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

Objective-To dissociate the effect of inotropy from activation change durin g 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 s tress. Amplitude, shortening and lengthening velocities, postejection short ening, Q wave to onset of shortening (Q-OS), and A2 to onset of lengthening (A2-OL) were measured. Inotropy was evaluated from peak aortic acceleratio n. Results-In controls, amplitude, shortening and lengthening velocities, and peak aortic acceleration increased with stress; QRS, Q-OS, and A2-OL shorte ned (all p < 0.001); and contraction remained coordinate. In the group of p atients with CAD and normal left ventricular cavity size, shortening veloci ty and peak aortic acceleration increased with stress (p < 0.005). However, amplitude and lengthening velocity did not change, QRS, Q-OS, and A2-OL le ngthened (p < 0.01), and incoordination appeared. Results were similar in t he group with DCM-NA. In the DCM-LBBB group, shortening velocity and peak a ortic acceleration increased modestly with stress (p < 0.01) but amplitude, lengthening velocity, QRS, Q-OS, A2-OL, and incoordination remained unchan ged. Overall, change in shortening velocity correlated with that in peak ao rtic acceleration (r(2) = 0.71), in amplitude with that in lengthening velo city (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 inotro py and rapid activation. In CAD, inotropy is preserved with development of ischaemia but the normal increase in amplitude is lost and prolonged activa tion delays the time course of shortening, causing pronounced incoordinatio n. Overall, shortening rate uniformly reflects inotropy while lengthening r ate depends mainly on systolic amplitude rather than primary diastolic invo lvement, even with overt ischaemia.