OBJECTIVE: To assess the prognostic value of wall motion abnormalities during the recovery phase of dobutamine stress echocardiography in addition to wall motion abnormalities at peak stress. METHODS: Wall motion abnormalities were assessed at peak and during recovery phase of dobutamine stress echocardiography in 187 consecutive patients, who were followed for occurrence of cardiac events. RESULTS: During follow-up (mean 36±28 months), 19 patients (10%) died from cardiac causes, 34 (18%) patients suffered nonfatal myocardial infarction, and 77 (41%) patients underwent late revascularization. Univariable predictors of cardiac events by Cox regression analysis were age (hazard ratio: 1.01; confidence interval: 1.00-1.03), dyslipidemia (hazard ratio: 1.41; confidence interval: 1.02-1.95), rest wall motion abnormalities (hazard ratio: 1.37; confidence interval: 1.14-1.64), new wall motion abnormalities (hazard ratio: 1.18; confidence interval: 0.95-1.45) at peak and new wall motion abnormalities (hazard ratio: 1.33; confidence interval: 1.11-1.59) at recovery phase of dobutamine stress echocardiography. The best multivariable model to predict cardiac events included new wall motion abnormality (hazard ratio: 5.34; confidence interval: 1.71-16.59) at recovery phase of dobutamine stress echocardiography, after controlling for clinical and peak dobutamine stress echocardiography data. CONCLUSIONS: Myocardial ischemia at recovery phase of dobutamine stress echocardiography is an independent predictor of cardiac events and has an incremental value when added to ischemia at peak.

Additional Metadata
Keywords Dobutamine stress echocardiography, Ischemia, Risk stratification
Persistent URL dx.doi.org/10.1097/MCA.0b013e32801682d0, hdl.handle.net/1765/36476
Citation
Karagiannis, S.E, Elhendy, A, Feringa, H.H.H, van Domburg, R.T, Bax, J.J, Vidakovic, R, … Poldermans, D. (2007). The long prognostic value of wall motion abnormalities during the recovery phase of dobutamine stress echocardiography after receiving acute β-blockade. Coronary Artery Disease, 18(3), 187–192. doi:10.1097/MCA.0b013e32801682d0