Technetium 99m-labeled sestamibi imaging reliably identifies retained contractile reserve in dyssynergic myocardial segments

Background

Recently there has been considerable controversy regarding the use of ^99mTc-labeled sestamibi as an agent for the detection of viable myocardium. In this study we have used dobutamine-induced left ventricular wall thickening by echocardiography in regions with evidence of resting dyssynergy of the left ventricle as an indicator of retained contractile reserve and compared this with 99m Tc-labeled sestamibi uptake in the same regions.

Methods and Results

Twenty-seven patients with documented coronary artery disease and severe regional wall motion abnormalities underwent low-dose (5 to 15 μg/kg/min) dobutamine echocardiography and maximal (15 to 40 μg/kg/min) stress dobutamine ^99mTc-labeled sestamibi single-photon emission computed tomographic imaging. Separate-day rest ^99mTc-labeled sestamibi scanning was also performed. ^99mTc-labeled sestamibi uptake was assessed semiquantitatively from grades from 1 to 4, from normal to absent perfusion. Regions with grade 3 or less uptake were considered viable by ^99mTc-labeled sestamibi. Of the 34 regions with severe wall motion abnormalities by echocardiography, 32 showed improved wall thickening with low-dose dobutamine. Rest ^99mTc-labeled sestamibi detected retained myocardial viability in 29 of these regions (91%) that were deemed to have contractile reserve by echocardiography (concordance: 91% [K=0.53; p<0.001]). Furthermore, stress-rest ^99mTc-labeled sestamibi revealed completely reversible defects in five regions (16%), partially reversible defects in 24 regions (75%), and grade 4 uptake and fixed (nonviable) defects in three (9%) of these 32 regions with retained contractile reserve.

Conclusion

Uptake of ^99mTc-labeled sestamibi at rest accurately identifies regions of segmental dyssynergy in which recovery of function may be provoked by inotropic stimulation. Addition of stress dobutamine ^99mTc-labeled sestamibi provides further proof of retained myocardial viability in these dysfunctional segments.