Peptídeo natriurético do tipo B e índices de deformação miocárdica (strain/strain rate) na doença pulmonar obstrutiva crônica estável e exacerbada

Abstract

Background: There is little information in the literature about possible cardiovascular hemodynamic alterations during acute exacerbations of chronic obstructive pulmonary disease (COPD). The identification of biochemical, neurohormonal or echocardiographic markers would be important for early diagnosis and even for prognosis. Objectives: The aim of the present study was to evaluate the behavior of B-type natriuretic peptide (BNP) and conventional echocardiography, Tissue Doppler and strain/ strain rate (/ SR) Imaging during COPD stable periods and acute exacerbations. Methods: Thirty stable COPD patients, with GOLD criteria stage II without any known cardiovascular disease underwent clinical, spirometric, radiological, eletrocardiographic, echocardiographic (including strain rate and strain) evaluations, along with plasma BNP measurement. Of these patients, twelve also underwent clinical, echocardiographic evaluation and BNP measurement during an acute exacerbation period. Seven patients without cardiac or pulmonary disease participated as controls. Results: Thirty stable COPD patients - 68 ±7 years old (20 men), with forced expiratory volume in one second (FEV1, percent of predicted) of 44±16%, average BNP level of 17.5±12.9 pg/mL and PsAP of 37.2±8.6 mm Hg - were studied. During stable periods, PsAP significantly correlated with oxygen saturation (r=-0.61/ p=0.00), FEV1 % predicted (r=-0.57/ p=0.01), Tei index (r=0.67/ p=0.00), the relation between early and late diastolic velocities (Em/Am) in basal segment (r=-0.49/ p=0.02), systolic and early diastolic in medium segment (r= 0.46/ p= 0.03 and r=-0.42/ p=0.05, respectively). BNP levels were loosely correlated with peak systolic velocities (Sm) (r=0.38/ p=0.04) and Em (r=0.38/ p=0.04) in the same segment. Only the Tei index was adjusted to the multivariate linear regression model: Tei= 1.602 0.012 x Sat.O2 (%) 0.00012 x FEV1 (mL), (p= 0.05 e 0.03, respectively; r2=0.44). Twelve patients were also studied during exacerbation. BNP levels (32.2±16.8 x 15.9±12.3 pg/mL, p=0.00) and PASP (47±6 x 37±7 mm Hg, p=0.00) were significantly higher and SatO2 (88±7 x 91±5 %, p=0.01) was significantly lower in exacerbated than in stable COPD patients, although there was no correlation between BNP and PsAP. There was a systolic SR reduction in all RV free wall segments (apical:-1.67±0.39 x -1.38±0.32; medium:-1.75±0.34 x - 1.47±0.22; basal:-1.55±0.23 x -1.31±0.19 s-1; p<0.05) and a systolic strain reduction in medium (-26.18±5.45 x -20.84±5.01%; p=0.02) and apical (-21.91± 5.06 x -17.06± 4.05%; p<0.02) segments; there was no significant variation in the Tei index between stable and exacerbated patients. Conclusions: During COPD acute exacerbations episodes, hemodynamic and neurohormonal alterations occur, characterized by elevations of PsAP and BNP serum levels. The best correlations with PsAP and BNP were between the systolic , SR and peak velocity Sm, mainly on the medium RV free wall segment. These indexes were the most robust markers of RV dysfunction, during exacerbation. During stable periods, ventilation and gas exchange lung function determinated 44% of the Tei index variation. The Tei index, however, did not identify the acute exacerbation.