,607; p = 0,0001), diastólica (PAD) (r = 0,447; p = 0,0001), insulina (r = 0,505; p = 0,0001), com a relação TG/HDL-C (r = 0,447; p = 0,0001), com o colesterol HDL (r = 0,353; p = 0,007), VAI (r = 0,432; p = 0,001) e MVI (r = 0,469; p = 0,0001). A espessura do TAE se correlacionou negativamente com a adiponectina (r = -0,499; p = 0,0001). Conclusão: Existe uma relação significativa entre a espessura do TAE, os componentes do SM e a concentração plasmática de adiponectina, o que poderia ser utilizado como um biomarcador para essa doença.

Objective: To study the relationship between epicardial adipose tissue (EAT) thickness and plasma levels of adiponectin in Venezuelan patients. Subjects and methods: Thirty-one patients diagnosed with metabolic syndrome (study group) and 27 controls were selected and tested for glycemia, lipids, and adiponectin. EAT thickness, ejection fraction, diastolic function, left ventricular mass (LVM), and left atrial volume (LAV) were determined by transthoracic echocardiography. Results: EAT thickness was greater in metabolic syndrome patients (5.69 ± 1.12 vs. 3.52 ± 0.80 mm; p = 0.0001), correlating positively with body mass index (BMI) (r = 0.661; p = 0.0001); waist circumference (WC) (r = 0.664; p = 0.0001); systolic (SBP) (r = 0.607; p = 0.0001), and diastolic blood pressure (DBP) (r = 0.447; p = 0.0001); insulin (r = 0.505; p = 0.0001); Tg/HDL-C ratio (r = 0.447; p = 0.0001), non-HDL-C (r = 0.353; p = 0.007); LAV (r = 0.432; p = 0.001), and LVM (r = 0.469; p = 0.0001). EAT thickness correlated negatively with adiponectin (r = -0.499; p = 0.0001). Conclusion: A significant association exists between EAT thickness and both metabolic syndrome components and adiponectin concentration, a link that might be used as a biomarker for this disease.

Objetivos: Determinar cambios hemodinámicos, estructurales y funcionales de pacientes con resistencia insulínica y sin síndrome metabólico. Métodos: Se seleccionaron diez pacientes de ambos sexos con diagnóstico de resistencia insulínica. Diez pacientes sanos ajustados por edad, sexo e índice de masa corporal (IMC) constituyeron el grupo control. El IMC y la presión arterial fueron registrados. Los pacientes fueron sometidos a una prueba de tolerancia oral a la glucosa. El índice de HOMAIR fue utilizado para el cálculo de la resistencia insulínica (HOMAIR: valor ≥ 2,5). La concentración de norepinefrina plasmática (NE) se cuantifico por HPLC. Los parámetros hemodinámicos, estructurales y funcionales del corazón fueron evaluados mediante el ecocardiograma bidimensional, eco doppler pulsado y doppler pulsado tisular. Resultados: La glucemia, la insulina basal y post-carga y el HOMAIR fueron significativamente más altos en el grupo de pacientes. El índice cardiaco resultó significativamente más bajo en el grupo de pacientes. La concentración de NE se correlacionó en forma positiva y estadísticamente significativa con las concentraciones de insulina basal y post-carga. La presión arterial diastólica se correlacionó en forma negativa y estadísticamente significativa con la insulina post-carga solo en el grupo control. El volumen diastólico final del ventrículo izquierdo se correlacionó en forma positiva y estadísticamente significativa con la insulina y el HOMAIR en el grupo de pacientes pero no en el grupo control. Conclusiones: Los niveles de insulina plasmática podrían desempeñar un papel muy importante en la modulación de los niveles plasmáticos de NE en pacientes con resistencia insulínica. La sobreactivación del sistema nervioso simpático podría condicionar anormalidades en el volumen sistólico final y el índice cardiaco, los cuales constituirían los cambios hemodinámicos adaptativos precoces en pacientes con resistencia insulínica sin síndrome metabólico.

Objective: To determine the haemodynamic, structural and functional changes in insulin-resistant subjects Methods: Ten insulin-resistant subjects were studied. Asymptomatic subjects were studied as a control group. Blood pressure and body mass index were registered. Standard oral glucose tolerance test was performed. Plasma glucose and insulin were measured at baseline and 2 hours post glucose load. Insulin resistance index HOMAIR was calculated. Insulin resistance was considered if HOMAIR value was ≥ 2.5. Plasma norepinephrine (NE) was measured by HPLC. In order to examine the mass and cardiac function, bi-dimensional echocardiogram and imaging doppler tissue were performed. Results: Plasma glucose, insulin and HOMAIR were significantly higher in insulin-resistant subjects. There was no significant difference in plasma NE concentration between groups. The cardiac index was the only haemodynamic variable found to be significantly lowers in insulin resistant subjects. A significant positive correlation between NE with fasting and post load insulin concentration was observed. In control group, a significant negative correlation between diastolic blood pressure and post load insulin concentration was observed. The left ventricle systolic end-volume was positively and significantly correlated with insulin and HOMAIR in insulin-resistant subjects, but not in controls. Conclusions: Insulin levels may play role in modulating plasma NE levels, particularly in insulin-resistant subjects. The increased sympathetic activity in these subjects might lead to an abnormality in the left ventricle systolic end-volume and cardiac index, which might be the earlier adaptative haemodynamic changes due to cardiac post-load.