Key result
In subendocardial infarction, subepicardial contraction increased with dobutamine (12.4% to 27.1%, P<0.005) while subendocardial contraction was lost, whereas in transmural infarction neither increased.
Why the study?
Does tissue strain imaging during dobutamine challenge accurately evaluate the transmural distribution of viable myocardium in a canine model of myocardial infarction?
Does tissue strain imaging during dobutamine challenge accurately evaluate the transmural distribution of viable myocardium in a canine model of myocardial infarction?
Tissue strain imaging during dobutamine stress can differentiate subendocardial from transmural infarction by assessing the transmural distribution of viable myocardium.
Dobutamine strain imaging distinguishes experimental infarction depth; leaves open human translation before clinical use.
Transmural distribution of viable myocardium in the ischemic myocardium has not been quantified and fully elucidated. To address this issue, we evaluated transmural myocardial strain profile (TMSP) in dogs with myocardial infarction using a newly developed tissue strain imaging. TMSP was obtained from the posterior wall at the epicardial left ventricular short-axis view in 13 anesthetized open-chest dogs. After control measurements, the left circumflex coronary artery was occluded for 90 min to induce subendocardial infarction (SMI). Subsequently, latex microbeads (90 microm) were injected in the same artery to create transmural infarction (TMI). In each stage, measurements were done before and after dobutamine challenge (10 microg.kg(-1).min(-1) for 10 min) to estimate transmural myocardial viability. Strain in the subendocardium in the control stage increased by dobutamine (from 53.6 +/- 17.1 to 73.3 +/- 21.8%, P < 0.001), whereas that in SMI and TMI stages was almost zero at baseline and did not increase significantly by dobutamine [from 0.8 +/- 8.8 to 1.3 +/- 7.0%, P = not significant (NS) for SMI, from -3.9 +/- 5.6 to -1.9 +/- 6.0%, P = NS for TMI]. Strain in the subepicardium increased by dobutamine in the control stage (from 23.9 +/- 6.1 to 26.3 +/- 6.4%, P < 0.05) and in the SMI stage (from 12.4 +/- 7.3 to 27.1 +/- 8.8%, P < 0.005), whereas that in the TMI stage did not change (from -1.0 +/- 7.8 to -0.7 +/- 8.3%, P = NS). In SMI, the subendocardial contraction was lost, but the subepicardium showed a significant increase in contraction with dobutamine. However, in TMI, even the subepicardial increase was not seen. Assessment of transmural strain profile using tissue strain imaging was a new and useful method to estimate transmural distribution of the viable myocardium in myocardial infarction.
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Maruo et al. (2006) studied Myocardial infarction (n=13). Dobutamine challenge vs. Baseline was evaluated on Transmural myocardial strain profile (subendocardial and subepicardial strain). In subendocardial infarction, subepicardial contraction increased with dobutamine (12.4% to 27.1%, P<0.005) while subendocardial contraction was lost, whereas in transmural infarction neither increased.