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NT-proBNP correlated with strain and strain rate imaging of the right ventricle before and after transcatheter closure of atrial septal defects.

BACKGROUND: Atrial septal defects (ASD) account for 10% of all congenital heart lesions and represent the third most congenital cardiac defect seen in adults.

OBJECTIVES: Using strain and strain rate imaging (SRI) to assess right ventricular (RV) function in patients with ASD and correlate the results with the level of N-terminal pro-brain natriuretic peptide (NT-proBNP) before and after transcatheter closure.

METHODS: At the Hungarian Institute of Cardiology, 27 females and 18 males (mean age 21.53 years) were diagnosed with ASD and admitted for percutaneous closure. Echocardiography was done to assess theleft ventricular (LV), RV and left atrial (LA) diameters. For assessment of systolic RV function, we measured Tricuspid annular plane systolic excursion (TAPSE), strain, and SRI. Amplatzer ASD closure was done under general anesthesia. NT-proBNP levels were measured before and three months after closure.

RESULTS: ASD closure was achieved in all patients. The mean ASD diameter was 15.15 mm. The size of the occluder ranged from 10 to 24 mm. The mean LA diameter in the pre-closure group was significantly higher than the control; mean left ventricular end diastolic diameter (LVEDD) showed a non-significant difference from either the control group or the post-closure group, while the mean right ventricular end diastolic diameter (RVEDD) markedly reduced post-closure, and it was significantly higher than the control group. Global RV strain and peak systolic strain rate (PSSR) were significantly higher in ASD group than in the control. The NT-proBNP levels were found to be correlated with pulmonary arterial pressure (PAP), TAPSE, global RV strain and PSSR.

CONCLUSION: Volume overload induced by ASD is associated with increased strain values, which return to normal after closure. NT-proBNP is a parameter which correlates to RV pressure, PAP and the amount of shunt volume caused by an ASD.

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