Systolic left ventricular long axis function during dobutamine stress echocardiography

K.P Bouki1, T.P Kakavas1 and A.I Kranidis2

1 General Hospital of Nikea, Pireaus, Greece
2 "Evaggelismos" General Hospital, Athens, Greece

We read with great interest the study by Mishra, Lythall, and Chambers,1 concerning systolic left ventricular long axis function during dobutamine stress echocardiography (DSE) as a quantitative adjunct to wall motion analysis for the detection of myocardial ischaemia, as well as the editorial by Henein and Gibson.2 We do concur with the conclusions of the original study and the thoughtful comments of the editorial. However, we want to mention that we have already reported, in an earlier study,3 the accuracy of the systolic long axis function during DSE, for identification of myocardial viability after revascularization, which escaped the attention of the authors.

In that series,3 we have shown, in a cohort of 30 patients with resting left ventricular wall motion abnormalities, that an increase >2 mm in the amplitude of long axis shortening on any side of the mitral annulus, predicts recovery of regional ventricular dyssynergies with a sensitivity of 91% and a specificity of 83%. When wall motion analysis was used for the detection of reversible dysfunction, sensitivity and specificity were found to be 81.5% and 87.5%, respectively. When the two methods were in agreement, the positive and negative predictive values were 100% and 84.2%, respectively.

In another very recent study of ours,4 we examined the response of long axis function during DSE in 10 healthy subjects and in 47 patients with severe left ventricular dysfunction of unknown cause and we estimated the diagnostic value of this parameter to identify the ischemic or non-ischemic origin of the disease. Healthy volunteers showed a significant increase in the amplitude of mean long axis shortening (LAS) from baseline to low and peak dobutamine dose (from 13.8±1.5 mm to 16.1±2.1 mm and 17.6±2.7 mm respectively, P=0.002 compared to baseline, ANOVA test). Ischaemic cardiomyopathy patients did not demonstrate any significant increase in mean LAS during either low or peak dobutamine infusion from 7.8±1.4 mm at baseline, to 8.1±1.5 mm and 8.6±1.3 mm at low and peak dobutamine dose respectively, P=0.17, ANOVA test). In non-ischaemic dilated cardiomyopathy patients, mean LAS increased significantly only with the maximal dose of the drug (8.4±2.0 mm at baseline, 9.5±2.5 mm at low dobutamine dose, 10.7±2.1 mm at peak dobutamine dose, P=0.01 peak dose vs baseline, ANOVA test). Use of a mean LAS increase ≥1.5 mm at peak dobutamine dose resulted in a sensitivity of 80% and a specificity of 95% for the detection of coronary artery disease in patients with dilated cardiomyopathy of unknown cause. Therefore, we suggested that assessment of mean LAS during DSE provides a simple and accurate quantitative method for the identification of coronary artery disease in patientswith left ventricular dysfunction of unknown origin.

It appears from the initial results of our studies, as well as from the study of Mishra, Lythall and Chambers, that systolic long axis function during DSE is a really promising new method which offers a quantifiable measurement, avoiding the partial subjectivity of wall motion analysis. Although all these results are preliminary, we do concur with Henein and Gibson that stress long axis echocardiography can readily be interpreted into the standard stress echo protocol and merits at least further trial.

References

  1. Mishra MB, Lythall DA, Chambers JB. A comparison of wall motion analysis and systolic left ventricular long axis function during dobutamine stress echocardiography. Eur Heart J. 2002;23:579–585.[Abstract/Free Full Text]
  2. Henein M, Gibson D. Dobutamine stress echocardiography: the long and short of it. Eur Heart J. 2002;23:520–522.[Free Full Text]
  3. Kranidis A, Bouki T, Kostopoulos K et al. The contribution of the left atrio-ventricular plane displacement during low dose dobutamine stress echocardiography, in predicting recovery of left ventricular dyssynergies. Echocardiography. 1996;13:587–598.[Medline]
  4. Bouki K, Kakavas T, Kostopoulos K et al. Differentiation between ischemic and non-ischemic dilated cardiomyopathy based on left atrioventricular plane displacement duringdobutamine echocardiography. J Am Coll Cardiol. 2001;37(Suppl): 187A.




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