Key result
During dobutamine stress, patients with coronary artery disease exhibited QRS prolongation by 9 ms (p<0.001) and a blunted 63% increase in peak aortic acceleration compared to normal controls.
Why the study?
Does dobutamine stress alter ventricular activation and inotropic state differently in patients with coronary artery disease compared to normal subjects?
Case-Control (n=39)
No
Does dobutamine stress alter ventricular activation and inotropic state differently in patients with coronary artery disease compared to normal subjects?
p-value: p=<0.001
Relative ejection and filling times reflect ventricular activation independent of inotropic state, while peak aortic acceleration reflects the positive inotropic effect of dobutamine regardless of activation changes.
Dobutamine stress may induce QRS prolongation and blunt inotropy in CAD; hypothesis-generating for activation-inotropy mismatch, needs prospective validation.
OBJECTIVE: To identify the effects of altered ventricular activation during dobutamine stress on left ventricular function in normal subjects and in patients with coronary artery disease, and to distinguish these from an inotropic response. DESIGN: Prospective analysis of 12 lead ECG and echocardiogram at rest and at peak stress. SETTING: Tertiary referral centre for cardiac disease equipped with non-invasive facilities for pharmacological stress testing. METHODS: 22 patients with coronary artery disease were compared with 17 age matched controls. Left ventricular ejection and filling patterns were assessed using Doppler echocardiography. Activation effects were correlated with relative left ventricular ejection and filling times, and the Z ratio ([left ventricular ejection + filling times]/RR interval). Inotropic response was measured from peak aortic acceleration. RESULTS: In controls, QRS shortened (by 4 ms, p < 0.001), and total ejection and filling periods lengthened (by 2 s/min, p < 0.01 and 5 s/min, p < 0.001, respectively). The Z ratio thus increased and correlated with QRS shortening (r(2) = 0.69). Peak aortic acceleration (PAA) increased by 135%, p < 0.001. In patients, QRS lengthened at peak stress (by 9 ms, p < 0.001). Total ejection and filling times did not change, but Z ratio fell, correlating with QRS prolongation (r(2) = 0.65). Nevertheless, PAA increased by 63%, p < 0.001. CONCLUSIONS: Relative ejection and filling times reflect ventricular activation at rest and during stress independent of changes in inotropic state. By contrast, peak aortic acceleration reflects the positive inotropic effect of dobutamine on the myocardium, regardless of changes in activation.
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Alison Duncan (2001) conducted a case-control in Coronary artery disease (n=39). Coronary artery disease vs. Normal subjects was evaluated on Change in QRS duration at peak stress (p=<0.001). During dobutamine stress, patients with coronary artery disease exhibited QRS prolongation by 9 ms (p<0.001) and a blunted 63% increase in peak aortic acceleration compared to normal controls.
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