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https://dspace.inc.saude.gov.br/handle/123456789/21

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Navegando Produção Docente por Autor "Albanesi Filho, Francisco M."

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    Impact of Carvedilol on QT Interval Dispersion in Patients with Chronic Heart Failure
    (Journal of Cardiac Failure, 2003) Albuquerque, Denilson C.; Paola, Angelo A.V. de; Rocha, Ricardo M.; Tura, Bernardo; Albanesi Filho, Francisco M.; Veloso, Henrique H.
    Background: The role of QT interval dispersion (QTD) in heart failure (HF) remains poorly defined and controversial. Our objective was to evaluate the impact of QTD in the clinical evolution of chronic HF patients under control due to the use of carvedilol (CVD). Methods: We selected 108 patients (22-82 years), 65.7% were male, 72.2% caucasians, with stable chronic HF and NYHA functional class (FC) II, III and IV on optimized treatment, with an left ventricle ejection fraction (LVEF) of 0.40 for therapy with CVD. All patients had complete history taken and physical exam performed, as well as, laboratorial evaluation, electrocardiogram, echocardiogram and followed-up at the HF clinic for an average period of 38.2 months. All used CVD at the maximum tolerated dose. The evaluated parameters were: general characteristics of the population, cardiopathy etiology, concomitant medication used, NYHA’s FC, maximum CVD dose, LVEF and QTD before and 6 months after CVD and deaths. Results: A QTD reduction (109ms to 72ms) and an increase in the LVEF (0.27 to 0.35) was found after 6 months of therapy with CVD (p 0.001). The general characteristics of the population (p 0.05), concomitant medications (p 0.05), CVD dose (p 0.80), cardiopathy etiology (p 0.959) did not influence in the QTD reduction. This reduction was related to the patients with worse NYHA FC pre-CVD (p 0.007) and with NYHA FC improvement (p 0.028). The ROC curve analysis post-CVD determined that QTD 90ms was a mortality predictor (p 0.034; OR 3.912) (AUC 0.061; sensibility 29.2%; specificity 90.5%; positive likelihood ratio 3.06; negative likelihood ratio 0.78). The multivariate analysis showed that the QTD reduction was an independent survival predictor (p 0.004; OR 5.48). Conclusions: CVD reduced the QTD and increased the LVEF in patients with chronic HF. We did not observe interaction among QTD reduction and population characteristics. The QTD reduction was not influenced by concomitant medications, cardiopathy etiology and CVD dose. The largest QTD reduction occurred specially in worst patients (NYHA FC III and IV). The presence of QTD reduction was an independent predictor of survival and the QTD 90ms post-CVD was predictor of mortality.