Introduction: In LV failure, it has been observed that a lower velocity is often combined with a slower increase in velocity, a more rounded curve form and peak velocity later in systole. From isolated cells, it was suggested that chronic ischemia decreases but prolongs contraction. Additionally, severe aortic stenosis shows, higher but often prolonged outflow velocities. Outflow velocities represent the pressure gradient between LV and aorta and thus influenced by either of them. However, a dynamically increasing resistance in the vessel tree reduces late velocities while late increases should be related to prolonged contraction. We assumed a relationship between the morphology and duration of aortic outflow velocities and myocardial function in coronary artery disease (CAD). Methods: We studied 85 patients (pts) undergoing routine dobutamine stress echo (DSE) (40 male, 45 female, mean age 62.4± 9.6 years). Pts were divided in 2 groups: group A: 37 pts without evidence of CAD and/or normal DSE, group B: 48 pts with angiographically proven CAD and/or positive DSE. 37 sex and age matched healthy volunteers with no signs or symptoms of cardiovascular disease served as a control group. Automated analysis using modeling was applied on digitally stored aortic CW traces. Time from onset of aortic flow to peak flow (Tmax) and ejection time (ET) were calculated both directly from the CW traces as well as from the modeled signal (Tmax_mat, ET_mat). The asymmetry measure (asymm) was measured from the modeled signal and was defined as the the difference between the areas of the right and left half of the signal. A normal curve was more triangular in shape, with an early peak, while curves of pts with CAD showed typical broadening with a much more rounded shape and later peak. *p<0, 02 vs. normal. † p<0, 05 vs normal, ‡ p<0, 02 vs group A. Results: Tmax and Tmax_mat were the longest in group B, followed by group A and normals (Tmax: 68, 54± 15, 72 ms*, 65, 97± 16, 96 ms† , 58, 61± 12, 46 ms ; Tmax_mat: 74, 26± 18, 36 ms‡ , 65, 07± 14, 43 ms*, 65, 79± 13, 68 ms, respectively). Tmax/ET was the largest in group B (0, 23± 0, 06‡ *), followed by group A (0, 21± 0, 06) and normals (0, 20± 0, 04), similarly to Tmax_mat/ET_mat (group B: 0, 24± 0, 55‡ *, group A: 0, 20± 0, 05 ; normals: 0, 21± 0, 04). Asymm. was the largest in group A: 0, 35± 0, 07, followed by normals (0, 32± 0, 06) while group B had the most symmetrical profiles: 0, 31± 0, 08‡ . A broadened profile (symm<0, 25) was present in 2, 6% normals, 5, 4% of group A pts and 25% of group B pts. Conclusion: These data show that a symmetrical, late peaking aortic outflow velocity profile is present in an important percentage of CAD patients which might be related to a reduction in global myocardial contractility. Automated analysis using modelling can be used to categorize Doppler data and provides additional clinical information on the functional impact of CAD.