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Atrioventricular plane displacement during low dose dobutamine infusion predicts recovery of left ventricular dyssynergies
  1. ATHANASIOS KRANIDIS,
  2. GERASIMOS FILIPPATOS,
  3. KOSTAS KAPPOS,
  4. LAMBROS ANTHOPOULOS
  1. First Department of Cardiology,
  2. Evangelismos Hospital,
  3. Athens, Greece

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    Sir,—We read with interest the study by Willenheimer et al regarding the prognostic significance of left atrioventricular plane displacement (AVPD) in patients with heart failure.1 This study showed that mortality in patients with heart failure is strongly related to systolic left atrioventricular plane motion. The movement of the left atrioventricular plane is a result of the longitudinal shortening of left ventricular fibres. During systole, the contraction of the longitudinal fibres of the left ventricle leads to a descent of the atrioventricular plane towards the relatively immobile cardiac apex. It should not be forgotten that assessment of left ventricular systolic function by cross sectional echocardiography is sometimes difficult because endocardium is inadequately visualised, especially in the elderly. In contrast, the mitral ring is distinctly outlined and easily studied by m mode recording,2-4 and, as it was related to mortality in cardiac failure patients,m mode echocardiography was recommended for general use.1

    Willenheimer et al proposed further studies of the effects of different drugs on systolic AVPD. We recently assessed the value of left AVPD during low dose dobutamine infusion to predict functional improvement of asynergic infarcted myocardial areas after revascularisation in patients with heart failure caused by ischaemic heart disease.5 In healthy subjects we found a significant increase of left AVPD at all four recorded sites (septal, lateral, anterior, and inferior walls of the left ventricle) after dobutamine infusion. Patients also had a significant increase of left systolic AVPD during dobutamine infusion, but only in the dyssynergic sites with functional improvement after revascularisation. In the dyssynergic areas without functional improvement left AVPD did not change. Selecting a maximum left AVPD increase of more than 2 mm at any site of the left ventricle to predict recovery of the regional dyssynergies resulted in a sensitivity of 91%, specificity of 83%, positive predictive value of 88%, and negative predictive value of 87%. Willenheimer et al found that mortality in patients with heart failure is related to systolic AVPD. We found that assessment of left systolic AVPD during low dose dobutamine infusion predicted left ventricular dyssynergy recovery after revascularisation in patients with heart failure caused by ischaemic heart disease.

    References

    This letter was shown to the authors, who reply as follows:

    We read with great interest the letter by Kranidiset al concerning their study on the value of AVPD in predicting functional recovery following revascularisation of akinetic/dyskinetic myocardium.1-1 These findings add further to the knowledge about the nature of AVPD.

    Why is AVPD improved in response to dobutamine infusion? The most obvious answer seems to be that dobutamine improves contractility of hibernating subendocardial fibres. In addition, improved diastolic function may play a role. In 54 patients with heart failure we found a clear relation between reduced AVPD and impaired transmitral Doppler indices of left ventricular diastolic function, especially a short deceleration time of early diastolic flow (Willenheimeret al, unpublished data). In patients with similar fractional shortening—that is, contractility in circumferential fibres, AVPD was lower in those with more compromised diastolic function. We believe that our results indicate that impaired myocardial diastolic properties result in decreased long axis lengthening. Consequently, because the long axis shortening must equal the lengthening, AVPD is reduced; concurrently, diastolic transmitral flow is disturbed. Diastolic dysfunction might thus be the primary cause of impaired AVPD.

    Our findings are somewhat supported by those of Henein and Gibson.1-2 They suggested that, because of a primarily disturbed long axis function, incoordination between long and short axis function can result in asynchrony of left ventricular diastolic function and associated filling abnormalities. An increased AVPD in response to dobutamine stimulation may thus, at least partly, be the result of improved diastolic function, which may coincide with improved contractility of circumferential fibres.

    An interesting finding in the study by Kranidis et al was that the regional (septal, lateral, inferoposterior, and anterior) AVPD increase during dobutamine infusion corresponded to the areas of functional recovery following revascularisation.1-1Alam et al found that, following exercise, regions of decreased AVPD corresponded to areas of reversible ischaemia on thallium scan.1-3 Furthermore, Höglundet al found that regional AVPD at rest was decreased corresponding to the site of first time acute Q wave myocardial infarction.1-4 These findings support a connection between regional AVPD and an area of ischaemic,1-3 hibernating,1-1 or infarcted1-4 myocardium. In contrast, in 173 patients with coronary artery disease undergoing coronary angiography, regional AVPD at rest was not related to areas of coronary artery stenosis or areas of prior myocardial infarction, although AVPD was decreased corresponding to the degree and extent of coronary artery disease (Willenheimer et al, unpublished data).

    The time elapsed between the ischaemic event and the assessment of AVPD may explain these contrasting findings. Short term alterations in the functional status of subendocardial, longitudinal fibres (in response to ischaemia or dobutamine infusion) may cause corresponding regional changes in AVPD. However, changes in functional status may, after some time, lead to an interdependence between longitudinal and circumferential fibres, smoothing out regional contractility differences, thus causing a more generalised decrease in AVPD. This hypothesis might not only explain the differences between our findings at rest and the findings by Kranidis et aland Alam et al using stress echocardiography,1-1 1-3 but also the different findings by us and Höglund et al in the resting situation.1-4 In the latter study, patients were examined shortly after an acute Q wave myocardial infarction, whereas most patients in our study were examined a longer time after a major ischaemic event.

    The nature of AVPD is still largely unknown and somewhat confusing. Future research in this field will hopefully provide important insight into systolic and diastolic left ventricular function.

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