DUS has the potential to be used as a diagnostic modality for thoracic aortic pathology, and may have a role in surveillance for some patients for whom CT scanning is contraindicated. Further validation and refinements to this technique are required. However, this study provides proof of concept.
Introduction
Brain natriuretic peptide (BNP) is a well-established marker for heart failure in the general population however limited data are available on the value of BNP as a diagnostic and prognostic marker in adults with congenital heart disease (ACHD). The purpose of our study is to evaluate the relation between BNP levels and biventricular systolic and diastolic function in patients with ACHD.
Methods
We evaluated clinically stable ACHD patients who underwent echocardiography from May 2015 until January 2018. We studied the correlation of BNP with the degree of systolic and diastolic dysfunction of the left ventricle. Moreover we also investigate the relation of BNP with the right tricuspid annular plane systolic excursion (TAPSE), the fractional area change (FAC) and the pulmonary arterial systolic pressure (PASP).
Results
In total, 385 patients were included in our study (median age, 43 ±12 years; 61% male). Of the 385 patients, 193 (50%) had tetralogy of Fallot, 94 (24%) had systemic RV, including patients with transposition of the great arteries (TGA) after atrial switch operation (Mustard or Senning) and congenitally corrected TGA -ccTGA , 43 (11%) had univentricular hearts and Fontan physiology, 55 (14%) had other lesions. BNP levels were 66 ± 26 pg/mL and 93, ±31pg/mL, for patients with EF > 50% and 50%> EF >35% respectively (p = 0.003). BNP levels correlate with parameters reflecting LV filling pressure, including transmitral early diastolic velocity (E) 81 ± 29pg/mL and its ratio to early diastolic annular myocardial tissue velocity (E/Ea) 77 ± 17pg/mL. (r=-0.607, p = 0.003 r=-0.598, p = 0.005, respectively) BNP levels were also significantly higher in patients with impaired tricuspid annular plane systolic excursion 87 ± 21 pg/mL (TAPSE < 14mm; p = 0.002) and decreased RV FAC 81 ± 18 pg/mL (FAC <35% P= 0.004) and in patients with PASP≥35 mmHg (p = 0.003). The ROC curve and logistic regression analysis spotted the role of BNP in identifying systolic and diastolic dysfunction patterns in ACHD patients. Conclusion: In clinical stable ACHD patiens BNP levels correlate well with LV systolic dysfunction as well as with impaired diastolic function. Furthermore patients with impaired RV function and increased PASP have raised BNP levels. Therefore monitoring BNP levels plays an important role in management of clinical stable ACHD patients
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