Myocardial gene expression alterations in peripheral blood mononuclear cells of patients with idiopathic dilated cardiomyopathy.

AIMS: To assess cardiac gene expression in peripheral blood cells of patients with idiopathic dilated cardiomyopathy (IDCM) and its relationship to echocardiographic left ventricular (LV) function. METHODS AND RESULTS: A complete echocardiographic study and blood sampling were performed in 65 consecutive stable IDCM patients with LV ejection fraction (LVEF) 31.76 +/- 10.07% and chronic mild to moderate heart failure (NYHA functional class II to III) for > or =9 months. Blood samples from 19 healthy individuals were included for comparison. Transcript levels of myocardin, GATA4, alpha- and beta-myosin heavy chain (MHC), sarcoplasmic reticulum calcium ATPase 2 (SERCA2), and phospholamban were determined by quantitative real-time reverse transcription-polymerase chain reaction. Myocardin (24.88 +/- 4.93 vs. 3.98 +/- 1.12, P = 0.0048) and GATA4 (17.85 +/- 4.85 vs. 0.45 +/- 0.15, P = 0.0069 x 10(-5)) were upregulated in IDCM patients compared with controls, whereas SERCA2 (5.11 +/- 0.42 vs. 8.93 +/- 1.07, P = 0.001) was downregulated. In IDCM patients, myocardin (r = 0.279, P = 0.025), GATA4 (r = 0.314, P = 0.011), beta-MHC (r = 0.444, P=0.0002), and alpha-MHC (r = 0.272, P = 0.034) showed positive correlations, whereas SERCA2 (r = -0.264, P = 0.034) exhibited a negative correlation with LVEF. Patients with elevated LV filling pressures had lower myocardin (15.06 +/- 3.10 vs. 43.12 +/- 12.03, P = 0.048), GATA4 (8.96 +/- 2.17 vs. 34.38 +/- 12.60, P = 0.026), beta-MHC (10.59 +/- 4.05 vs. 16.43 +/- 4.91, P = 0.013), and alpha-MHC (0.27 +/- 0.08 vs. 0.79 +/- 0.20, P = 0.033) and higher SERCA2 (5.65 +/- 0.54 vs. 3.90 +/- 0.61, P = 0.037) levels. Patients with atrial fibrillation (AF) had higher SERCA2 levels compared with sinus rhythm patients (6.75 +/- 0.84 vs. 4.54 +/- 0.45, P = 0.017). CONCLUSION: Our data indicate that cardiac gene expression alterations in peripheral blood cells of IDCM patients may reflect alterations in LV function, whereas the presence of AF may be associated with increased SERCA2 levels in these patients.

Noncompaction myocardium imaging with multiple echocardiographic modalities.

Noncompaction myocardium of the left ventricle (LV) is a genetically heterogeneous congenital cardiomyopathy, that has only been described during the last two decades. Echocardiography plays a pivotal role as a first line diagnostic tool of this rare abnormality. The present case describes the imaging of the noncompacted myocardium using varying echocardiographic modalities.

NT-proBNP response to dobutamine stress echocardiography predicts left ventricular contractile reserve in dilated cardiomyopathy.

BACKGROUND: Brain natriuretic peptide (BNP) and left ventricular (LV) inotropic reserve are major prognostic indexes in heart failure (HF). AIMS: To investigate the relationship between N-terminal-proBNP (NT-proBNP) changes in response to dobutamine stress echocardiography (DSE) and the LV inotropic reserve, in HF patients with dilated cardiomyopathy (DC). METHODS: We studied 41 patients with DC, LVEF 31.6+/-7.7%, NYHA class II-III and 15 controls. Plasma NT-proBNP levels were measured before and 60 min after three 5-min stages of dobutamine (5 to 15 microg/kg/min). RESULTS: Based on NT-proBNP changes in response to dobutamine, patients were categorized into two groups: In Group A circulating NT-proBNP levels fell (-16.6+/-7.8%), and in Group B they increased (8.4+/-9.1%). Group A had a marked improvement in WMSI compared to Group B (32.1+/-9.7% vs. 18.8+/-15.9%, p<0.001). Multivariate analysis showed that NT-proBNP changes were an independent predictor of LV inotropic reserve (b= -0.55, p<0.001). A reduction of 21.3% in plasma NT-proBNP levels in response to dobutamine predicted an improvement in WMSI of >25% with a sensitivity of 100% and a specificity of 92.3%. CONCLUSIONS: NT-proBNP changes in response to dobutamine reflect improvement in LV contractility and constitute an independent predictor of LV inotropic reserve in patients with DC.