Key result
Pulsed TDI during low-dose dobutamine stress differentiates normal, viable, and nonviable myocardial segments.
Why the study?
Does pulsed tissue Doppler imaging during low-dose dobutamine stress objectively quantify myocardial viability compared to 2-D DSE and PET in patients with prior myocardial infarction?
Observational (n=30)
Does pulsed tissue Doppler imaging during low-dose dobutamine stress objectively quantify myocardial viability compared to 2-D DSE and PET in patients with prior myocardial infarction?
p-value: p=<0.001
Pulsed tissue Doppler imaging during low-dose dobutamine stress provides an objective, quantitative measure of myocardial functional reserve that distinguishes between different viability states, complementing standard 2-D stress echocardiography.
May complement 2-D DSE for post-MI viability assessment; leaves open prospective validation against PET and outcomes.
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.
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Yuan et al. (2001) conducted an observational in Prior myocardial infarction (n=30). Pulsed tissue Doppler imaging (TDI) with low dose dobutamine stress vs. 2-D DSE and PET was evaluated on Increase of peak systolic myocardial velocity from baseline to low dose dobutamine (p=<0.001). Pulsed tissue Doppler imaging during low-dose dobutamine stress differentiated normal, viable, and nonviable myocardial segments (2.71 vs 1.86 vs 0.99 cm/sec, respectively; P<0.001).
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