الفهرس 
AbstractOnly 14 pages are availabe for public view
 |  | from | 180 |  |  |
| | | from | 180 | | |
Abstract
B-type natriuretic peptide (BNP), a 32–amino-acid polypeptide, is released predominately by the left and right cardiac ventricles and regulates a wide array of physiologic effects including natriuresis, diuresis, and vasodilatation. The main stimulus for the secretion of BNP is cardiac stress reflected by myocardial stretch and pressure or volume overload (Mueller et al, 2007). Additionally, BNP levels are significantly elevated in pulmonary arterial hypertension (PAH) and seem to correlate strongly with hemodynamic changes, functional impairment, and cardiac stress in PAH (Ishii et al, 2000; Leuchte et al, 2004). It is especially increased in proportion to the degree of right ventricular (RV) dysfunction (Yap et al, 2004; Kanat et al, 2007). Pro-inflammatory cytokines, the activation of the sympathetic nervous system, and hypoxia have also been identified as additional triggers inducing BNP secretion (Silver, 2006).
Since high plasma concentration of BNP is associated with increased strain on the ventricles, patients with COPD who have elevated plasma BNP levels should have some degree of RV strain, contributing to the raised BNP levels even in the absence of clinical findings of RV dysfunction. Therefore, patients suffering an acute attack of COPD with high plasma levels of BNP might benefit from mild diuretics to decrease the volumetric strain on the right ventricle.
Based on this, we planned this study that aims to evaluate the effect of mild diuretic treatment on the plasma BNP level in patients with an acute exacerbation of COPD without clinical findings of cor pulmonale and have high concentrations of BNP.
In the present study, Plasma BNP level was elevated in all studied 41 males COPD patients (31with acute exacerbation -group I- and 10 in stable states -group II). For AECOPD patients (group I) Measurement of plasma BNP level was done twice one measurement on the day of admission and the other on 8th day of treatment. All patients in group I received the standard treatment for acute COPD exacerbation but mild diuretic treatment (20 mg frusemide) in addition to the standard acute attack treatment was randomized to 16 patients only of group I who were categorized as (group IA) and the remaining 15 patients in group I were categorized as (group IB). For all studied patients (41 patients) full assessments were done including; history taking, physical examination, pulmonary functions test, echocardiography and plasma BNP measuring.
The fall in plasma BNP concentration post treatment was evident in both group of AECOPD patients; the group who received diuretics and conventional treatment (group I A) and the group received conventional treatment only (group I B) but the fall of BNP level was more sticking in group who received diuretics as add on therapy.
Statistically significant correlation between sPAP (systolic pulmonary artery pressure) and plasma brain natriuretic peptide levels was observed, and also between blood BNP levels and right ventricular end diastolic diameter (RVEDD).
Limitations of the study
The study was conducted on limited number of patients with AECOPD.
Evaluation of patients for pulmonary hypertension by echocardiography which has limited accuracy than right heart catheterization.
Follow up Echocardiography for evaluation of RVEDD and pulmonary artery pressure not done.