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      Systolic time intervals combined with Valsalva maneuver for the diagnosis of left ventricular dysfunction in COPD exacerbations

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          Abstract

          Background

          The goal of this study was to determine the value of systolic time intervals and their change during Valsalva maneuver (VM) in the diagnosis of left ventricular dysfunction (LVD) in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

          Methods

          We included 166 patients admitted to the emergency department for AECOPD. Measurement of systolic time intervals included electromechanical activation time (EMAT), left ventricular ejection time (LVET), and EMAT/LVET ratio. These were performed at baseline and during the first strain phase of the VM using a computerized phonoelectrocardiographic method. The diagnosis of LVD was determined on the basis of clinical examination, echocardiography, and brain natriuretic peptide. The values of systolic time intervals were compared between patients with and without LVD; their diagnostic performance was assessed using the area under receiver operating characteristic (ROC) curve.

          Results

          Patients with LVD (n=95) had a significantly higher EMAT and lower LVET and EMAT/LVET ratio compared to patients without LVD (n=71); the area under ROC curve was 0.79, 0.88, and 0.90, respectively, for EMAT, LVET, and EMAT/LVET ratio. All baseline systolic time intervals changed significantly during VM in patients without LVD but they did not change in patients with LVD. The area under ROC curve increased to 0.84 and 0.93, respectively, for EMAT and EMAT/LVET ratio but did not change for LVET.

          Conclusion

          Simple and noninvasive measurements of systolic time intervals combined with VM could be helpful to detect or rule out LVD in patients admitted to the emergency room for COPD excacerbation. The EMAT/LVET ratio seems to have the best diagnostic value.

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          Most cited references 26

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          Does this dyspneic patient in the emergency department have congestive heart failure?

          Dyspnea is a common complaint in the emergency department where physicians must accurately make a rapid diagnosis. To assess the usefulness of history, symptoms, and signs along with routine diagnostic studies (chest radiograph, electrocardiogram, and serum B-type natriuretic peptide [BNP]) that differentiate heart failure from other causes of dyspnea in the emergency department. We searched MEDLINE (1966-July 2005) and the reference lists from retrieved articles, previous reviews, and physical examination textbooks. We retained 22 studies of various findings for diagnosing heart failure in adult patients presenting with dyspnea to the emergency department. Two authors independently abstracted data (sensitivity, specificity, and likelihood ratios [LRs]) and assessed methodological quality. Many features increased the probability of heart failure, with the best feature for each category being the presence of (1) past history of heart failure (positive LR = 5.8; 95% confidence interval [CI], 4.1-8.0); (2) the symptom of paroxysmal nocturnal dyspnea (positive LR = 2.6; 95% CI, 1.5-4.5); (3) the sign of the third heart sound (S(3)) gallop (positive LR = 11; 95% CI, 4.9-25.0); (4) the chest radiograph showing pulmonary venous congestion (positive LR = 12.0; 95% CI, 6.8-21.0); and (5) electrocardiogram showing atrial fibrillation (positive LR = 3.8; 95% CI, 1.7-8.8). The features that best decreased the probability of heart failure were the absence of (1) past history of heart failure (negative LR = 0.45; 95% CI, 0.38-0.53); (2) the symptom of dyspnea on exertion (negative LR = 0.48; 95% CI, 0.35-0.67); (3) rales (negative LR = 0.51; 95% CI, 0.37-0.70); (4) the chest radiograph showing cardiomegaly (negative LR = 0.33; 95% CI, 0.23-0.48); and (5) any electrocardiogram abnormality (negative LR = 0.64; 95% CI, 0.47-0.88). A low serum BNP proved to be the most useful test (serum B-type natriuretic peptide <100 pg/mL; negative LR = 0.11; 95% CI, 0.07-0.16). For dyspneic adult emergency department patients, a directed history, physical examination, chest radiograph, and electrocardiography should be performed. If the suspicion of heart failure remains, obtaining a serum BNP level may be helpful, especially for excluding heart failure.
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            Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension.

            This study sought to investigate the influence of right ventricular (RV) hemodynamic variables and function on the secretion of brain natriuretic peptide (BNP) in patients with isolated RV overload. Plasma BNP is known to increase in proportion to the degree of left ventricular (LV) overload. However, whether BNP secretion is also regulated in the presence of RV overload remains unknown. Plasma BNP and atrial natriuretic peptide (ANP) levels in the pulmonary artery were measured in 44 patients with RV overload: 18 with RV volume overload (RVVO) due to atrial septal defect and 26 with RV pressure overload (RVPO) due to primary or thromboembolic pulmonary hypertension. Right heart catheterization was performed in all patients. RV and LV ejection fraction, myocardial mass and volume of the four chambers were determined by using electron beam computed tomography. Although both plasma BNP and ANP levels were significantly elevated in patients with RV overload compared with values in control subjects, plasma BNP and the BNP/ANP ratio were significantly higher in patients with RVPO than with RVVO (BNP 294 +/- 72 vs. 48 +/- 14 pg/ml; BNP/ANP 1.6 +/- 0.2 vs. 0.8 +/- 0.2, both p < 0.05). Plasma BNP correlated positively with mean pulmonary artery pressure (r = 0.73), total pulmonary resistance (r = 0.79), mean right atrial pressure (r = 0.79), RV end-diastolic pressure (r = 0.76) and RV myocardial mass (r = 0.71); it correlated negatively with cardiac output (r = -0.33) and RV ejection fraction (r = -0.71). Plasma BNP significantly decreased from 315 +/- 120 to 144 +/- 54 pg/ml with long-term vasodilator therapy (total pulmonary resistance decreased from 23 +/- 4 to 15 +/- 3 Wood U). Plasma BNP increases in proportion to the extent of RV dysfunction in pulmonary hypertension.
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              Global Strategy for Diagnosis, Management and Prevention of COPD

              (2015)
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2016
                15 September 2016
                : 11
                : 2237-2243
                Affiliations
                [1 ]Department of Emergency, Fattouma Bourguiba University Hospital
                [2 ]Research Laboratory (LR12SP18), University of Monastir
                [3 ]Department of Cardiology
                [4 ]Department of Biochemistry, Fattouma Bourguiba University Hospital, Monastir
                [5 ]Department of Emergency, Sahloul University Hospital, Sousse
                [6 ]Department of Emergency, Tahar Sfar University Hospital, Mahdia, Tunisia
                Author notes
                Correspondence: Semir Nouira, Department of Emergency, Fattouma Bourguiba University Hospital, University of Monastir, Monastir 5000, Tunisia, Tel +216 3 9867 7343, Fax +216 3 7346 0678, Email semir.nouira@ 123456rns.tn
                Article
                copd-11-2237
                10.2147/COPD.S96280
                5029838
                © 2016 Boubaker et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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