Ultrasound examination during microbubble infusion can be used to quantify total organ as well as regional nutrient blood flow to the kidney.

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Background-Currently, the detection of noncritical coronary stenoses requires some form of stress. We hypothesized that these stenoses can be detected at rest without recourse to stress by assessing adaptive changes that occur distally in the microcirculation. Methods and Results-Phasic changes in myocardial video intensity (VI) were measured at rest with continuous high-mechanical-index (MI) contrast echocardiography in 15 open-chest dogs. Data were acquired at baseline and in the presence of different degrees of noncritical coronary stenosis. In 6 of these dogs, capillary blood volume was also measured at baseline using high-MI intermittent imaging with triggering performed separately at both end diastole and end systole. During continuous high-MI imaging, a significant increase in systolic VI was noted with coronary stenoses that resulted in progressive increases in the systolic/diastolic VI ratio with greater degrees of stenosis (Pϭ0.003), with a mildly quadratic relation noted between the two: yϭ1.3 · 10 Ϫ6 · x 2 ϩ0.01xϩ0.32, PϽ0.001, rϭ0.76, SEEϭ0.14. There was no difference in capillary blood volume between end diastole and end systole at baseline. Conclusions-Capillary blood volume does not change between diastole and systole in vivo. Phasic changes in VI are noted at baseline during high-MI continuous imaging. The systolic component is negligible at baseline but increases with increasing levels of noncritical coronary stenosis because of adaptive changes in the microcirculation distal to the stenosis. Thus, the measurement of phasic changes in myocardial VI has the potential to detect coronary stenosis at rest without recourse to any form of stress. Key Words: stenosis Ⅲ echocardiography Ⅲ blood volume B ecause of autoregulation, coronary blood flow (CBF) remains normal at rest until a coronary stenosis exceeds Ϸ85% in severity. 1,2 In the absence of a prior infarction, therefore, noncritical coronary stenoses cannot be detected by cardiac imaging at rest, and some form of stress is required to induce either regional dysfunction or a perfusion abnormality. The same is true even for electrocardiography.When coronary arterioles dilate in the presence of a noncritical stenosis, their blood volume (aBV) increases. 3,4 A portion of these arterioles are intramyocardial. 5 We hypothesized that because the degree of dilation of the coronary arterioles is related to the severity of stenosis, 3,4,6 aBV should increase in proportion to coronary stenosis severity. If this phenomenon could be measured noninvasively, the presence and severity of noncritical coronary stenosis could be measured at rest without recourse to any form of stress.Whereas phasic changes in intramyocardial arteriolar dimensions have been documented during cardiac contraction, 7 there is controversy regarding changes in capillary dimensions during this period. 8 -11 We postulated that because arterioles and venules are larger than capillaries, their compression would occur early in systole, causing an increase in their resistance that would re...

Reversible perfusion defects on (99m)Tc-sestamibi imaging during hyperemia are thought to occur due to myocardial blood flow (MBF) "mismatch" between regions with and without stenosis. We have recently shown that myocardial blood 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 (99m)Tc-sestamibi imaging during hyperemia results from the same mechanism. We tested our hypothesis under the following conditions: 1) increases in MBF in the absence of changes in MBV by using direct intracoronary infusion of 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 coronary 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 (group III, n = 7 dogs). In group I dogs, no difference in MBV or (99m)Tc-sestamibi uptake was found between the two coronary beds despite an up to fourfold 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 mean MBF. A good correlation was found between (99m)Tc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.91, P < 0.001). In group III dogs, both MBF and MBV were decreased in the stenosed bed at rest with a good correlation noted between (99m)Tc-sestamibi uptake and MBV ratios from the stenosed versus normal bed (r = 0.92, P = 0.004). We conclude that reversible defects on (99m)Tc-sestamibi during vasodilator stress imaging are related to decreases in MBV distal to a stenosis and not to "flow mismatch" between beds. The decrease in MBV results in reduced (99m)Tc-sestamibi uptake during hyperemia.

Although the effects of dipyridamole and dobutamine on MBV and VEL are different, both are equally effective in detecting physiologically relevant coronary stenoses on MCE. Both can therefore be used interchangeably with myocardial perfusion imaging for the detection of CAD.

Background-We hypothesized that increased myocardial oxygen demand resulting from hypotension and reflex tachycardia unmasking a reduced endocardial myocardial blood flow (MBF) reserve is the mechanism of dipyridamole-induced regional dysfunction in chronic coronary artery disease. Methods and Results-Ameroid constrictors were placed around the proximal coronary arteries and their major branches in 15 dogs to create chronic coronary stenosis. Seven days later, radiolabeled microsphere-derived MBF and 2-dimensional echocardiography-derived percent wall thickening (%WT) were measured at rest and after 0.56 mg/kg dipyridamole. Dipyridamole caused an increase (mean, 21%) in the rate-pressure product secondary to reflex tachycardia resulting from mild systemic hypotension. %WT in myocardial segments with an endocardial MBF reserve (dipyridamole/resting MBF) of 1.5 to 2.5 (nϭ35) did not change after dipyridamole, whereas it decreased in segments with an endocardial MBF reserve of Ͻ1.5 (nϭ30) and increased in those with an endocardial MBF reserve of Ն2.5 (nϭ45) (PϽ0.05). Most (80%) segments with endocardial MBF reserve of Ͻ1.5 and 14% with an endocardial MBF reserve of 1.5 to 2.5 showed inducible dysfunction after dipyridamole, whereas none of the segments with an endocardial MBF reserve of Ն2.

MCE parameters of perfusion at low power can be significantly altered by microbubble destruction in the LV cavity and in the myocardial microcirculation during RLPI. Short microbubble destruction pulse sequences and imaging only at end-systole can reduce these effects.