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. 2001 Oct;86(4):397–404. doi: 10.1136/heart.86.4.397

Long axis electromechanics during dobutamine stress in patients with coronary artery disease and left ventricular dysfunction

A Duncan 1, C O'Sullivan 1, G Carr-White 1, D Gibson 1, M Henein 1
PMCID: PMC1729931  PMID: 11559677

Abstract

OBJECTIVE—To dissociate the effect of inotropy from activation change during dobutamine stress on left ventricular long axis function in patients with coronary artery disease (CAD).
METHODS—25 patients with CAD and normal left ventricular cavity size and 30 with cavity dilatation—18 with normal activation (DCM-NA) and 12 with left bundle branch block (DCM-LBBB)—were compared with 20 controls. 12 lead ECG and septal long axis echograms were assessed at rest and peak dobutamine stress. Amplitude, shortening and lengthening velocities, postejection shortening, Q wave to onset of shortening (Q-OS), and A2 to onset of lengthening (A2-OL) were measured. Inotropy was evaluated from peak aortic acceleration.
RESULTS—In controls, amplitude, shortening and lengthening velocities, and peak aortic acceleration increased with stress; QRS, Q-OS, and A2-OL shortened (all p < 0.001); and contraction remained coordinate. In the group of patients with CAD and normal left ventricular cavity size, shortening velocity and peak aortic acceleration increased with stress (p < 0.005). However, amplitude and lengthening velocity did not change, QRS, Q-OS, and A2-OL lengthened (p < 0.01), and incoordination appeared. Results were similar in the group with DCM-NA. In the DCM-LBBB group, shortening velocity and peak aortic acceleration increased modestly with stress (p < 0.01) but amplitude, lengthening velocity, QRS, Q-OS, A2-OL, and incoordination remained unchanged. Overall, change in shortening velocity correlated with that in peak aortic acceleration (r2 = 0.71), in amplitude with that in lengthening velocity (r2 = 0.74), and in QRS with both Q-OS (r2 = 0.69) and A2-OL (r2 = 0.63).
CONCLUSION—The normal long axis response to dobutamine reflects both inotropy and rapid activation. In CAD, inotropy is preserved with development of ischaemia but the normal increase in amplitude is lost and prolonged activation delays the time course of shortening, causing pronounced incoordination. Overall, shortening rate uniformly reflects inotropy while lengthening rate depends mainly on systolic amplitude rather than primary diastolic involvement, even with overt ischaemia.


Keywords: stress echocardiography; activation; inotropy; incoordination

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Figure 1  .

Figure 1  

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Left: long axis shortening during ejection normally increases during stress. In patients with dilated cardiomyopathy and normal activation (right), shortening during ejection, already lower than normal at rest, falls further during stress. A2, aortic valve closing; AO, aortic valve opening; PCG, phonocardiogram.    

Figure 2  .

Figure 2  

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At rest, the percentage of total systolic shortening that occurred during ejection fell as the severity of ventricular disease increased. In the control group, shortening during ejection increased during stress but fell further in all patient groups. R, rest; S, stress.    

Figure 3  .

Figure 3  

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(A) There was a close correlation between the change in total systolic amplitude and lengthening velocity in the control group and all patients when taken as a single group. (B) There was a close correlation between the change in shortening velocity and peak aortic acceleration (PAA) in individual subjects.

Figure 4  .

Figure 4  

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Correlation between the change in QRS duration and the time from the Q wave to the onset of shortening (Q-OS) in control and patient groups. In controls, Q-OS shortened with dobutamine, even when the change in QRS duration was zero. This effect was attenuated in all patient groups. Similar relations were found between the change in QRS duration and the time from A2 to the onset of lengthening (A2-OL) in all studied groups.    

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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