Mechanism of reversible (99m) Tc-sestamibi perfusion defects during pharmacologically induced vasodilatation

Reversible perfusion defects on Tc-99m-sestamibi imaging during hyperemia a re thought to occur due to myocardial blood flow (MBF) "mismatch" between r egions with and without stenosis. We have recently shown that myocardial bl ood volume (MBV) distal to a stenosis decreases during hyperemia, resulting in a reversible perfusion defect on myocardial contrast echocardiography ( MCE). In this study, we hypothesized that a reversible perfusion defect on Tc-99m-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MB F in the absence of changes in MBV by using direct intracoronary infusion o f adenosine (group I, n = 10 dogs); 2) decrease in MBV despite an increase in MBF by left main infusion of adenosine proximal to a noncritical coronar y stenosis placed on either coronary artery (group II, n = 13 dogs); and 3) reduction in both resting MBF and MBV by placement of a severe stenosis (g roup III, n = 7 dogs). In group I dogs, no difference in MBV or Tc-99m-sest amibi uptake was found between the two coronary beds despite an up to fourf old increase in MBF in one bed with adenosine. In group II dogs, MBV distal to the stenosis decreased during hyperemia despite a twofold increase in m ean MBF. A good correlation was found between 99m Tc-sestamibi uptake and M BV ratios from the stenosed versus normal bed (r = 0.91, P< 0.001). In grou p III dogs, both MBF and MBV were decreased in the stenosed bed at rest wit h a good correlation noted between Tc-99m-sestamibi uptake and MBV ratios f rom the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on Tc-99m-sestamibi during vasodilator stress imaging ar e related to decreases in MBV distal to a stenosis and not to "flow mismatc h" between beds. The decrease in MBV results in reduced Tc-99m-sestamibi up take during hyperemia.