Cardiovascular medicine
Long axis electromechanics during dobutamine stress in patients
with coronary artery disease and left ventricular dysfunction
A M Duncan, C A O'Sullivan, G S Carr-White, D G Gibson, M Y Henein
Department of
Echocardiography, The Royal Brompton Hospital, Sydney Street, London
SW3 6NP, UK
Correspondence to: Dr Henein m.henein{at}rbh.nthames.nhs.uk
Accepted 20 June 2001
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
© 2001 by Heart
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