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

Abstract

Objective-To dissociate the eVect 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. (Heart 2001;86:397-404)

Differentiation of Ischemic From Nonischemic Cardiomyopathy During Dobutamine Stress by Left Ventricular Long-Axis Function

“…The sensitivity and specificity of changes in septal systolic amplitude and early diastolic lengthening velocity were similar when all patients were considered, findings that are compatible with a previously demonstrated correlation between them. 11 Finally, the contrasting effects of stress in LBBB with or without ischemia meant that septal long-axis measurements performed particularly well in this group. This probably reflected their direct relation to QRS shortening with stress in nonischemic but not in ischemic cardiomyopathy.…”

“…11 Transthoracic echocardiography was performed with an echocardiographic system (Hewlett-Packard Sonos 5500), a multifrequency transducer, and harmonic imaging as appropriate. Two-dimensional echocardiography was performed from the parasternal long-and short-axis views and apical 4-and 2-chamber views.…”

“…10 Furthermore, stress-induced changes in long-axis function can be measured objectively. 11,12 Our study thus aimed to compare long-axis behavior at rest and during stress in ischemic and nonischemic cardiomyopathy, with and without LBBB, and thus define criteria for differentiating between them.…”

Relation of Biventricular Function Quantified by Stress Echocardiography to Cardiopulmonary Exercise Capacity in Adults With Mustard (Atrial Switch) Procedure for Transposition of the Great Arteries

“…This "q-OS" was previously found to be a sensitive marker of ischemia in patients with coronary artery disease. 9,10 We also measured the time interval between the second heart sound and the onset of long-axis lengthening (S2-OL, Figure 2), a measurement similar to isovolumic relaxation time in value despite the difference in their definitions. 10 We assessed the reproducibility of the timing measurements of the onset of shortening with respect to the onset of the QRS and the onset of lengthening with respect to S2.…”

“…Post-ejection shortening was measured as the extent of inward movement that occurred after the second heart sound. 9 We measured the delay between the onset of electrical activity (QRS) and the onset of shortening in the pulmonary and systemic ventricular free walls ( Figure 2). This "q-OS" was previously found to be a sensitive marker of ischemia in patients with coronary artery disease.…”