Journal List > J Korean Soc Echocardiogr > v.4(1) > 1075217

Park, Sohn, Lee, Rhee, Chai, Seo, and Lee: Myocardial Velocity Gradient during Low-dose Dobutamine Stress Echocardiography in the Prediction of Viable Myocardium in the infarct Zone

Abstract

Background

Clinical importance of predicting viability in the infarct zone has been well recognized and low dose dobutamine stress echocardiography has been used in this regards. Several experimental and clinical studies have shown that dobutamine can recruit a contraction reserve in postischemic viable but akinetic segment in patients with myocardial infarction. However, echocardiographic assessment of regional wall motion abnormality is relatively semiquantitative, ambiguous in differentiation between akinetic and hypokinetic segment. With the advent of Doppler tissue imaging, instantaneous wall motion velocity could be measured. This study was performed to evaluate the usefulness of myocardial velocity gradient during low-dose dobutamine stress echocardiography in the prediction of viable myocardium in the infarct zone.

Method

We assessed left ventricular wall motion in 10 normal subjects, 20 patients with myocardial infarction(anteroseptal in 10, inferior in 10). Myocardial velocity gradient was defined as the difference in the wall motion velocities between the endocardium and the epicardium divided by wall thickness in the parasternal short axis view at the mid-ventricular level.

Results

Myocardial velocity gradient in the infarct zones were significantly lower than the corresponding segments in normal subjects(anteroseptal 0.46 ± 0.42/sec vs 1.47 ± 0.39/sec, p <0.01; inferior 0.31 ± 0.18/sec vs 1.97 ± 0.72/sec, p<0.01). In normal subjects, myocardial velocity gradients during low-dose dobutamine infusion(5μg/kg/min), increased significantly compared to the resting myocardial velocity gradients(anteroseptal 1.47 ± 0.39/sec to 2.04 ± 0.68/sec, p<0.01; inferior 1.97 ± 0.72/sec to 2.48 ± 0.62/sec, p<0.05). However in the infarct zones, there were no sinificant increases in myocardial velocity gradients during low-dose dobutamine infusion(anteroseptal 0.46 ± 0.42/sec to 0.69 ± 0.76/sec, p=NS; inferior 0.31 ± 0.18/sec to 0.62 ± 0.72, p=NS). When the infarct zones were separated into two groups according to the presence of viable myocardium based on the 24 hour-delayed thallium 201 myocardial SPECT, infarct zones with viable myocardium(n=6, two in anteroseptal and four in inferior infarction) showed significant increase in myocardial velocity gradients during low-dose dobutamine infusion(0.61 ± 0.39/sec to 1.48 ± 0.71/sec, p<0.05), while infarct zones without viable myocardium(n=14) did not show significant difference(0.29 ± 0.25/sec to 0.30 ± 0.34/sec, p=NS)

Conclusions

Myocardial velocity gradient could be an objective parameter in the prediction of viable myocardium with low-dose doubutamine stress echocardiography.

References

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Fig. 1.
Example of measurement of myocardial velocity gradient on short axis view at the level of mid-ventricular. Myocardial velocity gradient was defined as the difference in velocity between the endocardium and epicardium divided by the myocardial wall thickness. We obtained intramyocardial velocity toward the hypothetical center of contraction by correcting incidental angle.
jkse-4-13f1.tif
Fig. 2.
Changes of myocardial velocity gradient with low-dose dobutamine infusion in normal subjects: During low dose dobutamine infusion, myocardial velocity gradients significantly increased in anteroseptal wall(a) and inferior wall(b). There was no significant difference in the amount of change of myocardial velocity gradient between the anteroseptal and inferior wall(c).
jkse-4-13f2.tif
Fig. 3.
Changes of myocardial velocity gradient with low-dose dobutamine infusion in patients with myocardial infarction. There was no significant difference of myocardial velocity gradient both in anteroseptal(a) and inferior wall(b).
jkse-4-13f3.tif
Fig. 4.
Changes of myocardial velocity gradient with low-dose dobutamine infusion in viable(a) and nonviable myocardium(b), which was differentiated in infart zones on the basis of 24 hour delayed Thallium scan. In infarct zones with viable myocardium, myocardial velocity gradients significantly increased, but, in infarct zones without viable myocardium, not changed.
jkse-4-13f4.tif
Table 1.
Basal myocardial velocity gradients in normal subjects and patients with myocardial infarction
  Anteroseptal segment(n=10) Inferior segment (n=10)
Normal(/s) 1.47 ± 0.39,# 1.97 ± 0.72,
MI(/s) 0.46 ± 0.42# 0.31 ± 0.18

p>0.05,

# p<0.05,

p<0.05

Table 2.
Comparison of the amount of change of myocardial velocity gradient during low-dose dobutamine infusion among normal wall and infarcted wall(viable and nonviable myocardium)
  Myocardial velocity gradients(/sec)
  Basal The amount of change during dobutamine
Normal regions(n=20) 1.72 ± 0.63 0.54 ± 0.56,#
Viable zones(n=6) 0.61 ± 0.39 0.87 ± 0.52#
Nonviable zones(n=14) 0.29 ± 0.25 0.01 ± 0.46

p<0.01,

# p>0.05,

p>0.05

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