title: Pulsed tissue Doppler imaging to assess myocardial viability by quantification of regional myocardial functional reserve.
abstract: Dobutamine stress echocardiography (DSE) is used widely to evaluate myocardial viability, but is limited by the subjective nature of test interpretation. Assessment of systolic function by pulsed tissue Doppler imaging (TDI) during dobutamine stimulation may allow a more objective evaluation of myocardial functional reserve and, thus, myocardial viability. In 30 patients (58 +/- 9 years) with prior myocardial infarction, pulsed TDI with low dose dobutamine stress (10 microg/kg/min) was performed to assess myocardial viability. Qualitative assessment of two-dimensional (2-D) DSE and positron emission tomography (PET) were used for comparison. Peak systolic myocardial velocity was measured for each left ventricular segment (16 segments) at baseline and low dose dobutamine stress using pulsed TDI. The absolute and relative increases of peak systolic velocity from rest to low dose dobutamine stress were calculated. Three hundred sixty-four segments with adequate pulsed TDI tracing were divided according to either 2-D DSE or PET findings into normal, viable (mismatch), and nonviable (match) segments. The increase of peak systolic myocardial velocity from baseline to low dose dobutamine was significantly different between segments defined as normal, viable, and nonviable by 2-D DSE (2.71 +/- 1.91 cm/sec, 1.86 +/- 2.15 cm/sec, and 0.99 +/- 1.16 cm/sec, respectively; P < 0.001). The increase of peak systolic myocardial velocity from rest to low dose dobutamine for normal, mismatch, and match segments defined by PET was 2.72 +/- 1.96, 1.01 +/- 0.96 and 0.80 +/- 1.07 cm/sec, respectively (P < 0.001). In conclusion, the increase of peak systolic myocardial velocity during low dose dobutamine stimulation determined by pulsed TDI distinguishes between different myocardial viability states. It complements the standard interpretation of stress echocardiograms.
authors.affiliation: Medical Clinic I, University RWTH Aachen, Pauwelsstrasse 30, 52057 Aachen, Germany. Rhof@pcserver.mk1.rwth-aachen.de
authors.forename: D
authors.initials: D
authors.lastname: Yuan
authors.forename: H
authors.initials: H
authors.lastname: Kühl
authors.forename: B
authors.initials: B
authors.lastname: Nowak
authors.forename: E
authors.initials: E
authors.lastname: Kleinhans
authors.forename: H J
authors.initials: HJ
authors.lastname: Kaiser
authors.forename: A
authors.initials: A
authors.lastname: Franke
authors.forename: U
authors.initials: U
authors.lastname: Büll
authors.forename: P
authors.initials: P
authors.lastname: Hanrath
authors.forename: R
authors.initials: R
authors.lastname: Hoffmann
mesh_terms: D000368:Aged; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology*; D002316:Cardiotonic Agents / Q000008:administration & dosage; D002470:Cell Survival / Q000187:drug effects / Q000502:physiology*; D023921:Coronary Stenosis / Q000150:complications / Q000503:physiopathology; D004280:Dobutamine / Q000008:administration & dosage; D004305:Dose-Response Relationship, Drug; D015150:Echocardiography, Doppler; D025401:Echocardiography, Stress; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging / Q000187:drug effects; D006801:Humans; D007089:Image Enhancement; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure*; D011674:Pulse; D012372:ROC Curve; D012680:Sensitivity and Specificity; D014055:Tomography, Emission-Computed; D016276:Ventricular Function / Q000187:drug effects / Q000502:physiology*
chemical_list: D002316:Cardiotonic Agents; D004280:Dobutamine