title: The shape of the aortic outflow velocity profile revisited: is there a relation between its asymmetry and ventricular function in coronary artery disease?
abstract: OBJECTIVE
  Myocardium contracts in the beginning of ejection causing outflow acceleration, resulting in asymmetric outflow velocity profiles peaking around one-third of ejection and declining when force development declines. This article aimed to demonstrate that decreased contractility in coronary artery disease (CAD) changes outflow timing and profile symmetry.
  
  
  RESULTS
  Seventy-nine patients undergoing routine full dose dobutamine stress-echo (DSE) were divided into two groups based on resting wall motion and DSE response: DSE negative (DSE(neg)) (35 of 79 patients) and positive (DSE(pos)) (44 of 79 patients) which were compared with 32 healthy volunteers. Aortic CW-Doppler traces at rest were analysed semi-automatically; time-to-peak (T(mod)), ejection-time (ET(mod)), rise-time (t(rise)), and fall-time (t(fall)) were quantified. Asymmetry (asymm) was calculated as the normalized difference of left and right half of the spectrum. Normal curves were triangular, early-peaking, whereas patients showed more rounded shapes and later peaks. T(rise) was longest in DSE(pos). T(fall) was shortest in DSE(pos), followed by controls and DSE(neg). Asymm was lowest in DSE(pos), followed by controls and DSE(neg). Abnormally symmetric profiles (asymm <0.25) were found in none of the controls, 2.9% DSE(neg), and 27.3% DSE(pos). A good correlation was found between assym and ejection fraction (EF) and T(mod)/ET(mod) and EF. Notably, an LV dynamic gradient was induced in 71.4% DSE(neg) and in 18.2% DSE(pos), associated with LV hypertrophy and supernormal (very asymmetric) traces.
  
  
  CONCLUSIONS
  Decreased myocardial function results in a more symmetrical outflow, while very asymmetrical traces suggest increased contractility, potentially inducing intra-cavity gradients during DSE. Therefore, including outflow symmetry as a clinical measurement provides additional information on patients with CAD.
authors.affiliation: Department for Cardiovascular Diseases, University Hospital Centre Zagreb and School of Medicine, University of Zagreb, Kispaticeva 12, Zagreb 10000, Croatia. maja_cikes@yahoo.com
authors.forename: Maja
authors.initials: M
authors.lastname: Cikes
authors.forename: Hrvoje
authors.initials: H
authors.lastname: Kalinic
authors.forename: Aigul
authors.initials: A
authors.lastname: Baltabaeva
authors.forename: Sven
authors.initials: S
authors.lastname: Loncaric
authors.forename: Chirine
authors.initials: C
authors.lastname: Parsai
authors.forename: Davor
authors.initials: D
authors.lastname: Milicic
authors.forename: Ivo
authors.initials: I
authors.lastname: Cikes
authors.forename: George
authors.initials: G
authors.lastname: Sutherland
authors.forename: Bart
authors.initials: B
authors.lastname: Bijnens
mesh_terms: D000368:Aged; D001021:Aortic Valve / Q000503:physiopathology*; D001783:Blood Flow Velocity; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009119:Muscle Contraction; D012189:Retrospective Studies; D018754:Ventricular Dysfunction / Q000000981:diagnostic imaging / Q000503:physiopathology*