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Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
Published on: February 10, 2013
Long axis electromechanics during dobutamine stress in patients with coronary artery disease and left ventricular
A M Duncan1, C A O'Sullivan, G S Carr-White
1Department of Echocardiography, The Royal Brompton Hospital, Sydney Street, London SW3 6NP, UK.
Insights
Dobutamine stress testing reveals that in coronary artery disease (CAD), preserved inotropy is masked by prolonged activation, leading to impaired left ventricular function and incoordination. Shortening rate reflects inotropy, while lengthening rate depends on systolic amplitude.
Area of Science:
- Cardiology
- Physiology
Background:
- Dobutamine stress echocardiography is used to assess left ventricular function.
- Coronary artery disease (CAD) can affect myocardial activation and contractility.
- Dissociating inotropic effects from activation changes is crucial for accurate functional assessment.
Purpose of the Study:
- To differentiate the impact of inotropy from activation changes on left ventricular long axis function during dobutamine stress in patients with CAD.
- To investigate the mechanisms underlying impaired left ventricular function in CAD during stress.
Main Methods:
- 25 patients with CAD and 30 with dilated cardiomyopathy (DCM) were compared to 20 controls.
- Echocardiography and ECG were performed at rest and peak dobutamine stress.
- Measurements included amplitude, velocities, Q-OS, A2-OL, and peak aortic acceleration to assess inotropy and activation.
Main Results:
- Controls showed increased amplitude, velocities, and peak aortic acceleration with stress.
- CAD patients exhibited preserved shortening velocity but reduced amplitude and prolonged activation (Q-OS, A2-OL), leading to incoordination.
- Dilated cardiomyopathy groups showed varying degrees of preserved or unchanged function and activation.
Conclusions:
- Normal dobutamine response involves inotropy and rapid activation.
- In CAD, ischemia preserves inotropy but prolonged activation impairs function and coordination.
- Shortening rate reflects inotropy, while lengthening rate is influenced by systolic amplitude, not solely diastolic function.
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 (r(2) = 0.71), in amplitude with that in lengthening velocity (r(2) = 0.74), and in QRS with both Q-OS (r(2) = 0.69) and A2-OL (r(2) = 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.
