EFFECTS OF DOBUTAMINE STRESS ON MYOCARDIAL BLOOD-FLOW, TC-99M SESTAMIBI UPTAKE, AND SYSTOLIC WALL THICKENING IN THE PRESENCE OF CORONARY-ARTERY STENOSES - IMPLICATIONS FOR DOBUTAMINE STRESS-TESTING

Background Although dobutamine stress is used with both Tc-99m sestami bi (sestamibi) myocardial perfusion imaging and echocardiography for d etecting coronary artery stenoses, the impact of stenosis severity on test end points (myocardial sestamibi uptake and systolic thickening, respectively) has not been clearly defined. Methods and Results In 15 open-chest dogs, dobutamine (2.5 to 30 mu g.kg(-1).min(-1)) was infuse d after placement of an LAD stenosis that reduced (n=8) or abolished ( n=7) flow reserve. In dogs with reduced flow reserve, the stenotic-to- normal sestamibi activity ratio (0.86+/-0.03) significantly underestim ated the approximate to 2-to-1 dobutamine-induced flow disparity at th e time of sestamibi injection (flow ratio, 0.53+/-0.04; P<.001). Steno tic-zone thickening increased at low but not at higher doses of dobuta mine (2.9+/-0.4 versus 4.2+/-0.4 mm in normal zone at peak dobutamine; P=.055) but did not fall below baseline (2.7+/-0.3 mm). Similarly, in dogs with absent flow reserve, the sestamibi activity ratio (0.78+/-0 .02) underestimated the approximate to 2.5-to-1 dobutamine-induced flo w disparity (flow ratio, 0.41+/-0.05; P<.001), and failure to increase systolic thickening was observed in the stenotic zone (2.7+/-0.4 vers us 4.6+/-0.3 mm in the normal zone at peak stress, P<.01). In both gro ups of dogs, myocardial sestamibi uptake and image defect magnitudes w ere less than expected for the dobutamine-induced hyperemia, suggestin g that dobutamine adversely affects myocardial sestamibi binding. Fina lly, a significant reduction in stenotic-zone thickening was seen duri ng postdobutamine recovery, consistent with myocardial stunning. Concl usions In the presence of stenoses that reduced or abolished regional flow reserve, (1) myocardial sestamibi uptake significantly underestim ated the dobutamine-induced flow heterogeneity, (2) a ''failure to inc rease systolic thickening'' rather than a reduction in thickening was observed during dobutamine stress, and (3) myocardial stunning was obs erved during postdobutamine recovery.