title: Determinants of tissue Doppler measures of regional diastolic function during dobutamine stress echocardiography.
abstract: BACKGROUND
  Diastolic dysfunction induced by ischemia may alter transmitral blood flow, but this reflects global ventricular function, and pseudonormalization may occur with increased preload. Tissue Doppler may assess regional diastolic function and is relatively load-independent, but limited data exist regarding its application to stress testing. We sought to examine the stress response of regional diastolic parameters to dobutamine echocardiography (DbE).
  
  
  METHODS
  Sixty-three patients underwent study with DbE: 20 with low probability of coronary artery disease (CAD) and 43 with CAD who underwent angiography. A standard DbE protocol was used, and segments were categorized as ischemic, scar, or normal. Color tissue Doppler was acquired at baseline and peak stress, and waveforms in the basal and mid segments were used to measure early filling (Em), late filling (Am), and E deceleration time. Significant CAD was defined by stenoses >50% vessel diameter.
  
  
  RESULTS
  Diastolic parameters had limited feasibility because of merging of Em and Am waves at high heart rates and limited reproducibility. Nonetheless, compared with normal segments, segments subtended with significant stenoses showed a lower Em velocity at rest (6.2 +/- 2.6 cm/s vs 4.8 +/- 2.2 cm/s, P <.0001) and peak (7.5 +/- 4.2 cm/s vs 5.1 +/- 3.6 cm/s, P <.0001). Abnormal segments also showed a shorter E deceleration time (51 +/- 27 ms vs 41 +/- 27 ms, P =.0001) at base and peak. No changes were documented in Am. The same pattern was seen with segments identified as ischemic with wall motion score. However, in the absence of ischemia, segments of patients with left ventricular hypertrophy showed a lower Em velocity, with blunted Em responses to stress.
  
  
  CONCLUSIONS
  Regional diastolic function is sensitive to ischemia. However, a number of practical limitations limit the applicability of diastolic parameters for the quantification of stress echocardiography.
authors.affiliation: University of Queensland, Brisbane, Australia.
authors.forename: Ofelia
authors.initials: O
authors.lastname: Najos-Valencia
authors.forename: Peter
authors.initials: P
authors.lastname: Cain
authors.forename: Colin
authors.initials: C
authors.lastname: Case
authors.forename: Sudhir
authors.initials: S
authors.lastname: Wahi
authors.forename: Thomas H
authors.initials: TH
authors.lastname: Marwick
mesh_terms: D001783:Blood Flow Velocity / Q000502:physiology; D006332:Cardiomegaly / Q000175:diagnosis / Q000503:physiopathology; D017023:Coronary Angiography; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000175:diagnosis* / Q000000981:diagnostic imaging / Q000503:physiopathology; D003971:Diastole / Q000502:physiology*; D018618:Echocardiography, Doppler, Color / Q000706:statistics & numerical data*; D025401:Echocardiography, Stress / Q000706:statistics & numerical data*; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D008875:Middle Aged; D008943:Mitral Valve / Q000502:physiology / Q000503:physiopathology; D009200:Myocardial Contraction / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D013318:Stroke Volume / Q000502:physiology; D018754:Ventricular Dysfunction / Q000175:diagnosis* / Q000503:physiopathology