Asthma Before 7after TTT Speckle Tracking

Pediatric Allergy, Immunology, and Pulmonology
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Pediatric Allergy, Immunology, and Pulmonology: http://mc.manuscriptcentral.com/pediatricasthma
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The Effect of Childhood Asthma Treatment on Left and Right

Ventricular Mechanical Functions
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Journal: Pediatric Allergy, Immunology, and Pulmonology
Manuscript ID: PED-2015-0498

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Manuscript Type: Original Research
Keyword: Asthma, Corticosteroids, Children, Bronchodilators

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Mary Ann Liebert, Inc., 140 Huguenot Street, New Rochelle, NY 10801
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Page 1 of 22 Pediatric Allergy, Immunology, and Pulmonology
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3 The Effect of Childhood Asthma Treatment on Left and Right Ventricular Mechanical
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Abstract:
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12 Background: It is well known that the presence of bronchial asthma (BA) is a cause of
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14 subclinical right and left ventricular dysfunction which is detected by tissue Doppler in
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16 pediatric population. In this study, we aimed to evaluate the possible changes in left and
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19 right ventricular mechanical functions after management of BA using speckle tracking
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21 echocardiography (STE).
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Methods: The study population consisted of 18 children with BA. These patients underwent
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27 transthoracic STE before treatment and STE was repeated 3 months after treatment. LV
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29 longitudinal strain / strain rate and RV longitudinal strain / strain rate (from apical 4, 3 and 2
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31 chambers view) were obtained using STE. Left and right atrial reservoir strain and strain rate
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34 were also recorded. Paired t test or Wilcoxon tests were used for statistical analysis.
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37 Results: A total of 18 patients with BA were enrolled in the study (mean age 11.6 + 2.0 years,
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39 range from 9-15, 50% male) Analysis of pre and post-treatment STE parameters revealed no
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42 change in left ventricular and left atrial functions. A significant increase was observed in right
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44 ventricular systolic strain, diastolic strain and systolic strain rate. RV-GLS-S(-21.6 ± 4.3 and
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46 24.1 ±-4.7, p = 0.025); RV-GLS-D (-17.5 ± 5.3 and -20.2 ± 4.3 p = 0.045); RV-SR-S (-1.39 ± 0.5
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49 and -1.08 ± 0.2, p = 0.038). Additionally, post-treatment right atrial peak longitudinal strain
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51 and strain rate values showed a significant increase compared to pre-treatment values. RA-
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PALS (35.9 ± 12.4 and 43.8 ± 13.9 p=0.044, RA-SR-L( -1.5 ± 0.4 and -1.9 ± 0.6 p=0.043).
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56 Conclusions: Mechanical functions of the right ventricle and right atrium were observed to
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58 increase in bronchial asthma patients receiving treatment while no significant change was
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Pediatric Allergy, Immunology, and Pulmonology Page 2 of 22
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3 detected in the left ventricle and left atrial mechanical functions. This may reflect a positive
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5 effect of bronchial asthma management on the right heart functions.
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12 Introduction
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15 Bronchial asthma (BA) is a chronic inflammatory disorder of the airways. The attacks, due to
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17 bronchial hyper responsiveness associated with the chronic airway inflammation, are
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accompanied by a variable degree of airway obstruction1. The narrowing of the airways
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22 results from the contraction of the bronchial smooth muscle, mucus hypersecretion,
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24 mucosal edema, cellular infiltration, and epithelial desquamation2. Chronic inflammation
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27 and recurrent hypoxemia lead to pulmonary hypertension, resulting in right ventricular
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29 hypertrophy and right ventricular dilatation. It is well known that severely asthmatic patients
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31 are likely to develop cor pulmonale at an advanced age; however, the effect on the right and
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34 left cardiac functions in the early period for these patients is less known.
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37 In pediatric population, BA is known to cause subclinical right and left ventricular
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39 dysfunction, which is detected by tissue Doppler echocardiography3. The available
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42 conventional echocardiographic assessments may be insufficient to evaluate the global

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44 ventricular functions even in patients with symptoms of cardiac failure. The newly developed
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46 echocardiographic imaging techniques allow for the quantitative assessment of the right and
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49 left ventricles 4,5. The speckle tracking imaging method, which is among these novel imaging
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51 techniques, is relatively a non-operator-dependent method, independent of the angle for
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assessing the local and global wall movements, and is more sensitive in detecting the
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56 subclinical right and left ventricular dysfunctions of the heart 6.
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3 The present study evaluated how the right and left ventricular mechanical functions changed
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5 after the treatment in BA patients from the pediatric population by using the speckle
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8 tracking method.
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11 Methods and Materials:
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14 The study included 38 patients diagnosed with BA. However, six patients did not present for
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16 the post-treatment (after three months) control echocardiography. 14 patients (11 patients
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19 who were receiving intermittent B2 agonists and three patients who had to receive
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21 continuous B2 agonists) were excluded. Therefore, the study included 18 children with BA,
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who were diagnosed with BA by symptoms, physical examination, family history, and
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26 respiratory function tests, and who did not previously receive any treatment. The patients
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28 were treated with a B2 agonist (Salbutamol) for five days, montelukast for one month and an
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31 inhaled steroid (Budesonide) or fluticasone furoate for three months. For the BA-diagnosed
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patients, the right-left ventricles and the right-left atria were evaluated by two cardiologists
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35 in the left lateral position using conventional transthoracic echocardiography and 2D speckle
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38 tracking echocardiography prior to the treatment. The echocardiographic assessments were

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40 repeated by the same operators at the post-treatment third month. The pre-treatment and
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42 post-treatment parameters were compared with each other. All participants gave an
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45 informed consent and the study protocol was approved by the local ethics committee.
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48 Transthoracic Echocardiography
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51 Conventional echocardiography was performed using commercially available equipment
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(Vivid-7, 3.5 MHz transducer; GE Vingmed, Milwaukee, WI). Scanning was performed by two
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56 experienced operators, with the patient in the left lateral position. Complete two-
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58 dimensional and Doppler assessment was performed per the recommendations of the
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3 American Society of Echocardiography7,8. Basic measurements included LV wall thickness,
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5 measured from the parasternal long-axis view. LVEF were calculated from the apical four-
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8 chamber and two-chamber views using Simpson’s biplane method. For the tricuspid annular
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10 point systolic excursion (TAPSE) by M-mode in the apical four-chamber assessment, the M-
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mode cursor was placed through the lateral tricuspid annulus. Based on the images
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15 obtained, the distance between the lateral tricuspid annulus at the apex to the atrium and at
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17 the descent to the ventricle was obtained. Mitral annular plane systolic excursion (MAPSE)
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was assessed at the lateral mitral annulus using the same method.
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23 Pulsed-wave Doppler of mitral as well as tricuspid inflow velocities, including early (E) and
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25 atrial (A) waves, were measured. Tissue Doppler imaging (TDI) measures of myocardial
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27 systolic, early diastolic and atrial velocities were assessed at the mitral annulus level and on
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30 the lateral tricuspid annulus wall. The isovolumic relaxation time for the LV and RV were also
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32 derived from TDI measurements. RV end-diastolic diameter at basal level were assessed in
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the apical four chamber view.
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41 Strain Echocardiography
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44 Left ventricular and right ventricular Strain Echocardiography
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47 STE was performed on standard two-dimensional grayscale images of the left ventricle,
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obtained from the apical two-chamber, three chamber, and four-chamber. The images were
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52 obtained during an end-expiratory breath-hold at a frame rate of 60 to 80 frames/sec. All
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54 images were transferred to a workstation for further offline analysis( EchoPac, GE, USA). For
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each view, the LV endocardial border was manually traced in the end-systolic frame. The
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3 software then automatically divided the left ventricle into six equal segments and generated
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5 myocardial strain curves by frame-by-frame tracking of the natural acoustic markers
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8 throughout the cardiac cycle. Longitudinal strains (systolic and diastolic) were derived from
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10 the apical two-chamber, three-chamber, and four-chamber views. For all strain parameters,
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peak systolic strain was measured for each of the myocardial segments and averaged to
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15 derive global values (global longitudinal strain) [GLS] which were used for the analysis.
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RV free wall longitudinal myocardial function was assessed from 2-D harmonic grey scale
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20 images in the apical 4-chamber view. The imaging sector was narrowed to optimal view and
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23 the frame rate was kept higher than 60 Hz in each case. Longitudinal strains and strain rates
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25 were measured at the basal, mid and apical segments of the free wall and averaged to give
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27 global strain (GLS) and strain rates. Diastolic strain rate was obtained from the peak value
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30 observed during the early filling period. To adjust all vector velocity imaging data for
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32 intersubject differences in heart rate, a specific toolbox was used to normalize time
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sequence as a percentage of systolic duration calculated from the timing of pulmonary valve
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37 closure.Strain rates were obtained by automatic program for each view.
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40 Left and right atrial Strain Echocardiography
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43 For speckle tracking analysis, apical four- and two-chamber views images were obtained
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using conventional two dimensional gray scale echocardiography, during breath hold and
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48 with a stable ECG recording. Care was taken to obtain true apical images using standard
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50 anatomic landmarks in each view and not foreshorten the left atrium/right atrium, allowing
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53 a more reliable delineation of the atrial endocardial border. Three consecutive heart cycles
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3 independent echocardiographer, who was not directly involved in the image acquisition and
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5 had no knowledge of hemodynamic mesasurements, using a commercially available semi-
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8 automated two-dimensional strain software (EchoPac, GE, USA) as previously described (9).
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10 LA/RA endocardial border is manually traced in both four- and two-chamber views, thus
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delineating a region of interest (ROI), composed by 6 segments. Then, after the segmental
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15 tracking quality analysis and the eventual manual adjustment of the ROI, the longitudinal
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17 strain curves are generated by the software for each atrial segment. Peak atrial longitudinal
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strain (PALS), measured at the end of the reservoir phase, was calculated by averaging
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22 values observed in all LA/RA segments (global PALS), and by separately averaging values
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observed in 4- and 2-chamber views (4- and 2-chamber average PALS, respectively). PALS
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27 was calculated by averaging values measured in the remaining segments.
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30 All measurements were taken from the onset of QRS complex, as previously described for
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32 left and right atria 9,16,17. RA peak atrial longitudinal strain (PALS) was calculated by averaging
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values observed in all RA segments. RA PALS was used to estimate RA reservoir function. The
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37 time to peak longitudinal strain (TPLS) was also measured as the average of all 12 segments
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39 (global TPLS) and by separately averaging values observed in the two apical views (4- and 2-
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chamber average TPLS). In patients in whom some segments were excluded because of the
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44 impossibility of achieving adequate tracking, PALS and TPLS were calculated by averaging
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46 values measured in the remaining segments. RA strain rate was also measured by
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49 quantifying RA endocardial velocities of contraction and relaxation and local deformation.
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55 Statistical Analysis:
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3 Continuous variables were expressed as mean+sd. Categorical variables were expressed as
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5 percentages. An analysis of normality of the continuous variables was performed with the
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8 Kolmogorov–Smirnov test. Comparison of parametric values between before and after
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10 treatment were performed by means of paired test. Comparisons of nonparametric values
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between the 2 groups were performed by wilcoxon test. Two tailed P values <0.05 were
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20 Results:
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The average age of the patients participating in the study was 11.6 + 2.0 (range from 9-15)
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26 and 50% of them were male. Baseline characteristics are shown in Table 1. No significant
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28 difference was observed between pre and post-treatment values of left ventricle EF, heart
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31 rate, LVEDV, LVESD, E, A, E / A, LAV max, LAV min, IVRT and MAPSE. Standard two-
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dimensional, Doppler and tissue Doppler echocardiographic parameters of left ventricle and
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35 left atrium are shown in Table 2. No significant difference was observed between pre and
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40 Tri-Em', Tri-Am' and TAPSE. Standard two-dimensional, Doppler and tissue Doppler
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42 echocardiographic parameters of right ventricle and right atrium are shown in Table 3. No
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LA-SR-S,LA-SR-E, LA-SR-A] strain and strain rate. Right and left ventricle ST and STR
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52 parameters are shown in Table 4. Post treatment right ventricular systolic strain, diastolic
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54 strain and systolic strain rate values showed a significant increase compared to the pre-
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treatment values. [RV-GLS-S (-21.6 ± 4.3 and-24.1 ± 4.7, p=0.025); RV-GLS-D(-17.5± 5.3 and -
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3 20.2±4.3 p=0.045) RV-SR-S (-1.39 ± 0.5and-1.08 ± 0.2 p=0.038) ]. Right atrial diastolic strain
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8 pre-treatment values. RA-LS-D [(17.8 ± 9.8 and 23.6 ± 10.5 p=0.045), RA-SR-E (-1.5 ± 0.4 and -
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10 1.9 ± 0.6 p=0.043) ; RA-SR-A (-1.5 ± 0.6 and -2.0 ± 0.3 p=0.037). Longitudinal strain and strain
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rate of the left - right atria during atrial contraction and atrial relaxation are shown in Table
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21 Discussion
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When the results from the present study were summarized, first, the right cardiac functions
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27 were affected in the asthmatic patients at the time of diagnosis. Second, the recovery of the
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29 cardiac functions after the patients were treated suggests that the cardiac exposure is
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31 reversible. Third, the early diagnosis and the early treatment of bronchial asthma will
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34 minimize the cardiac exposure and maybe delay the development of cor pulmonale. Finally,
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36 we should be aware that we treated the cardiac adverse effects while treating the bronchial
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asthma. As far as we know, the present study is the first to evaluate the right and left
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41 ventricular functions by 2D speckle tracking echocardiography in patients with bronchial
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43 asthma.
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46 BA is the most common cause of respiratory disorders and also the most important cause of
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49 mortality and morbidity in children10. The exposure to recurrent hypoxia due to BA leads to
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51 permanent pulmonary vasoconstriction and prolonged narrowing of the pulmonary vessels.
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As a consequence, pulmonary hypertension occurs, which causes RV hypertrophy and
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56 dilatation; this impaired cardiac pathology is known as cor pulmonale11. As normally
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58 expected, the right atrium and the right ventricle are affected by the respiratory changes
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3 much more extensively than on the left side; however, there are normally cyclic changes in
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5 the right cardiac functions during the inspiration and expiration, as well. Namely, the
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8 negative intrathoracic pressure is increased during inspiration and the positive intrathoracic
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10 pressure is increased during active expiration. The outweighing negative intrathoracic
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pressure contributes to the increased pulmonary pressure, and the increased venous return
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15 to the right ventricle contributes to the right ventricular dilatation12. Contrary to this
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17 pathology, which is known as cor pulmonale, there is relatively less information about how
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the right and left cardiac cavities are affected by this condition in the early stages of the
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22 disease or how these are changed after the treatment. The present study aimed to evaluate
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the pre- and post-treatment right and left cardiac functions by using the speckle tracking
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27 method, a new imaging method, in untreated BA patients, who were newly diagnosed.
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30 One study that evaluated left ventricular functions during an acute severe asthma attack,
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32 found that the transmitral peak A-wave increased and the E/A ratio decreased during the
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acute severe asthma attack, meaning that a left ventricular dysfunction developed13.
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37 Additionally, this study found the left ventricular diameters similar to the control group and
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39 the right ventricular hypertrophy ratio significantly higher than the control group. Melian et
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al. found that the right ventricular free wall thickness was higher in the BA patients
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44 compared to the healthy control group 12. The present study found no significant difference
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46 in pre- and post-treatment values for the right ventricular wall thicknesses and diameters.
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The left ventricular diastole includes four phases: isovolumetric relaxation (IVRT), rapid
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52 filling, slow filling (diastasis), and atrial contraction14. As is well known, the peak E/A ratio is
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54 the ventricular filling pattern 15. The present study found no significant change in pre- and
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post-treatment E/A ratio. This may have resulted from the short onset time of the disease
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3 and the short duration of the treatment. Furthermore, some studies established a strong
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5 correlation between the pulmonary artery pressure (PAP) and IVRT, and found significantly
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8 prolonged IVRT in patients with pulmonary hypertension . In fact, one of these studies
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10 predicted a systolic PAP ≥ 40 mmHg in the population with IVRT > 59 ms with a sensitivity of
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86% and a specificity of 89.5%. The present study did not find any significant changes in pre-
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15 and post-treatment IVRT. This may be because that the estimated pulmonary artery
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17 pressure could be measured from the tricuspid jet flow in only six of the patients included in
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the study. It may have been due to the fact that the IVRT is not sensitive enough to evaluate
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22 the subclinical RV.
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25 Zeybek et al. found significant differences their study in which they compared the tricuspid E
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27 flow velocity, the E/A ratio, and IVRT of a control group and the mild asthmatic patients and
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30 moderate to severe asthmatic patients 19. Another study, which was conducted using tissue
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32 Doppler, compared 60 BA patients with RV functions evaluated normal by conventional
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echocardiography and 60 healthy control subjects. In this study, the RV TDI assessment
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37 revealed a significant difference in the tricuspid lateral annulus peak E′ flow velocity, peak A′
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39 flow velocity, the E′/A′ ratio and IVRT compared to the control group and this was
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interpreted as subclinical RV dysfunction in the BA patients . The present study found no
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44 significant difference in pre- and post-treatment TDI assessment, whereas recovery was
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46 established upon treatment when assessed by speckle tracking, which is proof that this
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49 technique is more sensitive.
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52 In addition to impaired cardiac functions due to hypoxemia on its own, various etiologic
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54 factors may contribute to this, as well. In fact, Massoud et al. found evidence that chronic
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and permanent inflammation had an effect on myocardial functions in severe asthmatic
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3 patients. When the respiratory symptoms emerge, the inflammation mediators increase,
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5 along with inflammation; some of these mediators (such as tumor necrosis factor-alpha and
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8 IL-6) are known to have the potential to severely depress the cardiac contractility 21. Other
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10 than the mediators depressing such cardiac contractility, the chronic right ventricular
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hypertrophy and dilatation, which develops in case of pressure overload, may result in
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15 impaired coronary perfusion, and this may contribute to both systolic and diastolic
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20 In acute severe asthma, the cardiovascular functions change significantly as a direct effect of
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23 BA or secondary to the medication administered (especially B2-adrenergic receptor agonists)
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22,23
25 . Several studies found that the increased mortality and B2 agonists were correlated in
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27 BA patients, and furthermore found sudden cardiac death 24-26
and congestive heart failure
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30 associated with oral B2 agonists. In acute severe asthma, there may be ECG changes
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associated with myocardial ischemia due to the prolonged inhalation of fenoterol .
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Additionally, beclomethasone was shown to cause increased CK-MB in significant amounts,
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37 as not associated with ECG and patient’s symptoms when used alone or in combination with
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39 salmeterol 30. These studies suggested that B2 agonists and other medical treatments used
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to treat asthma are the cause of the cardiac dysfunction. In contrast to these studies, the
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44 present study found cardiac recovery after the treatment and found no adverse cardiac
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46 effects. This may be due to the positive cardiac effects of montelukast used in the treatment.
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49 As far as we know, the effects of montelukast on the right and left ventricular functions have
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51 not been investigated.
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54 The sensitivity of the conventional echocardiography to demonstrate the myocardial
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abnormalities is very low compared to the novel echocardiographic imaging methods.
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3 Speckle tracking analysis, which is among these novel techniques, is suggested to be more
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8 Additionally, such accurate measurements allow for both local and global (longitudinal,
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10 circumferential, and radial) assessment of the myocardial functions . Therefore, the
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present study used this novel echocardiographic imaging technique to assess both the right
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15 and the left cardiac functions. The results of the present study seem to support most of the
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17 previous cardiac imaging studies in this patient group. The present study found post-
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treatment recovery in the right cardiac functions; however, there were not any changes in
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22 the left cardiac functions. Under normal circumstances, the right ventricle has a thin wall,
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low pressure, and high compliance since it works against the lower pulmonary vascular
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27 resistance. Therefore, it may be said that the right ventricle is affected earlier than the left
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32 The study limitations may be listed as the low number of patients, the short duration of the
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treatment for the measurements (three months), and the absence of a control group. The
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37 main reason for not including a control group is that the presence of subclinical right
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39 ventricular dysfunction is already known in BA patients.
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42 In conclusion, when the bronchial asthmatic patients were evaluated before and
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45 after the treatment, the right cardiac functions recovered after the treatment, but there was
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47 no significant difference in the left cardiac functions. This may be due to the exposure of the
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right cardiac functions in the early stage of the disease, whereas the left cardiac functions
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52 are maintained during this period. Early diagnosis and optimal treatment contribute to the
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54 maintenance of the cardiac functions in bronchial asthmatic patients.
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57 References:
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3 1. Ioan I, Coutier L, Bonabel C, Albrecht J, Demoulin B, Marchal F, Schweitzer C, Varechova S.
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5 Airway obstruction, upper airway artifact and response to bronchodilator in asthmatic and
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8 healthy children. Pediatr Pulmonol. 2014 Nov 10. doi: 10.1002/ppul.23131. [Epub ahead of
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10 print]
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13 2. D'Alba I, Carloni I, Ferrante AL, Gesuita R, Palazzi ML, de Benedictis FM. Hyperventilation
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16 syndrome in adolescents with and without asthma. Pediatr Pulmonol. 2014 Dec 2. doi:
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10.1002/ppul.23145. [Epub ahead of print]
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21 3. Hirono O1, Kubota I, Minamihaba O, Fatema K, Kato S, Nakamura H, Tomoike H. Left
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ventricular diastolic dysfunction in patients with bronchial asthma with long-term oral beta2-
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26 adrenoceptor agonists. Am Heart J. 2001 ;142: 11.
27
28
LY
29 4. Becker M, Bilke E, Kühl H, Katoh M, Kramann R, Franke A, Bücker A, Hanrath P, Hoffmann

30
31 R. Analysis of myocardial deformation based on pixel tracking in 2D echocardiographic
32
;N
33
34 images allows quantitative assessment of regional left ventricular function. Heart 2006; 92:
35
36 1102-1108.
37
ot
38
39 5. Torrent-Guasp F, Kocica MJ, Corno AF, Komeda M, Carreras-Costa F, Flotats A, Cosin-
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41
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42 Aguillar J, Wen H. Towards new understanding of the heart structure and function. Eur J
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44 Cardiothorac Surg 2005; 27: 191-201.
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46
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47 6. Ng AC, Tran da T, Newman M, Allman C, Vidaic J, Kadappu KK, Boyd A, Thomas L, Leung
48
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DY. Comparison of myocardial tissue velocities measured by two-dimensional speckle
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52 tracking and tissue Doppler imaging. Am J Cardiol. 2008; 102: 784-789
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54
55 7. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, et al.
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ut
57 Recommendations for chamber quantification: a report from the American Society of

58
59
io
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14
1
2
rP
3 Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification
4
5 Writing Group, developed in conjunction with the European Association of
6
ee
7
8 Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr
9
rR
10 2005; 18: 1440-1463.
11
12
13 8.Quinones MA, Otto CM, Stoddard M, Waggoner A, Zoghbi WA. Recommendations for
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ev
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16 quantification of Doppler echocardiography: a report from the Doppler Quantification Task
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Force of the Nomenclature and Standards Committee of the American Society of
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20 Echocardiography. J Am Soc Echocardiogr 2002; 15: 167-184.
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22
23
9. Cameli M, Caputo M, Mondillo S, Ballo P, Palmerini E, Lisi M, Marino E, Galderisi M:
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ON
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26 Feasibility and reference values of left atrial longitudinal strain imaging by two-dimensional
27
28 speckle tracking. Cardiovascular Ultrasound 2009, 7:6.
LY
29
30
31 10. Zar HJ, Ferkol TW. The global burden of respiratory disease-impact on child health.
32
;N
33
34 Pediatr Pulmonol. 2014 ;49: 430-434.
35
36
37 11. Leuchte HH, Baumgartner RA, Nounou ME, Vogeser M, Neurohr C, Trautnitz M, Behr J.
ot
38
39 Brain natriuretic peptide is a prognostic parameter in chronic lung disease. Am J Respir Crit
40
41
fo
42 Care Med. 2006; 173: 744-750.

43
44
r
45 12. MeiLan KH, Vallerie VM, Gerard JC, Martinez FJ. Pulmonary diseases and the heart.
46
Di
47 Circulation 2007; 116: 2992-3005.

48
49
st
50 13. Elmasry OA, Attia HM, Abdelfattah NM. Assessment of left ventricular diastolic function
51
52
rib
53 in bronchial asthma: Can werely on transmitral inflow velocity patterns?

54
55 Eur.J.Echocardiography 2008; 7: 178-90.
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15
1
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3 14. C.Y. Ho, S.D. Solomon, A clinician’s guide to tissue Doppler imaging, Circulation.2006;
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5 113: 396–398.
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ee
7
8
9
15. Fujii J, Yazaki Y, Sawada H, Aizawa T, Watanabe H, Kato K. Noninvasive assessment of
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11 left and right ventricular filling in myocardial infarction with a two-dimensional Doppler
12
13 echocardiographic method. J.Am.Coll. Cardiol. 1985; 5: 1155-1160.
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16 16. Caso P, Galderisi M, Cicala S, Cioppa C, D'Andrea A, Lagioia G, Liccardo B, Martiniello AR,
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19 Mininni N. Association between myocardial right ventricular relaxation time and pulmonary
20
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21 arterial pressure in chronic obstructive lung disease: Analysis by pulsed Doppler tissue
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23
imaging. J Am Soc Echocardiogr 2001; 14: 970-977.
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ON
25
26
27 17. Dambrauskaite V, Delcroix M, Claus P, Herbots L, Palecek T, D'hooge J, Bijnens B,
28
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29 Rademakers F, Sutherland GR. The evaluation of pulmonary hypertension using right

30
31 ventricular myocardial isovolumic relaxation time. J Am Soc Echocardiogr 2005; 18: 1113-
32
;N
33
34 1120.
35
36
37 18. Bréchot N, Gambotti L, Lafitte S, Roudaut R. Usefulness of right ventricular isovolumic
ot
38
39 relaxation time in predicting systolic pulmonary artery pressure. Eur J Echocardiogr 2008; 9:
40
41
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42 547-554.
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44
r
45 19. Zeybek C, Yalcin Y, Erdem A, Polat TB, Aktuglu-Zeybek AC, Bayoglu V, Akdeniz C, Celebi A.
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Di
47 Tissue Doppler echocardiographic assessment of cardiac function in children with bronchial

48
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asthma. Pediatr.Int. 2007; 49: 911-917.
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53 20. Soad Shedeed. Right Ventricular Function in Children with Bronchial Asthma: A Tissue
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55 Doppler Echocardiographic Study. Pediatr Cardiol. 2010; 31: 1008-1015.
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3 21. Massoud MN, el Nawawy AA, el Nazar SY, Abdel-Rahman GM. Tumour necrosis factor-
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5 alpha concentration in severely asthmatic children. East Mediterr Health J 2000; 6: 432-436.
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ee
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8
9
22. Manthous CA. Management of severe exacerbations of asthma. Am J Med 1995; 99: 298-
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11 308.
12
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14 23. Levy BD, Kitch B, Fanta CH. Medical and ventilatory management of status asthmaticus.
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16 Intensive Care Med 1998; 24: 105-17.
17
ie
18
19
20
24. Robin ED, McCauley R. Sudden cardiac death in bronchial asthma, and inhaled beta-
w
21
22 adrenergic agonists. Chest 1992; 101: 1699-1702
23
24
ON
25 25.Suissa S, Hemmelgarn B, Blais L, Ernst P. Bronchodilators and acute cardiac death. Am J

26
27
Respir Crit Care Med. 1996; 154: 1598-1602.
28
LY
29
30
31 26. Au DH, Lemaitre RN, Curtis JR, Smith NL, Psaty BM. The risk of myocardial infarction
32
associated with inhaled B-adrenoceptor agonists. Am J Respir Crit Care Med 2000; 161: 827-
;N
33
34
35 830.
36
37
ot
38
27. Martin RM, Dunn NR, Freemantle SN, Mann RD. Risk of nonfatal cardiac failure and
39
40
41 ischaemic heart disease with long acting B2 agonists. Thorax 1998; 53: 558-62.
fo
42
43
44 28.Jenne JW. Can oral β2- agonists cause heart failure? Lancet 1998; 352: 1081-1082
r
45
46
Di
47 29. Zanoni LZ, Palhares DB, Consolo LC. Myocardial ischemia induced by nebulized fenoterol
48
49
for severe childhood asthma. Indian Pediatr 2005; 42: 1013-1018.
st
50
51
52
rib
53 30. Del Rio-Navarro BE, Sienra-Monge JJ, Alvarez-Anador M, Reyes- Ruiz N, Arelavo- Salas A,
54
55 Berber A. Serum potassium levels, CPK- MB and ECG in children suffering asthma treated
56
ut
57
58
59
io
60
n
Fo
17
1
2
rP
3 with beclomethasone or beclomethasone-salmeterol. Allergol Immunopathol (Madr). 2001;
4
5 29: 16-21.
6
ee
7
8
9
31. Blessberger H, Binder T. Two dimensional speckle tracking echocardiography: basic
rR
10
11 principles. Heart 2010; 96: 716–722.
12
13
14
ev
15
16
17
ie
18
19
20
w
21
22
23
24
ON
25
26
27
28
LY
29
30
31
32
;N
33
34
35
36
37
ot
38
39
40
41
fo
42
43
44
r
45
46
Di
47
48
49
st
50
51
52
rib
53
54
55
56
ut
57
58
59
io
60
n
Fo
1
2
rP
3 Table 1. Clinical and demographic characteristics
4
5 Patients with BA (n=18)
6
ee
7 Age, years 11.6 + 2.0
8
9 Male,n( %) 9(50)
rR
10
11
BMI, kg/m2 17 ± 2
12
13
14 Heart rate, bpm 78 ± 12
ev
15
16 SBP, mm Hg 107 ± 14
17
ie
18 DBP, mm Hg 59 ± 8
19
20 BA- bronchial asthma; Bpm-beats per minutes; BMI-
w
21
Body mass index; SBP- systolic blood pressure; DBP;
22
23 diastolic blood pressure
24
ON
25
26
27
28
LY
29
30
31
32
;N
33
34
35
36
37
ot
38
39
40
41
fo
42
43
44
r
45
46
Di
47
48
49
st
50
51
52
rib
53
54
55
56
ut
57
58
59
io
60
n
Fo
1
2
rP
3 Table 2. Standard two-dimensional, Doppler and tissue Doppler echocardiographic parameters of
4 left ventricle and left atrium.
5
6 Before treatment After treatment P value
ee
7
8
9
rR
10
11 EF(%) 68.8 ± 2.1 69.4 ± 3.5 0.653
12
13 LVEDV(ml) 56.4± 15 53.5± 14 0.229
14
ev
15 LVESV(ml) 25.8 ± 7.6 27.3± 4.6 0.278
16
17 IVSD(cm) 6.9 ± 1.1 6.9 ± 1.8 0.131
ie
18
19 PWD(cm) 6.8 ± 0.9 6.9 ± 1.7 0.117
20
w
21 Mit-E(m/s) 94 ± 21 0.235
96 ± 19
22
23
24 Mit-A(m/s) 64 ± 15 60 ± 19 0.189
ON
25
26 Mit-E/A 1.5 ± 1.4 1.6 ± 0.7 0.540
27
28 LAVmax(ml) 24.5±8.4 22.6±7.7 0.256
LY
29
30 LAVmin(ml) 11.1 ± 5.3 12 ± 6.7 0.328
31
32 IVRT(m/s) 64.0± 12.3 61±8.7 0.288
;N
33
34 MAPSE 1.5 ± 0.2 0.655
1.4 ± 0.2
35
36
37 EF- ejection fraction; LVEDV-left ventricle end diastolic volume; LVESV- left ventricle
ot
38
39 end systolic volume; IVSD - interventricular septum diastolic thickness diameter; PWD-
40
41 posterior wall diastolic thickness diameter; Mit- E/A - ratio between diastolic early (E)
fo
42
43 and late diastolic mitral inflow (A) velocities; LAV- left atrial volume; IVRT- isovolumic
44
r
45 relaxation time; MAPSE — mitral annular plane systolic excursion.

46
Di
47
48
49
st
50
51
52
rib
53
54
55
56
ut
57
58
59
io
60
n
Fo
1
2
rP
3 Table 3. Standard two-dimensional, Doppler and tissue Doppler echocardiographic parameters of
4 right ventricle and right atrium.
5
ee
7
8
9
rR
10 RVED(cm) 2.0 ± 0.4 2.0 ± 0.5 0.960
11
12 RVT(cm) 0.3 ±0.2 0.3 ± 0.1 0.949
13
14
ev
RAVmax(ml) 19.7± 7.1 19.6± 6.5 0.923
15
16
RAVmin(ml) 10.5± 5.3 9.8±4.3 0.446
17
ie
18
19 PAPs mmHg 16.5 ± 9.0 17.9 ±7.1 0.237
20
Tri-E (m/s)
w
21 64.5±11.5 67.4 ± 12.5 0.345
22
23 Tri-A(m/s) 42.1± 8.5 43.3± 7.3 0.515
24
ON
25 Tri-İVRT(m/s) 62.0 ± 18.3 57.2 ± 11.6 0.395

26
27 Tri-Sm (m/s) 14.7±2.5 13.6± 3.0 0.312
28
Tri-Em’ (m/s) 15.2± 3.4 15.4 ±2.9 0.919
LY
29
30
31 Tri-Am’ (m/s) 11.3± 3.5 11.2±2.9 0.125
32
TAPSE 1.8 ± 0.3 1.8 ± 0.4 0.790
;N
33
34
35 RVED-parasternal long axis view right ventricle enddiastolic diameter; RVT-right ventricle free wall
36 thickness; RAV - right atrium volüme; PAPs — systolic pulmonary artery pressure Tri-E - tricuspid
37
ot
valve early diastolic velocity; Tri-A - tricuspid valve late diastolic velocity; Tri- İVRT— tricuspid valve
38
39 isovolumic relaxation time; Tri-Sm- tricuspid annulus systolic myocardial velocity; Tri- E’ — tricuspid
40 annulus early diastolic myocardial velocity; Tri-A’ - tricuspid anulus late diastolic myocardial velocity;
41
fo
TAPSE - tricuspid annular plane systolic excursion;

42
43
44
r
45
46
Di
47
48
49
st
50
51
52
rib
53
54
55
56
ut
57
58
59
io
60
n
Fo
1
2
rP
3
4
5 Table 4. Left atrial and left ventricular strain and strain rate parameters.
6
ee
8
9
rR
10
11 LV
12
13 LV-GLS-S(%) -17.3 ±2.3 -18.6±2.4 0.456
14
ev
15 LV-GLS-D(%) -16.3 ± 3.3 -17.1 ± 3.4 0.214
16
17 LV-SR-S(1/s) -1.03 ± 0.3 -1.1±20.5 0.549
ie
18
19 LV-SR-E(1/s) 1.7 ± 0.4 1.5 ± 0.3 0.077
20
w
21
LV-SR-A(1/s) 0.7±0.1 0.7 ± 0.2 0.747
22
23
LA
24
ON
25
LA-PALS(%) 40.6 ± 10.8 38.7 ± 9.6 0.134
26
27
28 LA-SR-L(1/s) -2.1± 0.8 -1.9 ±0.7 0.126
LY
29
30 LA-TPLS(ms) 370.1 ± 43.5 389.6±33.3 0.236
31
32 LV-left ventricle; LA-left atrium; S -strain; GLS-S- global longutinal strain systolic; GLS-D-global
longutinal strain diastolic; SR-S - systolic strain rate; SR-E - early diastolic strain rate; PALS- peak atrial
;N
33
34 longitudinal strain; L-longitudinal; TPLS- time-to-peak longitudinal strain.
35
36
37
ot
38
39
40
41
fo
42
43
44
r
45
46
Di
47
48
49
st
50
51
52
rib
53
54
55
56
ut
57
58
59
io
60
n
Fo
1
2
rP
3
4
5 Table 5. Longitudinal strain and strain rate of right ventricle and right atrium during atrial
6 contraction and atrial relaxation.
ee
7
9
rR
10
11
12 RV
13
14
ev
RV-GLS-S(%) -21.6 ± 4.3 -24.1 ± 4.7 0.025
15
16
RV-GLS-D(%) -17.5± 5.3 -20.2±4.3 0.045
17
ie
18
19 RV-SR-S (1/s) -1.39 ± 0.5 -1.08 ± 0.2 0.038
20
RV-SR-E (1/s)
w
21 1.49± 0.4 1.44±0.4 0.686
22
23 RV-SR-A (1/s) 0.83± 0.3 0.87± 0.4 0.745
24
ON
25 RA
26
27 RA-PALS(%) 35.9 ± 12.4 43.8 ± 13.9 0.044
28
RA-SR-L(1/s) -1.5 ± 0.4 -1.9 ± 0.6
LY
29 0.043
30
31 RA-TPLS (ms) 362.1±36.9 365.7 ± 54.9 0.698
32
RV - right ventricle; RA-right atrium; S-strain; SR-strain rate; GLS-S-global longitudinal systolic strain;
;N
33
34 GLS-D-global longitudinal diastolic strain; SR-S-Systolic strain rate; SR-E-early diastolic strain rate; SR-
35
A- late diastolic strain rate; PALS- peak atrial longitudinal strain; L- longitudinal;TPLS- time-to-peak
36
37 longitudinal strain
ot
38
39
40
41
fo
42
43
44
r
45
46
Di
47
48
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st
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Asthma Before 7after TTT Speckle Tracking

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Asthma Before 7after TTT Speckle Tracking

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Pediatric Allergy, Immunology, and Pulmonology

The Effect of Childhood Asthma Treatment on Left and Right

Manuscript ID: PED-2015-0498

Manuscript Type: Original Research

Keyword: Asthma, Corticosteroids, Children, Bronchodilators

42 conventional echocardiographic assessments may be insufficient to evaluate the global

38 tracking echocardiography prior to the treatment. The echocardiographic assessments were

29 ventricle, which is why recovery is achieved by treatment.

29 4. Becker M, Bilke E, Kühl H, Katoh M, Kramann R, Franke A, Bücker A, Hanrath P, Hoffmann

57 Recommendations for chamber quantification: a report from the American Society of

42 Care Med. 2006; 173: 744-750.

47 Circulation 2007; 116: 2992-3005.

53 in bronchial asthma: Can werely on transmitral inflow velocity patterns?

29 Rademakers F, Sutherland GR. The evaluation of pulmonary hypertension using right

47 Tissue Doppler echocardiographic assessment of cardiac function in children with bronchial

25 25.Suissa S, Hemmelgarn B, Blais L, Ernst P. Bronchodilators and acute cardiac death. Am J

45 relaxation time; MAPSE — mitral annular plane systolic excursion.

25 Tri-İVRT(m/s) 62.0 ± 18.3 57.2 ± 11.6 0.395

TAPSE - tricuspid annular plane systolic excursion;

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