Electromechanical left ventricular resynchronisation by coronary artery bypass surgery

In patients with coronary artery disease (CAD), the normal electromechanical response to dobutamine stress is deranged: QRS duration lengthens rather than shortens, left ventricular asynchrony develops, post-ejection shortening appears, and total isovolumic time (the time in the cardiac cycle when the ventricle is neither ejecting nor filling) increases rather than falls, all of which blunt the normal rise in cardiac output. We aimed to study the effect of revascularisation on these stress-induced electromechanical abnormalities and their effect on peak cardiac output after coronary artery bypass grafting (CABG).

20 unselected patients were studied before and after CABG. Long axis asynchrony was determined by (i) delay in the onset of shortening, (ii) amplitude and (iii) duration of post-ejection shortening. Total isovolumic time (in s/min), calculated as [60-(total ejection time+total filling time)] and cardiac output were measured by Doppler echocardiography.

Before CABG: QRS duration broadened with stress (by 7+/-8 ms, P<0.01) and post-ejection shortening increased (amplitude by 1.1+/-0.7 mm, P<0.01, duration by 8+/-9 ms, P<0.01). Total isovolumic time increased (by 3+/-3 s/min, P<0.01) and cardiac output rose (by 2.8+/-1.2 l/min, P<0.01). After CABG: QRS duration shortened with stress (by 5+/-4 ms, P<0.01) post-ejection shortening decreased (amplitude and duration fell by 0.4+/-0.5 mm and 22+/-14 ms, respectively), total isovolumic time shortened (by 3+/-3 s/min) and cardiac output increased (by 5.1+/-1.8 l/min, all P<0.01). Changes in total isovolumic time and duration of post-ejection shortening with stress were independent predictors of the increase in peak cardiac output after revascularisation (total R(2)=0.69). Independent predictors of changes in total isovolumic time with stress were those in QRS duration and the duration of post-ejection shortening (total R(2)=0.75). In turn, changes in the duration of post-ejection shortening were closely associated with alterations in the delay in long axis shortening (r(2)=0.50) which correlated with changes in QRS duration (r(2)=0.59, all P<0.001).

Revascularisation resynchronises left ventricular wall motion by restoring the normal activation response to stress, thereby reducing total isovolumic time and normalising peak cardiac output response to stress.