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  <front>
    <journal-meta>
      <journal-id journal-id-type="nlm-ta">Arq Bras Cardiol</journal-id>
      <journal-id journal-id-type="publisher-id">abc</journal-id>
      <journal-title-group>
        <journal-title>Arquivos Brasileiros de Cardiologia</journal-title>
        <abbrev-journal-title abbrev-type="publisher">Arq. Bras. Cardiol.</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">0066-782X</issn>
      <issn pub-type="epub">1678-4170</issn>
      <publisher>
        <publisher-name>Sociedade Brasileira de Cardiologia</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v3">44WwhdvPtZ8j3wPyWD95bNF</article-id>
      <article-id pub-id-type="publisher-id" specific-use="scielo-v2">S0066-782X2015002500625</article-id>
      <article-id pub-id-type="doi">10.5935/abc.20150144</article-id>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Review Article</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Methodological Gaps in Left Atrial Function Assessment by 2D Speckle Tracking Echocardiography</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Rimba&#351;</surname>
            <given-names>Roxana Cristina</given-names>
          </name>
          <xref ref-type="aff" rid="aff01">1</xref>
          <xref ref-type="aff" rid="aff02">2</xref>
          <xref ref-type="aff" rid="aff03">3</xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Dulgheru</surname>
            <given-names>Raluca Elena</given-names>
          </name>
          <xref ref-type="aff" rid="aff02">2</xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Vinereanu</surname>
            <given-names>Drago&#351;</given-names>
          </name>
          <xref ref-type="aff" rid="aff01">1</xref>
          <xref ref-type="aff" rid="aff02">2</xref>
          <xref ref-type="corresp" rid="c01"/>
        </contrib>
      </contrib-group>
      <aff id="aff01">
        <label>1</label>
        <institution content-type="orgname">University and Emergency Hospital</institution>
        <institution content-type="normalized">University and Emergency Hospital</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">University and Emergency Hospital, Bucharest &#8211; Romania</institution>
      </aff>
      <aff id="aff02">
        <label>2</label>
        <institution content-type="orgname">University of Medicine and Pharmacy Carol Davila</institution>
        <institution content-type="normalized">University of Medicine and Pharmacy Carol Davila</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">University of Medicine and Pharmacy Carol Davila, Bucharest &#8211; Romania</institution>
      </aff>
      <aff id="aff03">
        <label>3</label>
        <institution content-type="orgname">"Victor Babe&#351;" National Institute of Pathology</institution>
        <institution content-type="normalized">"Victor Babe&#351;" National Institute of Pathology</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">"Victor Babe&#351;" National Institute of Pathology, Bucharest &#8211; Romania</institution>
      </aff>
      <author-notes>
        <corresp id="c01"><bold>Mailing Address: Drago&#351; Vinereanu</bold> University of Medicine and Pharmacy Carol Davila. Bucharest &#8211; Romania. E-mail: <email>vinereanu@gmail.com</email>
					</corresp>
        <fn fn-type="con">
          <p>
            <bold>Author contributions</bold>
          </p>
          <p>Conception and design of the research and Writing of the manuscript: Rimba&#351; RC, Dulgheru RE, Vinereanu D; Acquisition of data and Analysis and interpretation of the data: Rimba&#351; RC, Dulgheru RE; Critical revision of the manuscript for intellectual content: Rimba&#351; RC, Vinereanu D.</p>
        </fn>
        <fn fn-type="conflict">
          <p>
            <bold>Potential Conflict of Interest</bold>
          </p>
          <p>No potential conflict of interest relevant to this article was reported.</p>
        </fn>
      </author-notes>
      <pub-date pub-type="epub">
        <month>12</month>
        <year>2015</year>
      </pub-date>
      <volume>105</volume>
      <issue>6</issue>
      <fpage>625</fpage>
      <lpage>636</lpage>
      <permissions>
        <license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
        </license>
      </permissions>
      <abstract>
        <title>Abstract</title>
        <p>The assessment of left atrial (LA) function is used in various cardiovascular diseases. LA plays a complementary role in cardiac performance by modulating left ventricular (LV) function. Transthoracic two-dimensional (2D) phasic volumes and Doppler echocardiography can measure LA function non&#8209;invasively. However, evaluation of LA deformation derived from 2D speckle tracking echocardiography (STE) is a new feasible and promising approach for assessment of LA mechanics. These parameters are able to detect subclinical LA dysfunction in different pathological condition. Normal ranges for LA deformation and cut-off values to diagnose LA dysfunction with different diseases have been reported, but data are still conflicting, probably because of some methodological and technical issues. This review highlights the importance of an unique standardized technique to assess the LA phasic functions by STE, and discusses recent studies on the most important clinical applications of this technique.</p>
      </abstract>
      <kwd-group xml:lang="en">
        <title>Keywords</title>
        <kwd>Atrial Function, Left</kwd>
        <kwd>Heart Atria / abnormalities</kwd>
        <kwd>Echocardiography</kwd>
        <kwd>Diagnostic Imaging</kwd>
      </kwd-group>
      <pub-date pub-type="epub-ppub">
        <month>12</month>
        <year>2015</year>
      </pub-date>
    </article-meta>
  </front>
  <body>
    <sec sec-type="intro">
      <title>Introduction</title>
      <p>Left atrial (LA) remodeling was described as an important prognostic marker in different diseases, such as heart failure, myocardial infarction, hypertrophic cardiomyopathy, and atrial fibrillation<xref ref-type="bibr" rid="B01">1</xref><sup>-</sup><xref ref-type="bibr" rid="B05">5</xref>.Although the assessment of LA function can be obtained by conventional 2D echocardiography, Doppler analysis of transmitral and pulmonary vein flows, and tissue Doppler measurement of LA myocardial velocities, its detailed quantification remains challenging.</p>
      <p>2D Speckle tracking echocardiography (2DSTE) is a feasible technique for the assessment of myocardial LA deformation<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B09">9</xref>. Its quantification may provide more insights into the LA mechanics<xref ref-type="bibr" rid="B10">10</xref><sup>-</sup><xref ref-type="bibr" rid="B12">12</xref>. However, normal ranges for LA strain and strain rate (SR) are still debatable<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B13">13</xref><sup>-</sup><xref ref-type="bibr" rid="B16">16</xref>.</p>
      <p>The aim of our review is to discuss the main advantages and limitations of assessing LA deformation by 2DSTE.</p>
      <p>We will refer to atrial physiology in order to discuss the main functions of the LA, and how STE can be used to assess them. Since the vast majority of the studies looking to LA deformation used EchoPac (GE Medical Systems), we will exemplify our comments by using images derived from this software, which was previously validated for the analysis of LA strain with high feasibility and good agreement<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B17">17</xref>.</p>
      <sec>
        <title>Left atrial physiology</title>
        <p>The LA function contributes to LV filling by all three components: a reservoir (40%), a passive conduit (35%), and a pump component (25%)<xref ref-type="bibr" rid="B18">18</xref><sup>,</sup><xref ref-type="bibr" rid="B19">19</xref>. Prolonged ventricular relaxation leads to a decrease in conduit function, while the reservoir and pump functions increase. As diastolic dysfunction progresses, the passive conduit function increases, while the reservoir and active pump functions decrease significantly<xref ref-type="bibr" rid="B18">18</xref>.</p>
        <p>LA contractile function depends on preload, afterload, intrinsic contractility, atrial electrical activation, and electromechanical coupling. Propagation of electrical impulse occurs throught interatrial connections in the subepicardium of the LA<xref ref-type="bibr" rid="B17">17</xref>. This results in LA atrial activation from the interatrial septum to the inferior, anterior, and lateral LA walls during sinus rhythm. Changes in these pathways may prolong or abolish interatrial conduction, and create a substrate for atrial arrhthmyias<xref ref-type="bibr" rid="B17">17</xref>.</p>
      </sec>
      <sec>
        <title>Left atrial phasic functions assessed by STE</title>
        <p>Currently, strain and SR parameters derived from 2DSTE allow us to identify all components of LA function<xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. However, this technique has some limitations. It is frame-dependent and cannot be used in patients whose 2D image quality is suboptimal. Thus, STE needs high quality-scale images, and requires a learning curve. Otherwise, it is a very promising tool for the assessment of regional and global LA function<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B13">13</xref>.</p>
        <p>Longitudinal LA strain and SR parameters can assess atrial function in several pathological conditions, such as mitral valve disease, supraventricular arrhythmias, hypertension, heart failure, and cardiomyopathies. However, the lack of standardization is an important limitation to the widespread use of these parameters in routine clinical practice.</p>
        <p>Consequently, normal values for all these 3 components of the LA function are highly required.</p>
        <p>The atria and ventricles move in opposite directions during the cardiac cycle, so the atrial myocardium lengthens during ventricular systole (positive strain), while the ventricular myocardium shortens during ventricular systole (negative strain). This creates a mirror image for S/SR curves of the LA and LV.</p>
        <p>Cameli et al<xref ref-type="bibr" rid="B08">8</xref> described a 12-segments model for the analysis of LA strain, using 4- and 2-chamber apical views. Other studies proposed a 15-segments model for a complete evaluation of the LA strain, using 4-, 2-, and 3- chamber views<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B18">18</xref>. This variability of the model used is one of the technical factors that might create different normal values for strain and SR parameters, and also different cut-off values in pathological conditions.</p>
        <p>It is already known that there are regional differences in the LA segmental function during atrial contraction and relaxation,with the posterior wall having the lowest strain, probably due to the fact that its motion is limited by attachment of the pulmonary veins<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>, and the inferior wall exhibiting the highest deformation, attributable to its greater thickness. Therefore, ignoring the posterior wall by using a 12-segments model, might overestimate the global S and SR parameters. Similarly, the atrial reservoir strain is greater in the apical 2C than in the 4C view, since the 4C view incorporates two areas in which atrial strain is low (the interatrial septum and the area of the pulmonary veins).</p>
        <p>During atrial contraction and relaxation, a deformation gradient is observed from all views, with higher strain in the atrio-ventricular junction and lower strain in the atrial roof, because the atrial roof is fixed to the mediastinum (<xref ref-type="fig" rid="f01">Figure 1</xref>).</p>
        <fig id="f01">
          <label>Figure 1</label>
          <caption>
            <title>"Bull&#8217;s eye" view of the longitudinal 2D strain of the left atrial contraction in a normal subject. It is coded in red because it represents the atrial strain of the pump function. Basal values are higher than medial values, and further reduced in the center, which represents the atrial roof (light red). Antero-lateral values are lower than infero-posterior values. Values of the antero-septal wall were excluded, because they correspond to the ascending aorta.</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf01.jpg"/></fig>
        <p>In our opinion, full assessment of the LA function by 2DSTE must include apical 2-, 4-, and 3- chamber views, optimized for the visualization of the LA.</p>
        <p>The frame rate should be set between 60 and 80 frames per second<xref ref-type="bibr" rid="B16">16</xref><sup>,</sup><xref ref-type="bibr" rid="B17">17</xref>. To trace the region of interest (ROI) in the discontinuity of the left atrial wall corresponding to pulmonary veins, the direction of LA endocardial and epicardial surfaces at the junction with these structures should be extrapolated<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref>.</p>
        <p>Before processing, a cine loop preview confirms that the internal line follows the LA endocardium throughout the cardiac cycle. Manual adjustments will be made when tracking of the LA endocardium is unsatisfactory.</p>
        <p>LA segments with inadequate image quality must be rejected. We suggest excluding from the analysis the subjects with more than one non-acceptable segment per chamber. Tracing the LA cavity just before atrial contraction, when it is smaller, often eliminates myocardial wall dropout in the interatrial septum and the pulmonary veins and, therefore, improves tracking. Tracking the more hyperdynamic parts of the LA, such as the annular lateral, inferior, and inferior-posterior regions, can be challenging. Extending the LA endocardial trace a little apically below the mitral annulus and adjusting the post-processing settings to better define the LA in this area might be helpful.</p>
        <p>Longitudinal left atrial S and SR parameters must be assessed as the average of 6 segmental values per each view (<xref ref-type="fig" rid="f02">Figure 2</xref>). The final S/SR values will be the average of the values obtained for each apical view, excluding the three segments of the antero-septal wall from the 3-chamber view, corresponding to the ascending aorta.</p>
        <fig id="f02">
          <label>Figure 2</label>
          <caption>
            <title>Quad view of the longitudinal LA strain by 2DSTE. 2DSTE of the left atrium (LA) from the 2C view, depicting the region of interest (ROI) created by the STE software (panel A), and the corresponding regional strain values of the atrial function (panel B). In panel C, LA strain curves for each of the 6 segments are analyzed. The dashed curve represents the mean LA longitudinal strain. Reference point was placed at the onset of the P-wave. During the period in which the atrium acts as a reservoir atrial strain increases, reaching a peak just before mitral valve opening. During the conduit function, atrial strain decreases, with a plateau during diastasis, and a negative peak at the end of atrial contraction. In panel D, curved M-mode shows that atrial roof positive strain is lower (in light blue) than the other walls (in dark blue).</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf02.jpg"/></fig>
        <p>The strain curve evaluated by 2DSTE must follow the LA physiology. During the LA reservoir function, corresponding to the LV isovolumic contraction, ejection and isovolumic relaxation, LA strain increases, achieving the highest peak just before mitral valve opening. During the conduit function, LA strain decreases and achieves a negative peak at the end of the LA contraction (<xref ref-type="fig" rid="f03">Figure 3</xref>). Subsequently, during the diastasis, both the S and SR profiles are flat, demonstrating that no LA wall deformation occurs in the late phase of the conduit function<xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. Using global longitudinal S and SR curves, active, passive, and reservoir function can be defined as follows:</p>
        <fig id="f03">
          <label>Figure 3</label>
          <caption>
            <title>Measurement of parameters of left atrial longitudinal strain by 2DSTE. 2C view depicting the region of interest and curved M-mode created by the software (left), and the corresponding global left atrial longitudinal strain (right); AVC: Aortic valve closure. The reference point was placed at the onset of the P wave, allowing measurement of the negative global strain at maximal atrial contraction (GSA-) (pump function), positive global strain at mitral valve opening (GSA+) (conduit function), and also sum of GSA- and GSA+ (TGSA) (reservoir function).</title>
          </caption>
          <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf03.jpg"/></fig>
        <list list-type="order">
          <list-item>
            <p>Active (pump) function:</p>
            <list list-type="bullet">
              <list-item>
                <p>Negative global strain as a difference between the strain at pre-atrial contraction (after A vawe) and strain just before mitral valve closure (MVC) (GSA-) (<xref ref-type="fig" rid="f03">Figure 3</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>;</p>
              </list-item>
              <list-item>
                <p>Late diastolic global strain rate (GSRL) (<xref ref-type="fig" rid="f04">Figure 4</xref>)<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
              </list-item>
            </list>
          </list-item>
          <list-item>
            <p>Passive (conduit) function:</p>
            <list list-type="bullet">
              <list-item>
                <p>Positive global strain at MVO (GSA+) (<xref ref-type="fig" rid="f03">Figure 3</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>;</p>
              </list-item>
              <list-item>
                <p>Early negative diastolic global strain rate (GSRE) (<xref ref-type="fig" rid="f04">Figure 4</xref>)<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
                <p>
                  <fig id="f04">
                    <label>Figure 4</label>
                    <caption>
                      <title>Measurement of parameters of left atrial longitudinal strain rate by 2DSTE. 4C view depicting the region of interest created by the software (left), and the corresponding left atrial global longitudinal strain rate (right). GSR+, first positive global strain rate at the beginning of left ventricular systole; TGSR+, time from the P wave onset to peak positive strain rate; GSRE, early diastolic strain rate; GSRL, late diastolic strain rate.</title>
                    </caption>
                    <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf04.jpg"/></fig>
                </p>
              </list-item>
            </list>
          </list-item>
          <list-item>
            <p>Reservoir function:</p>
            <list list-type="bullet">
              <list-item>
                <p>Sum of GSA- and GSA+ (TGSA) (<xref ref-type="fig" rid="f02">Figure 2</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>;</p>
              </list-item>
              <list-item>
                <p>First positive global strain rate at the beginning of LV systole (GSR+) (<xref ref-type="fig" rid="f04">Figure 4</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>.</p>
              </list-item>
            </list>
          </list-item>
        </list>
        <p>However, different studies used different methodologies, based on different reference points from the ECG (R-wave or P-wave), for the generation of the strain curve, which might generate different normal values<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. Saraiva et al<xref ref-type="bibr" rid="B07">7</xref>, in a normal population, used the P-wave for the generation of the strain curves and found that GSA+ was 21.4 &#177; 6.7%, TGSA was 35.6 &#177; 7.9%, while GSA- was -14.2&#177;3.3%. Sun et al<xref ref-type="bibr" rid="B05">5</xref>, in a similar population, using the R-wave as the reference point, reported completely different values for TGSA+, of 46.8 &#177; 7.7%<xref ref-type="bibr" rid="B05">5</xref>. Moreover, due to an upward translation of the strain curve with the R-wave method, they found a positive strain of 19.6 &#177; 4.2%, interpreted as atrial contraction. The normal values for SR parameters were similar between studies<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B08">8</xref>.</p>
        <p>Taking into account atrial physiology, we can easily understand that studies using the R-wave ignore the real active pump function (negative peak), and create a positive strain for this function, inconsistent with the real physiological changes<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. In contrast to the assessment of LV strain, in which the R-wave from the ECG is used as a reference point, we considered that the use of the P-wave enables the negative global LA strain, which corresponds to the real LA contractile function.</p>
        <p>Our experience showed that the R-wave method, by comparison with the P-wave method, provided a non physiological positive value for the active LA function, whereas conduit and reservoir functions (GSA+, TGSA) were significantly overestimated (<xref ref-type="fig" rid="f05">Figure 5</xref>)<xref ref-type="bibr" rid="B20">20</xref>. These findings suggest that the difference between methods does not consist of a simple upward translation of the strain curve, as previously suggested by Cameli et al<xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
        <fig id="f05">
          <label>Figure 5</label>
          <caption>
            <title>Comparison between the P-wave and the R-wave methods, for LA phasic function. 4C view depicting the region of interest (ROI) (left), and the corresponding LA strain curves (right). The dashed curves represent the mean global atrial longitudinal strains along the cardiac cycle. The reference point was placed at the onset of the P-wave (panel A), and at the R-wave (panel B). MVC: Mitral valve closure; AVC: Aortic valve closure; MVO: Mitral valve opening.</title>
            <p>Panel A - Measurement of the negative global strain at atrial contraction (GSA-), the positive global strain at MVO (GSA+), and the total strain (TGSA) as a sum between GSA- and GSA+. The pump (AC), reservoir, and conduit functions are depicted. In the left inferior panel there is a clear delineation of the LA pump (red) and reservoir function (blue), with curved M-mode profile.</p>
            <p>Panel B - Measurement of the total positive global strain at MVO (TGSA) (reservoir), and late positive global strain (GSAC) at the atrial contraction. There is a positive strain for atrial pump function with this method. The conduit function is defined as a difference between TGSA and GSAC. In the left inferior panel there is no delineation at all for the LA contraction and reservoir function (all blue), with curved M-mode profile.</p>
          </caption>
          <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf05.jpg"/></fig>
        <p>Guidelines recommend the R-wave as a temporal landmark for the LV strain analysis, in order to correctly generate maximal negative strain during the contraction phase. Because after LA contraction the length of the LA is smaller than before contraction, LA contraction strain has to have a negative value. This reflects better the true principles of strain, in which not only the magnitude that represents the strain is important, but also the direction of deformation. We suggest that using P-wave as a reference point might estimate correctly all LA functions<xref ref-type="bibr" rid="B20">20</xref>.</p>
        <p>To standardize LA deformation, other settings, such as proper gain and ROI, should be considered. Firstly, low gain settings artificially eliminate anatomic structures. Alternatively, with excess gain, there is a decrease in resolution. In our experience, increasing gain from minimum to maximum overestimates all LA functions.</p>
        <p>Intermediary changes did not have significant impact on active and conduit functions, but they did on reservoir function<xref ref-type="bibr" rid="B20">20</xref>. This is very important, since many studies focused on reservoir function and its correlation with LV systolic and diastolic functions<xref ref-type="bibr" rid="B21">21</xref><sup>-</sup><xref ref-type="bibr" rid="B24">24</xref>. Secondly, increasing the ROI width decreases values of LA deformation, probably related to the contamination by surrounding structures. Taking into account the LA anatomy, higher ROIs could be used by mistake only if the initial or the postprocessing gain is very high. Because the LA walls are very thin, the minimum ROI should be used<xref ref-type="bibr" rid="B20">20</xref><sup>,</sup><xref ref-type="bibr" rid="B21">21</xref>.The potential difficulty of accurately obtaining a region of interest close enough to the effective shape of the LA, and the risk of contamination by signal components arising from structures surrounding the LA, should be considered also<xref ref-type="bibr" rid="B20">20</xref><sup>-</sup><xref ref-type="bibr" rid="B24">24</xref>.</p>
        <p>In conclusion, we suggest that a medium gain and a minimum ROI should be used as the best choice for a standard assessment of LA deformation.</p>
      </sec>
      <sec>
        <title>Clinical applications of the parameters of left atrial deformation</title>
        <sec>
          <title>General population</title>
          <p>LA size has been shown to be a prognostic marker for adverse cardiovascular events in the general population<xref ref-type="bibr" rid="B25">25</xref><sup>-</sup><xref ref-type="bibr" rid="B28">28</xref>. While some studies emphasize the role of both LA volume index (LAVi) and LV diastolic dysfunction as independent predictors of cardiovascular events<xref ref-type="bibr" rid="B29">29</xref><sup>,</sup><xref ref-type="bibr" rid="B30">30</xref>, others doubt the ability of LAVi to predict all cause mortality, independently of the degree of LV diastolic dysfunction<xref ref-type="bibr" rid="B31">31</xref>. More recently, LA emptying fraction (LAEF) was associated independently with mortality<xref ref-type="bibr" rid="B32">32</xref>, in a general population based study, and with development of atrial fibrillation (AF) or flutter in subjects &#8805; 65 years<xref ref-type="bibr" rid="B33">33</xref>. Other studies have suggested that LA pump function is also able to identify subjects at higher cardiovascular risk in the population<xref ref-type="bibr" rid="B34">34</xref><sup>,</sup><xref ref-type="bibr" rid="B35">35</xref>, and that minimum LAV may be an important prognostic marker<xref ref-type="bibr" rid="B36">36</xref><sup>,</sup><xref ref-type="bibr" rid="B37">37</xref>. In order to identify the incremental value of LA deformation analysis by 2DSTE as a cardiovascular risk marker, compared with LAVi or LAEF, Cameli et al<xref ref-type="bibr" rid="B38">38</xref> evaluated prospectively 312 adults older than 50 years. They showed that global positive strain, using the R-wave method and a 12 segments model of LA, is a strong and independent predictor of cardiovascular events, superior to the conventional parameters of LA analysis<xref ref-type="bibr" rid="B38">38</xref>.</p>
        </sec>
        <sec>
          <title>Atrial fibrillation</title>
          <p>Patients with AF have both electrical and morphological LA remodeling. Interstitial fibrosis is one of the landmark morphological changes in patients with AF, and extensive LA fibrosis was associated with impairment of LA function. LA deformation parameters are reduced in patients with non-valvular AF (<xref ref-type="fig" rid="f06">Figure 6</xref>) as compared with normal subjects<xref ref-type="bibr" rid="B39">39</xref><sup>,</sup><xref ref-type="bibr" rid="B40">40</xref>. An inverse correlation was shown between the degree of LA fibrosis, as assessed by MRI, and LA strain and SR, as assessed by vector velocity imaging<xref ref-type="bibr" rid="B41">41</xref>.</p>
          <fig id="f06">
            <label>Figure 6</label>
            <caption>
              <title>Comparison between left atrial strain in a patient with reccurent atrial fibrillation (panel A) and in a normal subject (panel B).</title>
              <p>Averaged strain (dotted line) is markedly reduced in the patient with reccurent atrial fibrillation during the pump function (GSA-) (-3% vs. -15%), during the conduit function (GSA+) (9% vs. 18%), and during the reservoir function (TGSA) (13% vs. 33%). There is also a complete dyssynchrony of contraction and relaxation between left atrial segments in the patient with atrial fibrillation versus the normal subject.</p>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf06.jpg"/></fig>
          <p>Different studies demonstrated that LA strain predicts the risk of cardiovascular events, or success in restoring sinus rhythm following electrical cardioversion or ablation procedures, in patients with AF. It also predicts the risk of AF recurrence after successful cardioversion<xref ref-type="bibr" rid="B40">40</xref><sup>,</sup><xref ref-type="bibr" rid="B42">42</xref><sup>,</sup><xref ref-type="bibr" rid="B43">43</xref>. Thus, in the study of Saha et al<xref ref-type="bibr" rid="B39">39</xref>, TGSA and total LAEF were reduced, and TGSA was the only index associated with greater odds of a CHADS2 score &#8805; 2. Furthermore, LA reservoir strain was incremental to the CHADS2 score in predicting death or hospitalization<xref ref-type="bibr" rid="B39">39</xref>. Another study showed a reduced GSA- and GSA+ in patients with paroxysmal AF and a CHADS2 score &#8804; 1 before their index stroke, by comparison with age and sex matched controls, with paroxysmal AF and no history of stroke. Moreover, GSA- was associated significantly with stroke. These results suggest that LA strain might help the decision for oral anticoagulation in this group of patients<xref ref-type="bibr" rid="B44">44</xref>.</p>
          <p>Shih et al. showed that LA strain during atrial filling and SR during reservoir phase were decreased in patients with AF and stroke, and were associated independently with stroke<xref ref-type="bibr" rid="B45">45</xref>. Another study showed that although GSA+ was not predictive of AF recurrence in patients who needed cardioversion, the change in peak positive LA strain was significantly higher in subjects who maintained sinus rhythm<xref ref-type="bibr" rid="B46">46</xref>. The lack of predictive power may be related only to the small sample size. More recently, abnormalities of the timing of atrial deformation showed to predict recurrence of AF after cardioversionm<xref ref-type="bibr" rid="B47">47</xref><sup>,</sup><xref ref-type="bibr" rid="B48">48</xref>. Thus, in patients referred for cardioversion for AF the standard deviation of the time-to-peak strain, using a six segments model of the LA, was an independent predictor of AF recurrence<xref ref-type="bibr" rid="B47">47</xref>. Similar results have been published after catheter ablation procedures for AF<xref ref-type="bibr" rid="B49">49</xref>.</p>
        </sec>
        <sec>
          <title>Cardiomyopathies</title>
          <p>LA strain is reduced in hypertrophic cardiomyopathy (HCM) by comparison to healthy controls (<xref ref-type="fig" rid="f07">Figure 7</xref>), but also compared to patients with secondary LV hypertrophy due to hypertension<xref ref-type="bibr" rid="B22">22</xref><sup>,</sup><xref ref-type="bibr" rid="B24">24</xref>. Moreover, in another study it was suggested that LA strain might have an additive value over conventional parameters, such as LAVi, E/A and E/E' ratio, in differentiating HCM from other types of hypertrophy, with a cut-off value of -10.8% for the pump function<xref ref-type="bibr" rid="B22">22</xref>. Meanwhile, Rosca et al<xref ref-type="bibr" rid="B02">2</xref> showed that LA pump function, evaluated only from the SR curves, is an independent determinant of heart failure symptoms in patients with HCM.</p>
          <fig id="f07">
            <label>Figure 7</label>
            <caption>
              <title>Comparison between left atrial strain in a patient with hypertrophic cardiomyopathy (panel A) and in a normal subject (panel B). </title>
              <p>Averaged strain is markedly reduced in the patient with hypertrophic cardiomyopathy during the pump function (GSA-) (-4% vs. -10%), during the conduit phase (GSA+) (8% vs. 26%), and during the reservoir phase (TGSA) (12% vs. 36%).</p>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf07.jpg"/></fig>
          <p>In patients with cardiac amyloidosis, LA dysfunction is also common. In one study using tissue Doppler, peak LA systolic strain and SR were lower in patients with cardiac amyloidosis than in patients with LV diastolic dysfunction of other causes, suggesting that tissue Doppler can be used to detect subtle changes in LA function in these patients<xref ref-type="bibr" rid="B50">50</xref>. Another study using STE confirmed that LA dysfunction is a common component of amyloidosis, even in the absence of the traditional echocardiographic features. Thus, GSRL and GSA- were significantly lower in amyloidosis compared with the control group, suggesting that assessment of LA deformation is able to detect subtle differences in LA function, not recognized by most conventional parameters. Therefore, it appears that amyloidosis affects LA function above the dysfunction secondary to LV diastolic dysfunction<xref ref-type="bibr" rid="B51">51</xref>.</p>
          <p>In patients with dilated cardiomyopathy (DCM), LA function assessed by STE was severely altered in idiopathic, by comparison with ischemic DCM. In a study on 314 patients, peak systolic LA strain was significantly reduced in idiopathic DCM as opposed to ischemic DCM<xref ref-type="bibr" rid="B11">11</xref>. However, this study used the R-wave method for the generation of the strain curves, and what they defined as "peak systolic LA strain" was in fact the LA reservoir function (TGSA). Another recent study investigated the importance of LA functional reserve, during dobutamine stress echocardiography (DSE), in patients with depressed LV systolic function<xref ref-type="bibr" rid="B52">52</xref>. They concluded that the assessment of LA reservoir and passive emptying function during DSE provides important incremental value over standard clinical and echocardiographic parameters to predict cardiovascular events in DCM, since a decreased LA functional reserve was associated with a higher cardiovascular event rate<xref ref-type="bibr" rid="B52">52</xref>. In another study, in patients with heart failure, TGSA correlated well with the pulmonary capillary wedge pressure (r = -0.81, p &lt; 0.0001), providing a better estimation of LV filling pressure (AUC = 0.93) than E/E' ratio<xref ref-type="bibr" rid="B12">12</xref>.</p>
          <p>LA strain analysis by STE might reveal relevant information in patients with DCM, candidates for cardiac resynchronization therapy (CRT). One study including 90 patients with DCM of either idiopathic or ischemic etiology confirmed that LA systolic function (GSA-) is considerably more impaired in patients with idiopathic than ischemic DCM. Furthermore, CRT responders with ischemic DCM were more likely to have an improvement of LA function after resynchronization (<xref ref-type="fig" rid="f08">Figure 8</xref>). In fact, the only independent determinants of LA functional recovery after CRT were positive response to CRT and the ischemic etiology of DCM<xref ref-type="bibr" rid="B53">53</xref>. Another study using tissue Doppler showed that in patients with heart failure and CRT, atrial strain was higher in the right atrium, interatrial septum, and left atrium in atrial-sensed compared to atrial-paced mode<xref ref-type="bibr" rid="B54">54</xref>. This study emphasized that, despite no difference in intraventricular dyssynchrony, patients with atrial-sensed mode had significantly lower atrial dyssynchrony that contributed to a better LV performance after CRT.</p>
          <fig id="f08">
            <label>Figure 8</label>
            <caption>
              <title>Comparison between left atrial strain in a patient with idiopathic dilated cardiomyopathy, before (panel A) and after (panel B) cardiac resynchronization therapy (CRT). Averaged strain is markedly reduced before than after CRT during the pump function (GSA-) (-5.1% vs. -9%), during the conduit function (GSA+) (2.4% vs. 5%), and also during the reservoir function (TGSA) (7.5% vs. 14%). A significant improvement of the atrial synchrony for both pump and reservoir functions was observed after CRT (panel B), compared to a complete disorganized pattern of strain before CRT (panel A).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf08.jpg"/></fig>
        </sec>
        <sec>
          <title>Ischemic heart disease</title>
          <p>LA dysfunction is also common after acute myocardial infarction. In a study on 320 patients evaluated by STE 48 hours after admission for acute myocardial infarction, LA reservoir strain (TGSA) and maximum LAVi were independent predictors of all-cause mortality, re-infarction, and re-hospitalization for chronic heart failure, after adjustment for clinical and other echocardiographic parameters<xref ref-type="bibr" rid="B55">55</xref>. On contrary, in a study on 843 patients with myocardial infarction, TGSA measured within 48 hours after hospitalization was significantly associated with the composite outcome of heart failure and death, but failed to predict this outcome after adjustment (for age, global longitudinal LV strain, and maximum LAVi). This study suggested that LA strain in these patients is dependent on global LV longitudinal strain and LA size and, therefore, the added prognostic value of LA reservoir function in patients with impaired LV longitudinal function is questionable<xref ref-type="bibr" rid="B56">56</xref>.</p>
        </sec>
        <sec>
          <title>Valvular heart disease</title>
          <p>LA enlargement and impaired LA function, resulting from volume or pressure overload, is frequent in chronic mitral regurgitation (MR) and aortic stenosis (AS).</p>
          <p>LA size proved to be a good predictor of outcome in primary MR: a LA diameter more than 55 mm was associated with a lower 8-year survival rate, while a LA volume more than 60 ml/m<sup>2</sup> was associated with an increased mortality and cardiac events (AF and heart failure). However, few data are published regarding LA function, as assessed by STE, and its prognostic role in primary MR. A recent study on 121 patients with severe MR reported significant LA reservoir and pump dysfunction, which were more pronounced in patients already having an indication for surgery. Of all indices of LA function, the LA reservoir strain had the highest accuracy to identify patients with indication for mitral valve surgery. Moreover, after mitral valve surgery, patients with LA reservoir strain &#8804; 24% showed worse survival after a median follow up of 6.4 years, regardless of the symptomatic status before surgery<xref ref-type="bibr" rid="B57">57</xref>. This emphasizes once more the importance of a correct assessment of the LA reservoir strain.</p>
          <p>Preserved atrial pump function is important for maintenance of cardiac output in patients with severe aortic stenosis. In patients with severe AS, all atrial functions (reservoir, conduit, and pump) were impaired, by comparison with matched controls<xref ref-type="bibr" rid="B58">58</xref>. As expected, LA reservoir dysfunction was related to LV filling pressures, while LA conduit dysfunction depended on the degree of impaired LV relaxation<xref ref-type="bibr" rid="B58">58</xref>. Another recent study investigated the role of LA function, assessed by STE, as a predictor of postoperative AF in severe patients with AS undergoing conventional surgery. GSRL was the only independent predictor of postoperative AF, suggesting its role in risk stratification of patients with severe AS<xref ref-type="bibr" rid="B59">59</xref>.</p>
        </sec>
      </sec>
    </sec>
    <sec sec-type="conclusions">
      <title>Conclusions</title>
      <p>The assessment of LA deformation by 2D speckle tracking echocardiography may represent a rapid and easy-to-perform technique to explore LA function. These new parameters of atrial function are more sensitive than traditional indices of atrial function, and could be incorporated into the routine assessment of various heart diseases, such as atrial fibrillation, hypertrophic and dilated cardiomyopathies, ischaemic heart disease, and valvular valve disease. We suggest that methodological standardization is essential in order to introduce LA deformation analysis into the clinical practice. In order to define the normal values and the cut-off values for diagnosis and prognosis in different diseases, we suggest to use the P-wave method for the generation of the strain curve. This method allows a complete evaluation of all LA functions: pump, passive conduit, and reservoir. Gain should be set in the mid range, and ROI at the minimum level. A 15-segments model is indicated for a complete evaluation of the LA deformation, because this model incorporates all available segments, and has the potential to create a real map of the LA electromechanical activation.</p>
    </sec>
  </body>
  <back>
    <fn-group>
      <fn fn-type="supported-by">
        <p>
          <bold>Sources of Funding</bold>
        </p>
        <p>This study was partially funded by Sectorial Operational Programme Human Resources Development (SOPHRD) and CNCS &#8211; UEFISCDI.</p>
      </fn>
      <fn fn-type="other">
        <p>
          <bold>Study Association</bold>
        </p>
        <p>This study is not associated with any thesis or dissertation work.</p>
      </fn>
    </fn-group>
    <ack>
      <p>Acknowledgments</p>
      <p>The authors would like to thank to Dr. Leabu Mircea for his useful comments on the final version of this article. This paper was partly supported by the Sectorial Operational Programme Human Resources Development (SOPHRD), financed by the European Social Fund and the Romanian Government under the contract number POSDRU 141531, and also by the Romanian National Authority for Scientific Research, CNCS - UEFISCDI, project number PN-II-ID-PCE-2011-3-0791.</p>
    </ack>
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      </article-categories>
      <title-group>
        <article-title>Lacunas Metodol&#243;gicas na Avalia&#231;&#227;o da Fun&#231;&#227;o do &#193;trio Esquerdo por Ecocardiografia Bidimensional com <italic>Speckle Tracking</italic></article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Rimba&#351;</surname>
            <given-names>Roxana Cristina</given-names>
          </name>
          <xref ref-type="aff" rid="aff04">1</xref>
          <xref ref-type="aff" rid="aff05">2</xref>
          <xref ref-type="aff" rid="aff06">3</xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Dulgheru</surname>
            <given-names>Raluca Elena</given-names>
          </name>
          <xref ref-type="aff" rid="aff05">2</xref>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Vinereanu</surname>
            <given-names>Drago&#351;</given-names>
          </name>
          <xref ref-type="aff" rid="aff04">1</xref>
          <xref ref-type="aff" rid="aff05">2</xref>
          <xref ref-type="corresp" rid="c02"/>
        </contrib>
      </contrib-group>
      <aff id="aff04">
        <label>1</label>
        <institution content-type="orgname">University and Emergency Hospital</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">University and Emergency Hospital, Bucharest &#8211; Romania</institution>
      </aff>
      <aff id="aff05">
        <label>2</label>
        <institution content-type="orgname">University of Medicine and Pharmacy Carol Davila</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">University of Medicine and Pharmacy Carol Davila, Bucharest &#8211; Romania</institution>
      </aff>
      <aff id="aff06">
        <label>3</label>
        <institution content-type="orgname">"Victor Babe&#351;" National Institute of Pathology</institution>
        <addr-line>
          <named-content content-type="city">Bucharest</named-content>
        </addr-line>
        <country country="RO">Romania</country>
        <institution content-type="original">"Victor Babe&#351;" National Institute of Pathology, Bucharest &#8211; Romania</institution>
      </aff>
      <author-notes>
        <corresp id="c02"><bold>Correspond&#234;ncia: Drago&#351; Vinereanu</bold> Universidade de Medicina e Farm&#225;cia Carol Davila. Bucareste &#8211; Rom&#234;nia. E-mail: <email>vinereanu@gmail.com</email>
					</corresp>
        <fn fn-type="con">
          <p>
            <bold>Contribui&#231;&#227;o dos autores</bold>
          </p>
          <p>Concep&#231;&#227;o e desenho da pesquisa e Reda&#231;&#227;o do manuscrito: Rimba&#351; RC, Dulgheru RE, Vinereanu D; Obten&#231;&#227;o de dados e An&#225;lise e interpreta&#231;&#227;o dos dados: Rimba&#351; RC, Dulgheru RE; Revis&#227;o cr&#237;tica do manuscrito quanto ao conte&#250;do intelectual importante: Rimba&#351; RC, Vinereanu D.</p>
        </fn>
        <fn fn-type="conflict">
          <p>
            <bold>Potencial conflito de interesse</bold>
          </p>
          <p>Declaro n&#227;o haver conflito de interesses pertinentes.</p>
        </fn>
      </author-notes>
      <abstract>
        <title>Resumo</title>
        <p>A avalia&#231;&#227;o da fun&#231;&#227;o do &#225;trio esquerdo (AE) &#233; utilizada em v&#225;rias doen&#231;as cardiovasculares. O AE tem um papel complementar no desempenho card&#237;aco atrav&#233;s da modula&#231;&#227;o da fun&#231;&#227;o do ventr&#237;culo esquerdo (VE).A ecocardiografia com Doppler e a ecocardiografia transtor&#225;cica bidimensional (2D) de volumes de fase podem medir a fun&#231;&#227;o do AE de forma n&#227;o-invasiva. No entanto, a avalia&#231;&#227;o da deforma&#231;&#227;o do AE derivada da ecocardiografia bidimensional com <italic>speckle tracking</italic> (EST) &#233; uma abordagem nova, promissora e fact&#237;vel para avaliar a mec&#226;nica do AE. Estes par&#226;metros s&#227;o capazes de detectar disfun&#231;&#227;o do AE subcl&#237;nica em diferentes patologias. H&#225; relatos da varia&#231;&#227;o normal da deforma&#231;&#227;o do AE e dos valores de corte para o diagn&#243;stico de disfun&#231;&#227;o do AE em diferentes doen&#231;as, mas os dados ainda s&#227;o conflitantes, provavelmente devido a alguns problemas t&#233;cnicos e metodol&#243;gicos. Esta revis&#227;o destaca a import&#226;ncia de uma t&#233;cnica &#250;nica padronizada para a avalia&#231;&#227;o das fun&#231;&#245;es f&#225;sicas do AE por EST, e discute estudos recentes sobre as aplica&#231;&#245;es cl&#237;nicas mais importantes desta t&#233;cnica.</p>
      </abstract>
      <kwd-group xml:lang="pt">
        <title>Palavras-chave</title>
        <kwd>Fun&#231;&#227;o do &#193;trio Esquerdo</kwd>
        <kwd>&#193;trio Esquerdo / anormalidades</kwd>
        <kwd>Ecocardiografia</kwd>
        <kwd>Diagn&#243;stico por Imagem</kwd>
      </kwd-group>
    </front-stub>
    <body>
      <sec sec-type="intro">
        <title>Introdu&#231;&#227;o</title>
        <p>O remodelamento do AE foi descrito como um marcador progn&#243;stico importante em diferentes patologias como a insufici&#234;ncia card&#237;aca, infarto do mioc&#225;rdio, miocardiopatia hipertr&#243;fica e fibrila&#231;&#227;o atrial<xref ref-type="bibr" rid="B01">1</xref><sup>-</sup><xref ref-type="bibr" rid="B05">5</xref>. Embora a avalia&#231;&#227;o da fun&#231;&#227;o do AE possa ser obtida por ecocardiografia bidimensional convencional, an&#225;lise por Doppler dos fluxos transmitral e na veia pulmonar, e medida por Doppler tecidual das velocidades mioc&#225;rdicas do AE, sua quantifica&#231;&#227;o detalhada continua sendo desafiadora.</p>
        <p>A ecocardiografia bidimensional com <italic>speckle tracking</italic> (E2DST) &#233; uma t&#233;cnica fact&#237;vel para a avalia&#231;&#227;o da deforma&#231;&#227;o mioc&#225;rdica do AE<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B09">9</xref>. Sua quantifica&#231;&#227;o pode fornecer uma maior compreens&#227;o sobre a mec&#226;nica do AE<xref ref-type="bibr" rid="B10">10</xref><sup>-</sup><xref ref-type="bibr" rid="B12">12</xref>. No entanto, a varia&#231;&#227;o normal da deforma&#231;&#227;o do AE e da taxa de deforma&#231;&#227;o (TD) ainda s&#227;o discut&#237;veis<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B13">13</xref><sup>-</sup><xref ref-type="bibr" rid="B16">16</xref>.</p>
        <p>O objetivo de nossa revis&#227;o &#233; discutir as principais vantagens e limita&#231;&#245;es da avalia&#231;&#227;o da deforma&#231;&#227;o do AE por E2DST. Faremos refer&#234;ncia &#224; fisiologia atrial a fim de discutir as principais fun&#231;&#245;es do AE e como a EST pode ser usada para avali&#225;-las. Uma vez que a grande maioria dos estudos sobre deforma&#231;&#227;o do AE usaram o EchoPac (GE Medical Systems), exemplificaremos nossos coment&#225;rios atrav&#233;s de imagens derivadas deste software, que foi anteriormente validado para a an&#225;lise da deforma&#231;&#227;o do AE mostrando alta factibilidade e boa concord&#226;ncia<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B17">17</xref>.</p>
        <sec>
          <title>Fisiologia do &#225;trio esquerdo</title>
          <p>A fun&#231;&#227;o do AE contribui para o enchimento do VE atrav&#233;s dos tr&#234;s componentes: de reservat&#243;rio (40%), de conduto passivo (35%), e de bomba (25%)<xref ref-type="bibr" rid="B18">18</xref><sup>,</sup><xref ref-type="bibr" rid="B19">19</xref>. O relaxamento ventricular prolongado leva a uma redu&#231;&#227;o na fun&#231;&#227;o de conduto, enquanto as fun&#231;&#245;es de reservat&#243;rio e de bomba aumentam. &#192; medida que a disfun&#231;&#227;o diast&#243;lica progride, a fun&#231;&#227;o de conduto passivo aumenta, ao passo que as fun&#231;&#245;es de reservat&#243;rio e de bomba ativa diminuem sensivelmente<xref ref-type="bibr" rid="B18">18</xref>.</p>
          <p>A fun&#231;&#227;o contr&#225;til do AE depende da pr&#233;-carga, p&#243;s-carga, contratilidade intr&#237;nseca, ativa&#231;&#227;o el&#233;trica atrial, e do acoplamento eletromec&#226;nico. A propaga&#231;&#227;o do impulso el&#233;trico ocorre atrav&#233;s de conex&#245;es interatriais no subepic&#225;rdio do AE<xref ref-type="bibr" rid="B17">17</xref>. Isto resulta na ativa&#231;&#227;o do AE a partir do septo interatrial em dire&#231;&#227;o &#224;s paredes inferior, anterior e lateral do AE durante o ritmo sinusal. Altera&#231;&#245;es nessas vias podem prolongar ou abolir a condu&#231;&#227;o interatrial e criar um substrato para arritmias atriais<xref ref-type="bibr" rid="B17">17</xref>.</p>
        </sec>
        <sec>
          <title>Fun&#231;&#245;es f&#225;sicas do &#225;trio esquerdo avaliadas por est</title>
          <p>Atualmente, os par&#226;metros de deforma&#231;&#227;o e TD derivados do E2DST nos permitem identificar todos os componentes da fun&#231;&#227;o do AE<xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. No entanto, esta t&#233;cnica tem algumas limita&#231;&#245;es. Ela depende do enquadramento e n&#227;o pode ser usada em pacientes em que a qualidade da imagem 2D &#233; inferior &#224; ideal. Assim, a EST requer imagens em escala de alta qualidade e uma curva de aprendizado. N&#227;o obstante, trata-se de uma ferramenta muito promissora para a avalia&#231;&#227;o da fun&#231;&#227;o regional e global do AE<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref><sup>,</sup><xref ref-type="bibr" rid="B13">13</xref>. A deforma&#231;&#227;o longitudinal do AE e os par&#226;metros da TD podem avaliar a fun&#231;&#227;o atrial em v&#225;rias doen&#231;as como valvulopatia mitral, arritmias supraventriculares, hipertens&#227;o, insufici&#234;ncia card&#237;aca e miocardiopatias. No entanto, a falta de padroniza&#231;&#227;o &#233; uma limita&#231;&#227;o importante para o uso difundido desses par&#226;metros na pr&#225;tica cl&#237;nica. Consequentemente, os valores normais para todos esses 3 componentes da fun&#231;&#227;o do AE s&#227;o extremamente necess&#225;rios.</p>
          <p>Os &#225;trios e ventr&#237;culos movem-se em dire&#231;&#245;es opostas durante o ciclo card&#237;aco, de forma que o mioc&#225;rdio atrial se alonga durante a s&#237;stole ventricular (deforma&#231;&#227;o positiva), enquanto que o mioc&#225;rdio ventricular encurta durante a s&#237;stole ventricular (deforma&#231;&#227;o negativa). Isto cria uma imagem espelhada para as curvas D/TD do AE e VE.</p>
          <p>Cameli e cols.<xref ref-type="bibr" rid="B08">8</xref> descreveram um modelo de 12 segmentos para a an&#225;lise da deforma&#231;&#227;o do AE usando cortes apicais de 4 e 2 c&#226;maras. Outros estudos propuseram um modelo de 15 segmentos para uma avalia&#231;&#227;o completa da deforma&#231;&#227;o do AE usando cortes de 4, 2 e 3 c&#226;maras<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B18">18</xref>. Esta variabilidade de modelos utilizados &#233; um dos fatores t&#233;cnicos que pode criar valores normais diferentes para os par&#226;metros de deforma&#231;&#227;o e TD, al&#233;m de diferentes valores de corte em estados patol&#243;gicos.</p>
          <p>J&#225; se sabe que h&#225; diferen&#231;as regionais na fun&#231;&#227;o segmentar do AE durante a contra&#231;&#227;o e o relaxamento atrial, com a parede posterior sofrendo a menor deforma&#231;&#227;o, provavelmente devido ao fato de que sua movimenta&#231;&#227;o &#233; limitada pela liga&#231;&#227;o das veias pulmonares<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>, e a parede inferior sofrendo a maior deforma&#231;&#227;o, o que &#233; atribu&#237;vel a sua maior espessura. Portanto, ao ignorar a parede posterior quando se usa um modelo de 12 segmentos pode-se superestimar os par&#226;metros globais de D e TD. De maneira semelhante, a deforma&#231;&#227;o do reservat&#243;rio atrial &#233; maior no corte apical 2C do que no 4C, uma vez que o corte 4C incorpora duas &#225;reas em que a deforma&#231;&#227;o atrial &#233; baixa (o septo interatrial e a &#225;rea das veias pulmonares).</p>
          <p>Durante a contra&#231;&#227;o e o relaxamento atrial, observa-se um gradiente de deforma&#231;&#227;o a partir de todos os cortes, com maior deforma&#231;&#227;o na jun&#231;&#227;o atrioventricular e menor deforma&#231;&#227;o no teto atrial, porque este &#233; fixado ao mediastino (<xref ref-type="fig" rid="f09">Figura 1</xref>).</p>
          <fig id="f09">
            <label>Figura 1</label>
            <caption>
              <title>Vista em "alvo" da deforma&#231;&#227;o longitudinal 2D da contra&#231;&#227;o do &#225;trio esquerdo em indiv&#237;duo normal. Est&#225; codificado em vermelho porque representa a deforma&#231;&#227;o atrial da fun&#231;&#227;o de bomba. Os valores basais s&#227;o maiores que os valores mediais e ainda mais reduzidos ao centro, que representa o teto atrial (vermelho claro). Os valores anterolaterais s&#227;o mais baixos que os inferoposteriores. Os valores da parede anterosseptal foram exclu&#237;dos porque correspondem &#224; aorta ascendente.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf01-pt.jpg"/></fig>
          <p>Em nossa opini&#227;o, a avalia&#231;&#227;o complete da fun&#231;&#227;o do AE por E2DST deve incluir cortes apicais de 2, 4 e 3 c&#226;maras otimizados para a visualiza&#231;&#227;o do AE. A taxa de aquisi&#231;&#227;o de imagens deve ser ajustada entre 60 e 80 quadros por segundo<xref ref-type="bibr" rid="B16">16</xref><sup>,</sup><xref ref-type="bibr" rid="B17">17</xref>. Para tra&#231;ar a RDI (regi&#227;o de interesse) na descontinuidade da parede atrial esquerda correspondente &#224;s veias pulmonares, a dire&#231;&#227;o das superf&#237;cies endoc&#225;rdica e epic&#225;rdica do AE na jun&#231;&#227;o com estas estruturas deve ser extrapolada<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B08">8</xref>. Antes do processamento, uma pr&#233;-visualiza&#231;&#227;o em al&#231;a em modo cine confirma que a linha interna acompanha o endoc&#225;rdio do AE durante todo o ciclo card&#237;aco. S&#227;o feitos ajustes manuais quando o rastreamento do endoc&#225;rdio do AE &#233; insatisfat&#243;rio. Os segmentos de AE com qualidade de imagem inadequada devem ser descartados. Sugerimos que os indiv&#237;duos com mais de um segmento n&#227;o aceit&#225;vel por c&#226;mara sejam exclu&#237;dos da an&#225;lise. O rastreamento da cavidade do AE pouco antes da contra&#231;&#227;o atrial, quando menor, frequentemente elimina a perda de sinal da parede mioc&#225;rdica no septo interatrial e nas veias pulmonares e, portanto, melhora o rastreamento. O rastreamento das partes mais hiperdin&#226;micas do AE, como as regi&#245;es anulares lateral, inferior e inferoposterior, pode ser desafiador. Pode ser &#250;til estender o tra&#231;o endoc&#225;rdico do AE um pouco apicalmente abaixo do anel mitral e ajustar as configura&#231;&#245;es p&#243;s-processamento para definir melhor o AE nesta regi&#227;o.</p>
          <p>Os par&#226;metros de D e TD longitudinais do &#225;trio esquerdo devem ser avaliados como a m&#233;dia de 6 valores segmentares por cada corte (<xref ref-type="fig" rid="f10">Figura 2</xref>). Os valores de D/TD finais corresponder&#227;o &#224; m&#233;dia dos valores obtidos para cada corte apical, excluindo-se os tr&#234;s segmentos da parede anterosseptal do corte de 3 c&#226;maras, que corresponde &#224; aorta ascendente.</p>
          <fig id="f10">
            <label>Figura 2</label>
            <caption>
              <title>Vista em 4 imagens da deforma&#231;&#227;o longitudinal do AE por E2DST. E2DST do &#225;trio esquerdo (AE) a partir do corte 2C, mostrando a regi&#227;o de interesse (RDI) criada pelo software STE (painel A), e os valores de deforma&#231;&#227;o regional da fun&#231;&#227;o atrial correspondentes (painel B). No painel C, s&#227;o analisadas as curvas de deforma&#231;&#227;o do AE para cada um dos 6 segmentos. A curva tracejada representa a deforma&#231;&#227;o longitudinal m&#233;dia do AE. O ponto de refer&#234;ncia foi colocado no in&#237;cio da onda P. Durante o per&#237;odo em que o &#225;trio atua como reservat&#243;rio, a deforma&#231;&#227;o atrial aumenta, atingindo um pico pouco antes da abertura da v&#225;lvula mitral. Durante a fun&#231;&#227;o de conduto, a deforma&#231;&#227;o atrial diminui, com um plat&#244; durante a di&#225;stase e um pico negativo ao final da contra&#231;&#227;o atrial. No painel D, o modo unidimensional curvo mostra que a deforma&#231;&#227;o positiva do teto do &#225;trio &#233; menor (em azul claro) que o de outras paredes (em azul escuro).</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf02-pt.jpg"/></fig>
          <p>A curva de deforma&#231;&#227;o avaliada por E2DST deve seguir a fisiologia do AE. Durante a fun&#231;&#227;o de reservat&#243;rio do AE, que corresponde &#224; contra&#231;&#227;o isovolum&#233;trica, eje&#231;&#227;o e relaxamento isovolum&#233;trico do VE, a deforma&#231;&#227;o do AE aumenta, atingindo o pico m&#225;ximo pouco antes da abertura da v&#225;lvula mitral. Durante a fun&#231;&#227;o de conduto, a deforma&#231;&#227;o do AE diminui, atingindo um pico negativo ao final da contra&#231;&#227;o do AE (<xref ref-type="fig" rid="f11">Figura 3</xref>). Subsequentemente, durante a di&#225;stase, tanto o perfil de D quanto o de TD tornam-se planos, demonstrando que n&#227;o ocorre deforma&#231;&#227;o da parede do AE durante a fase tardia da fun&#231;&#227;o de conduto<xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. Usando as curvas de D e TD globais longitudinais, as fun&#231;&#245;es ativa, passiva e de reservat&#243;rio podem ser assim definidas:</p>
          <fig id="f11">
            <label>Figura 3</label>
            <caption>
              <title>Medida dos par&#226;metros de deforma&#231;&#227;o longitudinal do &#225;trio esquerdo por E2DST. Corte em 2C mostrando a regi&#227;o de interesse e o modo unidimensional curvo criado pelo software (esquerda) e a deforma&#231;&#227;o longitudinal global do &#225;trio esquerdo correspondente (direita). O ponto de refer&#234;ncia foi colocado no in&#237;cio da onda P, permitindo a medida da deforma&#231;&#227;o negativa global &#224; contra&#231;&#227;o atrial m&#225;xima (DGA-) (fun&#231;&#227;o de bomba), deforma&#231;&#227;o global positivo &#224; abertura da v&#225;lvula mitral (DGA+) (fun&#231;&#227;o de conduto), e tamb&#233;m a soma de DGA- e DGA+ (DGTA) (fun&#231;&#227;o de reserva). FVA: Fechamento da v&#225;lvula a&#243;rtica.</title>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf03-pt.jpg"/></fig>
          <list list-type="order">
            <list-item>
              <p>Fun&#231;&#227;o ativa (de bomba):</p>
              <list list-type="bullet">
                <list-item>
                  <p>Deforma&#231;&#227;o global negativa como diferen&#231;a entre a deforma&#231;&#227;o na contra&#231;&#227;o pr&#233;-atrial (ap&#243;s a onda A) e a deforma&#231;&#227;o pouco antes do fechamento da v&#225;lvula mitral (FVM) (DGA-) (<xref ref-type="fig" rid="f11">Figura 3</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>;</p>
                </list-item>
                <list-item>
                  <p>Taxa de deforma&#231;&#227;o global diast&#243;lica tardia (TDGT) (<xref ref-type="fig" rid="f12">Figura 4</xref>)<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
                </list-item>
              </list>
            </list-item>
            <list-item>
              <p>Fun&#231;&#227;o passiva (de conduto):</p>
              <list list-type="bullet">
                <list-item>
                  <p>Deforma&#231;&#227;o global positiva &#224; AVM (DGA+) (<xref ref-type="fig" rid="f11">Figura 3</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>;</p>
                </list-item>
                <list-item>
                  <p>Taxa de deforma&#231;&#227;o global diast&#243;lica negativa precoce (TDGP) (<xref ref-type="fig" rid="f12">Figura 4</xref>)<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
                </list-item>
              </list>
              <p>
                <fig id="f12">
                  <label>Figura 4</label>
                  <caption>
                    <title>Medida de par&#226;metros da taxa de deforma&#231;&#227;o longitudinal do &#225;trio esquerdo por E2DST. Corte 4C mostrando a regi&#227;o de interesse criada pelo software (esquerda) e a taxa de deforma&#231;&#227;o longitudinal global do &#225;trio esquerdo correspondente (direita). TDG+, primeira taxa de deforma&#231;&#227;o positiva no in&#237;cio da s&#237;stole do ventr&#237;culo esquerdo; TTDG+ tempo do in&#237;cio da onda P at&#233; o pico da taxa de deforma&#231;&#227;o positiva; TDGP, taxa de deforma&#231;&#227;o diast&#243;lica precoce; TDGT, taxa de deforma&#231;&#227;o diast&#243;lica tardia.</title>
                  </caption>
                  <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf04-pt.jpg"/></fig>
              </p>
            </list-item>
            <list-item>
              <p>Fun&#231;&#227;o de reservat&#243;rio:</p>
              <list list-type="bullet">
                <list-item>
                  <p>Soma de DGA- e DGA+ (DGTA) (<xref ref-type="fig" rid="f10">Figura 2</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>
										</p>
                </list-item>
                <list-item>
                  <p>Primeira taxa de deforma&#231;&#227;o global positiva no in&#237;cio da s&#237;stole do VE (TDG+) (<xref ref-type="fig" rid="f12">Figura 4</xref>)<xref ref-type="bibr" rid="B06">6</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref>.</p>
                </list-item>
              </list>
            </list-item>
          </list>
          <p>No entanto, diferentes estudos usaram metodologias diversas com base em pontos de refer&#234;ncia distintos do ECG (onda R ou P) para a gera&#231;&#227;o da curva de deforma&#231;&#227;o, o que pode ter gerado valores normais diferentes<xref ref-type="bibr" rid="B06">6</xref><sup>-</sup><xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. Numa popula&#231;&#227;o normal, Saraiva e cols.<xref ref-type="bibr" rid="B07">7</xref> utilizaram a onda P para a gera&#231;&#227;o de curvas de deforma&#231;&#227;o e verificaram que o valor de DGA+ foi de 21,4 &#177; 6,7%; o de DGTA, de 35,6 &#177; 7,9%; e o de DGA-, de -14,2 &#177; 3,3%. Em popula&#231;&#227;o semelhante, Sun e cols.<xref ref-type="bibr" rid="B05">5</xref> usaram a onda R como ponto de refer&#234;ncia e relataram valores completamente diferentes para DGTA+, de 46,8 &#177; 7,7%. Al&#233;m disso, devido a uma transla&#231;&#227;o para cima da curva de deforma&#231;&#227;o usando o m&#233;todo da onda R, encontraram um deforma&#231;&#227;o positiva de 19,6 &#177; 4,2%, interpretada como contra&#231;&#227;o atrial. Os valores normais para os par&#226;metros de TD foram semelhantes nos dois estudos<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B07">7</xref><sup>,</sup><xref ref-type="bibr" rid="B08">8</xref>.</p>
          <p>Levando-se em considera&#231;&#227;o a fisiologia atrial, podemos compreender facilmente que os estudos que utilizam a onda R ignoram a fun&#231;&#227;o de bomba ativa real (pico negativo), e criam uma deforma&#231;&#227;o positiva para esta fun&#231;&#227;o, o que &#233; incompat&#237;vel com as altera&#231;&#245;es fisiol&#243;gicas reais<xref ref-type="bibr" rid="B05">5</xref><sup>,</sup><xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref><sup>,</sup><xref ref-type="bibr" rid="B16">16</xref>. Em contraste com a avalia&#231;&#227;o da deforma&#231;&#227;o do VE, em que a onda R do ECG &#233; usada como ponto de refer&#234;ncia, consideramos que o uso da onda P possibilita a deforma&#231;&#227;o global negativa do AE, que corresponde &#224; fun&#231;&#227;o contr&#225;til real do AE.</p>
          <p>Nossa experi&#234;ncia mostrou que o m&#233;todo da onda R, em compara&#231;&#227;o ao m&#233;todo da onda P, forneceu um valor positivo n&#227;o fisiol&#243;gico para a fun&#231;&#227;o ativa do AE, ao passo que as fun&#231;&#245;es de conduto e de reservat&#243;rio (DGA-, DGTA) foram significativamente superestimadas (<xref ref-type="fig" rid="f13">Figura 5</xref>)<xref ref-type="bibr" rid="B20">20</xref>. Esses achados sugerem que a diferen&#231;a entre os m&#233;todos n&#227;o condiz com uma simples transla&#231;&#227;o para cima da curva de deforma&#231;&#227;o, como foi anteriormente sugerido por Cameli e cols.<xref ref-type="bibr" rid="B09">9</xref><sup>,</sup><xref ref-type="bibr" rid="B12">12</xref>.</p>
          <fig id="f13">
            <label>Figura 5</label>
            <caption>
              <title>Compara&#231;&#227;o entre os m&#233;todos da onda P e onda R para a fun&#231;&#227;o f&#225;sica do AE. Corte 4C mostrando a regi&#227;o de interesse (RDI) (esquerda) e as curvas de deforma&#231;&#227;o do AE correspondentes (direita). As curvas tracejadas representam as deforma&#231;&#245;es longitudinais globais atriais m&#233;dias durante o ciclo card&#237;aco. O ponto de refer&#234;ncia foi colocado no in&#237;cio da onda P (painel A) e da onda R (painel B). FVM: Fechamento da v&#225;lvula mitral; FVA: Fechamento da v&#225;lvula a&#243;rtica; AVM: Abertura da v&#225;lvula mitral.</title>
              <p>Painel A - Medida da deforma&#231;&#227;o global negativa da contra&#231;&#227;o atrial (DGA-), deforma&#231;&#227;o global positiva &#224; AVM (DGA+), e deforma&#231;&#227;o total (DGTA) como soma de DGA- e DGA+. S&#227;o mostradas as fun&#231;&#245;es de bomba (AC), reservat&#243;rio e conduto. No painel inferior &#224; esquerda, h&#225; um delineamento claro da fun&#231;&#227;o de bomba (vermelho) e de reservat&#243;rio (azul) do AE, com perfil em modo unidimensional curvo.</p>
              <p>Painel B - Medida da deforma&#231;&#227;o global positiva total &#224; AVM (DGTA) (reservat&#243;rio), e deforma&#231;&#227;o global positivo tardia (DGTC) &#224; contra&#231;&#227;o atrial. H&#225; uma deforma&#231;&#227;o positiva para a fun&#231;&#227;o de bomba atrial usando este m&#233;todo. A fun&#231;&#227;o de conduto &#233; definida como a diferen&#231;a entre DGTA e DGAC. No painel inferior esquerdo n&#227;o h&#225; nenhum delineamento para a contra&#231;&#227;o do AE e fun&#231;&#227;o de reservat&#243;rio (todo azul), com perfil em modo unidimensional curvo.</p>
            </caption>
            <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf05-pt.jpg"/></fig>
          <p>As diretrizes recomendam que a onda R seja utilizada como marco temporal para a an&#225;lise da deforma&#231;&#227;o do VE, a fim de gerar corretamente a deforma&#231;&#227;o negativa m&#225;xima durante a fase de contra&#231;&#227;o. Uma vez que ap&#243;s a contra&#231;&#227;o do AE o comprimento do AE &#233; menor que antes da contra&#231;&#227;o, o valor da deforma&#231;&#227;o da contra&#231;&#227;o do AE tem que ser negativo. Isto reflete melhor os princ&#237;pios verdadeiros da deforma&#231;&#227;o, segundo os quais n&#227;o apenas a magnitude que representa a deforma&#231;&#227;o, mas tamb&#233;m a dire&#231;&#227;o da deforma&#231;&#227;o &#233; importante. Sugerimos que, com o uso da onda P como ponto de refer&#234;ncia, pode-se estimar corretamente as fun&#231;&#245;es do AE<xref ref-type="bibr" rid="B20">20</xref>.</p>
          <p>Para padronizar a deforma&#231;&#227;o do AE, devem ser considerados outros ajustes, como um ganho adequado e a RDI. Em primeiro lugar, ajustes de ganho baixos eliminam artificialmente estruturas anat&#244;micas. Por outro lado, com ganho excessivo h&#225; uma redu&#231;&#227;o da resolu&#231;&#227;o.</p>
          <p>Em nossa experi&#234;ncia, aumentar o ganho do m&#237;nimo para o m&#225;ximo leva &#224; superestimativa de todas as fun&#231;&#245;es do AE.</p>
          <p>Altera&#231;&#245;es intermedi&#225;rias n&#227;o produziram impacto significativo nas fun&#231;&#245;es ativa e de conduto, mas sim na de reservat&#243;rio<xref ref-type="bibr" rid="B20">20</xref>, o que &#233; muito importante, uma vez que muitos estudos se concentram na fun&#231;&#227;o de reservat&#243;rio e sua correla&#231;&#227;o com as fun&#231;&#245;es sist&#243;lica e diast&#243;lica do VE<xref ref-type="bibr" rid="B21">21</xref><sup>-</sup><xref ref-type="bibr" rid="B24">24</xref>. Em segundo lugar, diminuir a largura da RDI reduz os valores da deforma&#231;&#227;o do AE, provavelmente por contamina&#231;&#227;o de estruturas adjacentes. Levando-se em considera&#231;&#227;o a anatomia do AE, RDIs maiores podem ser usados por engano apenas se o ganho inicial ou p&#243;s-processamento forem muito altos. Uma vez que as paredes do AE s&#227;o muito finas, deve-se usar uma RDI m&#237;nima<xref ref-type="bibr" rid="B20">20</xref><sup>,</sup><xref ref-type="bibr" rid="B21">21</xref>. Devem tamb&#233;m ser consideradas a dificuldade potencial de obter com precis&#227;o a regi&#227;o de interesse pr&#243;xima o suficiente da forma do AE real e o risco de contamina&#231;&#227;o por componentes do sinal provenientes de estruturas adjacentes ao AE<xref ref-type="bibr" rid="B20">20</xref><sup>-</sup><xref ref-type="bibr" rid="B24">24</xref>.</p>
          <p>Concluindo, sugerimos o uso de um ganho m&#233;dio e de uma RDI m&#237;nima como a melhor escolha para a avalia&#231;&#227;o padr&#227;o da deforma&#231;&#227;o do AE.</p>
        </sec>
        <sec>
          <title>Aplica&#231;&#245;es cl&#237;nicas dos par&#226;metros de deforma&#231;&#227;o do &#225;trio esquerdo</title>
          <sec>
            <title>Popula&#231;&#227;o geral</title>
            <p>O tamanho do AE tem-se mostrado um marcador progn&#243;stico de eventos cardiovasculares adversos na popula&#231;&#227;o geral<xref ref-type="bibr" rid="B25">25</xref><sup>-</sup><xref ref-type="bibr" rid="B28">28</xref>. Enquanto alguns estudos enfatizam o papel tanto do &#237;ndice de volume do AE (VAEi) quanto o da disfun&#231;&#227;o diast&#243;lica do VE como fatores preditivos independentes de eventos cardiovasculares<xref ref-type="bibr" rid="B29">29</xref><sup>,</sup><xref ref-type="bibr" rid="B30">30</xref>, outros duvidam de que o VAEi seja capaz de predizer mortalidade por todas as causas, independentemente do grau de disfun&#231;&#227;o diast&#243;lica do VE<xref ref-type="bibr" rid="B31">31</xref>. Mais recentemente, num estudo baseado em uma popula&#231;&#227;o geral, a fra&#231;&#227;o de esvaziamento do AE (FEAE) mostrou-se independentemente associada &#224; mortalidade<xref ref-type="bibr" rid="B32">32</xref> e ao desenvolvimento de fibrila&#231;&#227;o atrial (FA) ou flutter em indiv&#237;duos &#8805; 65 anos<xref ref-type="bibr" rid="B33">33</xref>. Outros estudos sugeriram que a fun&#231;&#227;o de bomba do AE tamb&#233;m &#233; capaz de identificar indiv&#237;duos com maior risco cardiovascular na popula&#231;&#227;o<xref ref-type="bibr" rid="B34">34</xref><sup>,</sup><xref ref-type="bibr" rid="B35">35</xref>, e que o VAE m&#237;nimo pode ser um marcador progn&#243;stico importante<xref ref-type="bibr" rid="B36">36</xref><sup>,</sup><xref ref-type="bibr" rid="B37">37</xref>. Para identificar o valor adicional da an&#225;lise da deforma&#231;&#227;o do AE por E2DST como marcador de risco cardiovascular em compara&#231;&#227;o com o VAEi ou a FEAE, Cameli e cols.<xref ref-type="bibr" rid="B38">38</xref> avaliaram prospectivamente 312 adultos com mais de 50 anos de idade e mostraram que a deforma&#231;&#227;o positiva global, usando o m&#233;todo da onda R e um modelo de 12 segmentos do AE, &#233; um fator preditivo forte e independente de eventos cardiovasculares superior aos par&#226;metros convencionais da an&#225;lise do AE<xref ref-type="bibr" rid="B38">38</xref>.</p>
          </sec>
          <sec>
            <title>Fibrila&#231;&#227;o atrial</title>
            <p>Os pacientes com FA apresentam remodelamento do AE tanto el&#233;trico quanto morfol&#243;gico. A fibrose intersticial &#233; uma das altera&#231;&#245;es morfol&#243;gicas principais em pacientes portadores de FA, e fibrose extensa do AE mostrou-se associada ao comprometimento da fun&#231;&#227;o do AE. Os par&#226;metros de deforma&#231;&#227;o do AE est&#227;o diminu&#237;dos em pacientes portadores de FA n&#227;o valvular (<xref ref-type="fig" rid="f14">Figura 6</xref>) em compara&#231;&#227;o com indiv&#237;duos normais<xref ref-type="bibr" rid="B39">39</xref><sup>,</sup><xref ref-type="bibr" rid="B40">40</xref>. Foi mostrada correla&#231;&#227;o inversa entre o grau de fibrose do AE determinado por RM e deforma&#231;&#227;o do AE e TD determinadas por exame de imagem com velocidade vetorial<xref ref-type="bibr" rid="B41">41</xref>.</p>
            <fig id="f14">
              <label>Figura 6</label>
              <caption>
                <title>Compara&#231;&#227;o entre a deforma&#231;&#227;o do &#225;trio esquerdo em um paciente portador de fibrila&#231;&#227;o atrial recorrente (painel A) e em um indiv&#237;duo normal (painel B).</title>
                <p>A deforma&#231;&#227;o m&#233;dia (linha pontilhada) est&#225; pronunciadamente reduzida no paciente com fibrila&#231;&#227;o atrial recorrente durante a fun&#231;&#227;o de bomba (DGA-) (-3% versus -15%), durante a fun&#231;&#227;o de conduto (DGA+) (9% versus 18%), e durante a fun&#231;&#227;o de reservat&#243;rio (DGTA) (13% versus 33%). Tamb&#233;m h&#225; completa dissincronia da contra&#231;&#227;o e relaxamento entre os segmentos atriais esquerdos no paciente portador de fibrila&#231;&#227;o atrial em compara&#231;&#227;o com um indiv&#237;duo normal.</p>
              </caption>
              <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf06-pt.jpg"/></fig>
            <p>Diferentes estudos mostraram que a deforma&#231;&#227;o do AE prediz o risco de eventos cardiovasculares ou o sucesso no reestabelecimento do ritmo sinusal ap&#243;s cardiovers&#227;o el&#233;trica ou procedimentos de abla&#231;&#227;o em pacientes portadores de FA, al&#233;m do risco de recorr&#234;ncia de FA ap&#243;s cardiovers&#227;o bem-sucedida<xref ref-type="bibr" rid="B40">40</xref><sup>,</sup><xref ref-type="bibr" rid="B42">42</xref><sup>,</sup><xref ref-type="bibr" rid="B43">43</xref>. Assim, no estudo de Saha e cols.<xref ref-type="bibr" rid="B39">39</xref>, os valores de DGTA e FEAE mostraram-se diminu&#237;dos, e DGTA foi o &#250;nico &#237;ndice associado a uma maior chance de escore de CHADS2 &#8805; 2. Al&#233;m disso, a deforma&#231;&#227;o do reservat&#243;rio do AE apresentou-se como valor adicional ao escore de CHADS2 na predi&#231;&#227;o de morte ou hospitaliza&#231;&#227;o<xref ref-type="bibr" rid="B39">39</xref>. Outro estudo mostrou uma redu&#231;&#227;o da DGA- e DGA+ em pacientes portadores de FA parox&#237;stica e um escore de CHADS2 &#8804; 1 antes do primeiro AVC em compara&#231;&#227;o com controles pareados por idade e sexo, portadores de FA parox&#237;stica e sem antecedente de AVC. Al&#233;m disso, houve associa&#231;&#227;o significativa entre DGA- e AVC. Esses resultados sugerem que a deforma&#231;&#227;o do AE pode auxiliar na decis&#227;o por anticoagula&#231;&#227;o oral neste grupo de pacientes<xref ref-type="bibr" rid="B44">44</xref>.</p>
            <p>Shih e cols.<xref ref-type="bibr" rid="B45">45</xref> mostraram que a deforma&#231;&#227;o do AE durante o enchimento atrial e a TD durante a fase de reservat&#243;rio estavam diminu&#237;das em pacientes com FA e AVC, e estavam independentemente associados a AVC. Outro estudo mostrou que embora DGA+ n&#227;o fosse fator preditivo de recorr&#234;ncia de FA em pacientes que necessitaram de cardiovers&#227;o, a mudan&#231;a no pico da deforma&#231;&#227;o positiva do AE foi significativamente maior nos indiv&#237;duos que mantiveram ritmo sinusal<xref ref-type="bibr" rid="B46">46</xref>. A falta de poder preditivo pode estar relacionada apenas ao pequeno tamanho amostral. Mais recentemente, demonstrou-se que anormalidades no momento de deforma&#231;&#227;o atrial predizem recorr&#234;ncia de FA ap&#243;s cardiovers&#227;o<xref ref-type="bibr" rid="B47">47</xref><sup>,</sup><xref ref-type="bibr" rid="B48">48</xref>. Assim, em pacientes encaminhados para cardiovers&#227;o por FA, o desvio padr&#227;o do tempo at&#233; a deforma&#231;&#227;o de pico utilizando um modelo de seis segmentos do AE foi um fator preditivo independente de recorr&#234;ncia de FA<xref ref-type="bibr" rid="B47">47</xref>. Foram publicados resultados semelhantes ap&#243;s procedimentos de abla&#231;&#227;o por cateter para FA<xref ref-type="bibr" rid="B49">49</xref>.</p>
            <p>A deforma&#231;&#227;o do AE est&#225; diminu&#237;da em miocardiopatias hipertr&#243;ficas (MCH) em compara&#231;&#227;o a controles h&#237;gidos (<xref ref-type="fig" rid="f15">Figura 7</xref>) bem como em compara&#231;&#227;o a pacientes portadores de hipertrofia do VE secund&#225;ria &#224; hipertens&#227;o<xref ref-type="bibr" rid="B22">22</xref><sup>,</sup><xref ref-type="bibr" rid="B24">24</xref>. Al&#233;m disso, em outro estudo, foi sugerido que a deforma&#231;&#227;o do AE pode apresentar um valor adicional sobre par&#226;metros convencionais como VAEi, raz&#227;o E/A e E/E' na diferencia&#231;&#227;o de MCH de outros tipos de hipertrofia, com valor de corte de -10,8% para a fun&#231;&#227;o de bomba<xref ref-type="bibr" rid="B22">22</xref>. Enquanto isso, Rosca e cols.<xref ref-type="bibr" rid="B02">2</xref> mostraram que a fun&#231;&#227;o de bomba do AE, avaliada apenas a partir de curvas de TD, &#233; um determinante independente de sintomas de insufici&#234;ncia card&#237;aca em pacientes portadores de MCH.</p>
            <fig id="f15">
              <label>Figura 7</label>
              <caption>
                <title>Compara&#231;&#227;o entre a deforma&#231;&#227;o do &#225;trio esquerdo em paciente portador de miocardiopatia hipertr&#243;fica (painel A) e um indiv&#237;duo normal (painel B).</title>
                <p>Deforma&#231;&#227;o m&#233;dia marcadamente reduzida em paciente portador de miocardiopatia hipertr&#243;fica durante a fun&#231;&#227;o de bomba (DGA-) (-4% versus -10%), durante a fase de conduto (GDA+) (8% versus 26%) e durante a fase de reservat&#243;rio (DGTA) (12% versus 36%).</p>
              </caption>
              <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf07-pt.jpg"/></fig>
            <p>Em pacientes com amiloidose card&#237;aca, tamb&#233;m &#233; comum a disfun&#231;&#227;o do AE. Em um estudo usando Doppler tecidual, a deforma&#231;&#227;o sist&#243;lica do AE de pico e a TD foram menores em pacientes com amiloidose card&#237;aca do que naqueles com disfun&#231;&#227;o diast&#243;lica do VE de outras causas, sugerindo que o Doppler tecidual pode ser usado para detectar altera&#231;&#245;es sutis na fun&#231;&#227;o do AE nesses pacientes<xref ref-type="bibr" rid="B50">50</xref>. Outro estudo usando EST confirmou que a disfun&#231;&#227;o do AE &#233; um componente comum da amiloidose, mesmo na aus&#234;ncia de padr&#245;es ecocardiogr&#225;ficos tradicionais. Assim, TDGT e DGA- foram significativamente menores no grupo com amiloidose em compara&#231;&#227;o com o grupo controle, sugerindo que a avalia&#231;&#227;o da deforma&#231;&#227;o do AE &#233; capaz de detectar diferen&#231;as sutis na fun&#231;&#227;o do AE n&#227;o identificadas pela maioria dos par&#226;metros convencionais. Portanto, parece que a amiloidose afeta a fun&#231;&#227;o do AE ainda mais al&#233;m da disfun&#231;&#227;o secund&#225;ria &#224; disfun&#231;&#227;o diast&#243;lica do VE<xref ref-type="bibr" rid="B51">51</xref>.</p>
            <p>Em pacientes portadores de miocardiopatia dilatada (MCD), a fun&#231;&#227;o do AE avaliada por EST mostrou-se severamente alterada na forma idiop&#225;tica em compara&#231;&#227;o com a forma isqu&#234;mica. Em um estudo em 314 pacientes, a deforma&#231;&#227;o sist&#243;lica do AE de pico mostrou-se significativamente reduzida em MCD idiop&#225;tica em compara&#231;&#227;o &#224; MCD isqu&#234;mica<xref ref-type="bibr" rid="B11">11</xref>. Entretanto, esse estudo usou o m&#233;todo da onda R para a gera&#231;&#227;o das curvas de deforma&#231;&#227;o, e o que foi definido como "deforma&#231;&#227;o sist&#243;lica do AE de pico" era, na verdade, a fun&#231;&#227;o de reservat&#243;rio do AE (DGTA). Outro estudo recente investigou a import&#226;ncia da reserva funcional do AE durante ecocardiografia de estresse por dobutamina (EED) em pacientes com depress&#227;o da fun&#231;&#227;o sist&#243;lica do VE<xref ref-type="bibr" rid="B52">52</xref>. Os autores conclu&#237;ram que a avalia&#231;&#227;o do reservat&#243;rio do AE e da fun&#231;&#227;o de esvaziamento passivo durante EED fornece um valor adicional importante sobre par&#226;metros cl&#237;nicos e ecocardiogr&#225;ficos padr&#227;o na predi&#231;&#227;o de eventos cardiovasculares em MCD, uma vez que uma reserva funcional do AE diminu&#237;da se mostrou associada a uma taxa de eventos cardiovasculares mais alta<xref ref-type="bibr" rid="B52">52</xref>. Em outro estudo, em pacientes com insufici&#234;ncia card&#237;aca, a DGTA mostrou boa correla&#231;&#227;o com a press&#227;o capilar pulmonar (r = -0,81, p &lt; 0,0001), fornecendo uma estimativa melhor da press&#227;o de enchimento do VE (ASC = 0,93) do que a raz&#227;o E/E' <xref ref-type="bibr" rid="B12">12</xref>.</p>
            <p>A an&#225;lise da deforma&#231;&#227;o do AE por EST pode revelar informa&#231;&#245;es relevantes em pacientes com MCD, candidatos a terapia de ressincroniza&#231;&#227;o card&#237;aca (TRC). Um estudo incluindo 90 pacientes com MCD tanto de etiologia idiop&#225;tica quanto isqu&#234;mica confirmou que a fun&#231;&#227;o sist&#243;lica do AE (DGA-) est&#225; consideravelmente mais comprometida em pacientes portadores da forma idiop&#225;tica do que da isqu&#234;mica. Al&#233;m disso, os pacientes com MCD isqu&#234;mica que responderam &#224; TRC tiveram mais chance de apresentar melhora da fun&#231;&#227;o do AE ap&#243;s a ressincroniza&#231;&#227;o (<xref ref-type="fig" rid="f16">Figura 8</xref>). De fato, os &#250;nicos determinantes independentes da recupera&#231;&#227;o funcional do AE ap&#243;s TRC foram a resposta positiva &#224; TRC e etiologia isqu&#234;mica de MCD<xref ref-type="bibr" rid="B53">53</xref>. Outro estudo usando Doppler tecidual mostrou que, em pacientes com insufici&#234;ncia card&#237;aca e TRC, a deforma&#231;&#227;o atrial foi maior no &#225;trio direito, septo interatrial e &#225;trio esquerdo no modo de detec&#231;&#227;o atrial em compara&#231;&#227;o com o modo de estimula&#231;&#227;o atrial<xref ref-type="bibr" rid="B54">54</xref>. Esse estudo enfatizou que apesar de n&#227;o haver diferen&#231;a na dissincronia intraventricular, os pacientes com modo de detec&#231;&#227;o atrial apresentavam dissincronia atrial significativamente menor, o que contribu&#237;a para um melhor desempenho do VE ap&#243;s TRC.</p>
            <fig id="f16">
              <label>Figura 8</label>
              <caption>
                <title>Compara&#231;&#227;o entre a deforma&#231;&#227;o do &#225;trio esquerdo em paciente portador de miocardiopatia dilatada idiop&#225;tica antes (painel A) e depois (painel B) de terapia de ressincroniza&#231;&#227;o card&#237;aca (TRC). A deforma&#231;&#227;o m&#233;dia mostra-se marcadamente mais diminu&#237;da antes do que depois da TRC durante a fun&#231;&#227;o de bomba (DGA-) (- 5,1% versus -9%), durante a fun&#231;&#227;o de conduto (DGA+) (2,4 versus 5%) e tamb&#233;m durante a fun&#231;&#227;o de reservat&#243;rio (DGTA) (7,5% versus 14%). Foi observada melhora significativa da sincronia atrial tanto para a fun&#231;&#227;o de bomba, quanto para a de reservat&#243;rio ap&#243;s TRC (painel B), em compara&#231;&#227;o a um padr&#227;o de deforma&#231;&#227;o completamente desorganizado antes da TRC (painel A).</title>
              </caption>
              <graphic xlink:href="1678-4170-abc-105-06-0625-50144-gf08-pt.jpg"/></fig>
          </sec>
          <sec>
            <title>Doen&#231;a card&#237;aca isqu&#234;mica</title>
            <p>A disfun&#231;&#227;o do AE tamb&#233;m &#233; comum ap&#243;s infarto agudo do mioc&#225;rdio. Em um estudo de 320 pacientes avaliados por EST 48 horas ap&#243;s interna&#231;&#227;o por infarto agudo do mioc&#225;rdio, a deforma&#231;&#227;o do reservat&#243;rio do AE (DGTA) e o VAEi m&#225;ximo foram fatores preditivos independentes de mortalidade por todas as causas, reinfarto e reinterna&#231;&#227;o por insufici&#234;ncia card&#237;aca cr&#244;nica ap&#243;s ajuste para par&#226;metros cl&#237;nicos e outros par&#226;metros ecocardiogr&#225;ficos<xref ref-type="bibr" rid="B55">55</xref>. Por outro lado, em um estudo de 843 pacientes com infarto do mioc&#225;rdio, a DGTA medida dentro de 48 horas ap&#243;s interna&#231;&#227;o mostrou-se significativamente associada ao desfecho composto de insufici&#234;ncia card&#237;aca e &#243;bito, mas n&#227;o conseguiu predizer este desfecho ap&#243;s ajuste (para idade, deforma&#231;&#227;o global longitudinal do VE, e VAEi m&#225;ximo). Esse estudo sugeriu que a deforma&#231;&#227;o do AE nesses pacientes &#233; dependente da deforma&#231;&#227;o longitudinal global do VE e do tamanho do AE e, portanto, o valor progn&#243;stico adicional da fun&#231;&#227;o de reservat&#243;rio do AE em pacientes com comprometimento da fun&#231;&#227;o longitudinal do VE &#233; discut&#237;vel<xref ref-type="bibr" rid="B56">56</xref>.</p>
          </sec>
          <sec>
            <title>Valvopatias</title>
            <p>Aumento do AE e comprometimento da fun&#231;&#227;o do AE resultante de sobrecarga de volume ou press&#227;o s&#227;o frequentes em estenose a&#243;rtica (EA) e insufici&#234;ncia mitral (IM) cr&#244;nica.</p>
            <p>O tamanho do AE mostrou-se um bom fator preditivo de desfecho em IM prim&#225;ria: um di&#226;metro de AE maior que 55 mm mostrou-se associado a uma taxa de sobreviv&#234;ncia menor em 8 anos, enquanto que um volume de AE maior que 60 mL/m<sup>2</sup> mostrou-se associado a um aumento da mortalidade e de eventos card&#237;acos (FA e insufici&#234;ncia card&#237;aca). Entretanto, h&#225; poucos dados publicados sobre a fun&#231;&#227;o do AE avaliada por EST e seu papel progn&#243;stico em IM prim&#225;ria. Estudo recente em 121 pacientes portadores de IM grave relatou disfun&#231;&#227;o significativa da bomba e reservat&#243;rio do AE, que foram mais pronunciadas em pacientes que j&#225; tinham indica&#231;&#227;o de cirurgia. De todos os &#237;ndices de fun&#231;&#227;o do AE, a deforma&#231;&#227;o do reservat&#243;rio do AE apresentou a maior precis&#227;o na identifica&#231;&#227;o de pacientes com indica&#231;&#227;o para cirurgia de v&#225;lvula mitral. Al&#233;m disso, ap&#243;s a cirurgia de v&#225;lvula mitral, os pacientes com deforma&#231;&#227;o do reservat&#243;rio do AE &#8804; 24% apresentaram menor sobreviv&#234;ncia ap&#243;s um seguimento mediano de 6,4 anos, independentemente da sintomatologia antes da cirurgia<xref ref-type="bibr" rid="B57">57</xref>. Mais uma vez, isto enfatiza a import&#226;ncia de uma correta avalia&#231;&#227;o da deforma&#231;&#227;o do reservat&#243;rio do AE.</p>
            <p>Uma fun&#231;&#227;o de bomba atrial preservada &#233; importante para a manuten&#231;&#227;o do d&#233;bito card&#237;aco em pacientes com estenose a&#243;rtica (EA) grave. Em pacientes com EA grave, todas as fun&#231;&#245;es atriais (reservat&#243;rio, conduto e bomba) mostraram-se comprometidas em compara&#231;&#227;o com controles pareados<xref ref-type="bibr" rid="B58">58</xref>. Como esperado, a disfun&#231;&#227;o do reservat&#243;rio do AE mostrou-se relacionada &#224;s press&#245;es de enchimento do VE, enquanto que a disfun&#231;&#227;o de conduto do AE dependeu do grau de comprometimento do relaxamento do VE<xref ref-type="bibr" rid="B58">58</xref>. Outro estudo recente investigou o papel da fun&#231;&#227;o do AE avaliada por EST como fator preditivo de FA p&#243;s-operat&#243;ria em pacientes com EA grave submetidos a cirurgia convencional. TDGT foi o &#250;nico fator preditivo independente de FA p&#243;s-operat&#243;ria, sugerindo seu papel na estratifica&#231;&#227;o de risco de pacientes com EA grave<xref ref-type="bibr" rid="B59">59</xref>.</p>
          </sec>
        </sec>
      </sec>
      <sec sec-type="conclusions">
        <title>Conclus&#245;es</title>
        <p>A avalia&#231;&#227;o da deforma&#231;&#227;o do AE por ecocardiografia bidimensional com <italic>speckle tracking</italic> pode representar uma t&#233;cnica r&#225;pida e f&#225;cil na explora&#231;&#227;o da fun&#231;&#227;o do AE. Esses novos par&#226;metros da fun&#231;&#227;o atrial s&#227;o mais sens&#237;veis que os &#237;ndices tradicionais de fun&#231;&#227;o atrial e podem ser incorporados &#224; avalia&#231;&#227;o de rotina de v&#225;rias cardiopatias como fibrila&#231;&#227;o atrial, miocardiopatia hipertr&#243;fica e dilatada, doen&#231;a card&#237;aca isqu&#234;mica, e valvopatias. Sugerimos que uma padroniza&#231;&#227;o metodol&#243;gica &#233; essencial para introduzir a an&#225;lise da deforma&#231;&#227;o do AE na pr&#225;tica cl&#237;nica. A fim de definir os valores normais e de corte para o diagn&#243;stico e progn&#243;stico em diferentes doen&#231;as, sugerimos o uso do m&#233;todo da onda P para a gera&#231;&#227;o da curva de deforma&#231;&#227;o. Esse m&#233;todo permite uma avalia&#231;&#227;o completa de todas as fun&#231;&#245;es do AE: de bomba, conduto passivo e reservat&#243;rio. O ganho deve ser ajustado na faixa m&#233;dia, e a RDI, no n&#237;vel m&#237;nimo. Est&#225; indicado um modelo de 15 segmentos para uma avalia&#231;&#227;o completa da deforma&#231;&#227;o do AE, porque esse modelo incorpora todos os segmentos dispon&#237;veis e tem o potencial de criar um mapa real da ativa&#231;&#227;o eletromec&#226;nica do AE.</p>
      </sec>
    </body>
    <back>
      <fn-group>
        <fn fn-type="supported-by">
          <p>
            <bold>Fontes de financiamento</bold>
          </p>
          <p>O presente estudo foi parcialmente financiado pelo Programa Operacional Setorial Desenvolvimento de Recursos Humanos (<italic>Sectorial Operational Programme Human Resources Development</italic> - SOPHRD) e CNCS &#8211; UEFISCDI.</p>
        </fn>
        <fn fn-type="other">
          <p>
            <bold>Vincula&#231;&#227;o acad&#234;mica</bold>
          </p>
          <p>N&#227;o h&#225; vincula&#231;&#227;o deste estudo a programas de p&#243;s&#8209;gradua&#231;&#227;o.</p>
        </fn>
      </fn-group>
    </back>
  </sub-article>
</article>
