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OBJECTIVE: To test the hypothesis that myocardial stunning is due to myofibrillar oedema. METHODS: Experiments were performed in anaesthetised closed-chest pigs. In 15 pigs (group 1), myocardial stunning was produced by repetitive ischaemia and reperfusion; 5 pigs each were studied at 2 hours, 2 days, and 5 days later. Circumferential left ventricular (LV) mid-wall myocardial strain (E(cc)) was estimated in vivo using tagged magnetic resonance imaging. Myocardial water content (MWC) was measured post mortem, from which interfilament lattice distance (d) was calculated. In 6 pigs (group 2), myocardial dysfunction was produced by intracoronary administration of a mast cell degranulator. Animals were euthanised immediately upon induction of regional LV dysfunction to avoid development of inflammation. In 4 pigs (group 3), transmission electron microscopy (EM) was performed to quantify d in stunned versus normal myocardium. RESULTS: In group 1 pigs, MWC was raised in the stunned compared with normal myocardium (p<0.02) and decreased over time. An inverse relation was found between E(cc) and MWC in the stunned myocardium (r = -0.81) and between E(cc) and d (r = -0.90). A similar relation was noted between wall thickening and increase in MWC in group 2 (r = -0.84) pigs. In group 3 pigs, d on EM was significantly lower (40 (3) nmol/l) in normal myocardium than in stunned myocardium (46.4 (4) nmol/l), p<0.001. CONCLUSIONS: Ischaemia-reperfusion results in myocardial oedema, with consequent myocyte swelling and myofibrillar oedema. The latter leads to an increase in d, causing myosin heads to either fail to latch, or to latch improperly, onto the actin filament with poor force generation, leading to myocardial dysfunction. As the myocardial oedema abates, myocyte function improves.

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OBJECTIVE: To determine whether, when the vasomotor capacity of the coronary arterioles is exhausted at rest, myocardial blood volume decreases in order to maintain a normal capillary hydrostatic pressure, even at the expense of myocardial oxygen delivery. METHODS: 18 dogs were studied. In group 1 (n = 9), coronary driving pressure (CDP) was reduced by 10-80 mm Hg below normal by a stenosis; in group 2 (n = 9), it was increased 20-80 mm Hg above baseline by increasing aortic pressure with phenylephrine. Myocardial contrast echocardiography (MCE) was undertaken to measure the myocardial blood volume fraction and myocardial blood flow (MBF). RESULTS: In group 1 dogs, as CDP was reduced, both coronary blood flow (CBF) and MBF decreased. Myocardial blood volume fraction also decreased and myocardial vascular resistance increased, while coronary sinus PO2 decreased. In group 2 dogs, as CDP was increased, epicardial CBF increased but MBF remained unchanged because of a decrease in myocardial blood volume fraction. Myocardial vascular resistance decreased, however, implying the presence of coronary arteriovenous shunting, which was supported by a progressive increase in the coronary sinus PO2. CONCLUSIONS: When arteriolar tone is exhausted so that CBF becomes dependent on CDP, myocardial blood volume decreases in order to maintain a constant capillary hydrostatic pressure, which takes precedence over myocardial oxygen delivery. These novel findings implicate capillaries in the regulation of CBF beyond the autoregulatory range.

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BACKGROUND: There is no method of quantifying the severity of mitral regurgitation (MR) from injection of tracer directly into the left ventricular (LV) cavity, a method commonly used in the cardiac catheterization laboratory. METHODS AND RESULTS: We used a previously validated mathematical model that derives regurgitant fraction (RF) from the relative tracer washout from the left atrial (LA) and LV cavities. Thirty-nine patients referred for diagnostic cardiac catheterization with clinical evidence of possible MR were included in the study. Five milliliters of a microbubble mixture was power-injected into the LV during simultaneously performed contrast echocardiography. Relative changes in background-subtracted video intensity were measured from the LV and LA, and the resultant model-derived RF was correlated with the severity of MR on cineangiography. The severity of MR ranged from 0 to 4+ on cineangiography with corresponding model-derived RF of 0 to 0.69 on contrast echocardiography. A close linear relation was noted between angiographic severity of MR and model-derived RF on contrast echocardiography (y = 0.1x + 0.03, r = 0.89, P <.001). Contrast echocardiography was more sensitive than cineangiography for detecting mild MR. CONCLUSIONS: We describe a new method of measuring the severity of MR in the cardiac catheterization laboratory. Apart from being quantitative, this method can be safely used during cardiac catheterization in patients in whom iodinated contrast agents may be potentially harmful.

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To define the role of capillaries in the control of coronary blood flow (CBF) reserve, we developed a model of the coronary circulation and evaluated experimental data in its context. Our model comprised three compartments connected in series (arterial, capillary, and venous), each with its own resistance. The resistance in each vascular compartment was derived from the model based on hemodynamic data obtained in nine dogs during baseline and stenosis, both at rest and during hyperemia. The capillary hydrostatic pressure was assumed to be constant in all stages. Although in the absence of stenosis, the contribution of capillaries to total myocardial vascular resistance was only 25 +/- 5% at rest, it increased to 75 +/- 14% during hyperemia, despite the total myocardial vascular resistance decreasing by 51 +/- 13%. In the presence of a noncritical stenosis, total myocardial vascular resistance decreased by 22 +/- 10% at rest, with no change in capillary resistance. During hyperemia, total myocardial vascular resistance increased by 58 +/- 50% in the presence of the noncritical stenosis. In this situation, because arteriolar and venular resistances were already minimal, the increase in myocardial vascular resistance was due to increased capillary resistance, making it the predominant source (84 +/- 8%) of total myocardial vascular resistance. Myocardial video intensity (VI) on myocardial contrast echocardiography (MCE), which reflects capillary blood volume, decreased distal to the stenosis during hyperemia. In the presence of a flow-limiting stenosis at rest, myocardial VI also decreased, indicating that decrease in CBF was associated with an increase in capillary resistance. Our findings also provide an alternative explanation for the critical coronary closing pressure. Thus, contrary to previously held notions, capillaries play a vital role in the regulation of CBF.

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BACKGROUND: We hypothesized that the persistence of albumin microbubbles within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-reperfusion (I-R) occurs because of endothelial injury. METHODS AND RESULTS: The myocardial transit rate of albumin microbubbles was measured in 18 dogs perfused with different CP solutions and in 12 dogs undergoing I-R. Electron microscopy with cationized ferritin labeling of the glycocalyx was performed in 9 additional dogs after CP perfusion and in 3 additional dogs undergoing I-R. Microbubble transit was markedly prolonged during crystalloid CP perfusion. The addition of whole blood to the CP solution accelerated the transit rate in a dose-dependent fashion (P<0.05), which was greater with venous than with arterial blood (P<0.05). The addition of plasma or red blood cells to CP solutions was less effective in improving transit rate than addition of whole blood (P<0.05). Microbubble transit rate was independent of the temperature, K+ content, pH, PO2, osmolality, viscosity, and flow rate of the perfusate. Similarly, a proportion of microbubbles persisted in the myocardium after I-R, which was related to the duration of ischemia (P<0.01) but not of reflow. Crystalloid CP perfusion and I-R resulted in extensive loss of the endothelial glycocalyx without other ultrastructural changes. This effect was partially reversed in the case of crystalloid CP when it was followed by blood CP. CONCLUSIONS: Sonicated albumin microbubbles persist within the myocardium in situations in which the endothelial glycocalyx is damaged. The measurement of the myocardial transit rate of albumin microbubbles may provide an in vivo assessment of endothelial glycocalyx damage.

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BACKGROUND: We hypothesized that by using our newly defined method of destroying microbubbles and measuring their rate of tissue replenishment, we could assess the transmural distribution of myocardial perfusion. METHODS AND RESULTS: We studied 12 dogs before and after creation of left anterior descending coronary artery stenoses both at rest and during hyperemia (n=62 stages). Microbubbles were administered as a constant infusion, and myocardial contrast echocardiography (MCE) was performed with the use of different pulsing intervals. The video intensity versus pulsing interval plots derived from each myocardial pixel were fitted to an exponential function: y=A(1-ebetat), where A reflects microvascular cross-sectional area (or myocardial blood volume), and beta reflects mean myocardial microbubble velocity. The product A . beta represents myocardial blood flow (MBF). Average values for these parameters were derived from the endocardial and epicardial regions of interest placed over the left anterior descending coronary artery bed. Radiolabeled microsphere-derived MBF was also measured from the same regions. There was poor correlation between radiolabeled microsphere-derived MBF and A-endocardial/epicardial ratios (EER) (r=0.46). The correlation with beta-EER was better (r=0. 69, P<0.01). The best correlation with radiolabeled microsphere-derived MBF-EER was noted with A . beta-EER (r=0.88, P<0. 01). CONCLUSIONS: The transmural distribution of myocardial perfusion can be accurately assessed with MCE with the use of our newly described method of tissue replenishment of microbubbles after their ultrasound-induced destruction. In the model studied, an uncoupling of the transmural distribution of MBF and myocardial blood volume was observed during reversal of the MBF-EER.

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OBJECTIVES: This study sought to determine the basis of detection of stenosis by myocardial contrast echocardiography using venous administration of microbubbles and to define the relative merits of bolus injection versus continuous infusion. BACKGROUND: The degree of video intensity (VI) disparity in myocardial beds supplied by stenosed and normal coronary arteries can be used to quantify stenosis severity after venous administration of microbubbles. However, the comparative merits of administering microbubbles as a bolus injection or continuous infusion has not been studied. METHODS: Coronary stenoses of varying severity were created in either the left anterior descending or the left circumflex coronary artery in 18 dogs. Imagent US (AF0150) was given as a bolus injection in 10 dogs (Group I) and as both a bolus injection and a continuous infusion in 8 dogs (Group II). For bolus injections, peak VI was derived from time-intensity plots. During continuous infusion, microbubble velocity and microvascular cross-sectional area were derived from pulsing interval versus VI plots. Myocardial blood flow (MBF) was determined using radiolabeled microspheres. RESULTS: During hyperemia, VI ratios from the stenosed versus normal beds correlated with radiolabeled microsphere-derived MBF ratios from those beds for both bolus injections (r = 0.81) and continuous infusion (r = 0.79). The basis for detection of stenosis common to both techniques was the decrease in myocardial blood volume distal to the stenosis during hyperemia. The advantage of continuous infusion over bolus injection was the abolition of posterior wall attenuation and the ability to quantify MBF. CONCLUSIONS: Both bolus injection and continuous infusion provide quantitative assessment of relative stenosis severity. Compared with bolus injection, continuous infusion also allows quantification of MBF and data acquisition without attenuation of any myocardial bed.

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BACKGROUND: Ultrasound can cause microbubble destruction. If microbubbles are administered as a continuous infusion, then their destruction within the myocardium and measurement of their myocardial reappearance rate at steady state will provide a measure of mean myocardial microbubble velocity. Conversely, measurement of their myocardial concentration at steady state will provide an assessment of microvascular cross-sectional area. Myocardial blood flow (MBF) can then be calculated from the product of the two. METHODS AND RESULTS: Ex vivo and in vitro experiments were performed in which either flow was held constant and pulsing interval (interval between microbubble destruction and replenishment) was altered, or vice versa. In vivo experiments were performed in 21 dogs. In group 1 dogs (n=7), MBF was mechanically altered in a model in which coronary blood volume was constant. In group 2 dogs (n=5), MBF was altered by direct coronary infusions of vasodilators. In group 3 dogs (n=9), non-flow-limiting coronary stenoses were created, and MBF was measured before and after the venous administration of a coronary vasodilator. In all experiments, microbubbles were delivered as a constant infusion, and myocardial contrast echocardiography was performed using different pulsing intervals. The myocardial video intensity versus pulsing interval plots were fitted to an exponential function: y=A(1-e[-betat]), where A is the plateau video intensity reflecting the microvascular cross-sectional area, and beta reflects the rate of rise of video intensity and, hence, microbubble velocity. Excellent correlations were found between flow and beta, as well as flow and the product of A and beta. CONCLUSIONS: MBF can be quantified with myocardial contrast echocardiography during a venous infusion of microbubbles. This novel approach has potential for measuring tissue perfusion in any organ accessible to ultrasound.

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The dispersion and dilution of contrast medium through the myocardial vasculature is examined first with a serial model comprised of arterial, capillary, and venous components in series to determine their time-concentration curves (TCC) and the myocardial dilution curve (MDC). Analysis of general characteristics shows that the first moment of the MDC, adjusted for that of the aortic TCC and mean transit time (MTT) from the aorta to the first intramyocardial artery, is one-half the MTT of the myocardial vasculature and that the ratio of the area of the MDC and aortic TCC is the fractional myocardial blood volume (MBV). The use of known coronary vascular morphometry and a set of transport functions indicates that the temporal change in MDC is primarily controlled by the MTT. An analysis of several models with heterogeneous flow distributions justifies the procedures to calculate MTT and MBV from the measured MDC. Compared with previously described models, the present model is more general and provides a physical basis for the effects of flow dispersion and heterogeneity on the characteristics of the MDC.

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Venous injection of Albunex does not consistently produce left ventricular (LV) cavity opacification during conventional echocardiography. We postulated that by increasing the signal-to-noise ratio, harmonic imaging will result in more successful LV cavity opacification and provide a better assessment of regional LV systolic function. Forty-two patients with poor baseline endocardial delineation were given 10 ml intravenous injections of Albunex during continuous fundamental and harmonic imaging. Change in segmental wall-thickening scores and the confidence levels for these scores were assessed for 3 observers with various levels of experience. Compared with fundamental imaging, harmonic imaging significantly improved the success of LV cavity opacification (83% vs 62%, p <0.05). The background-subtracted video intensity within the central two thirds of the LV cavity increased threefold (from 10 +/- 15 to 31 +/- 29, p <0.05) with harmonic imaging. The spatial extent of opacification increased from 40% of the LV cavity during fundamental imaging to 65% with harmonic imaging (p <0.001). The confidence level for assessing regional LV systolic function improved (p <0.05) after contrast administration, particularly when observer experience was limited. We conclude that in patients with poor endocardial definition, injection of intravenous Albunex should be combined with harmonic imaging to improve LV cavity opacification.

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OBJECTIVES: We attempted to examine the interactions between ultrasound and microbubbles. BACKGROUND: The interactions between microbubbles and ultrasound are poorly understood. We hypothesized that 1) ultrasound destroys microbubbles, and 2) this destruction can be minimized by limiting the exposure of microbubbles to ultrasound. METHODS: We performed in vitro and in vivo experiments in which microbubbles were insonated at different frequencies, transmission powers and pulsing intervals. Video intensity decay was measured in vitro and confirmed by measurements of microbubble size and concentrations. Peak video intensity and mean microbubble myocardial transit rates were measured in vivo. RESULTS: Imaging at lower frequencies and higher transmission powers resulted in more rapid video intensity decay (p = 0.01), and decreasing exposure of microbubbles to ultrasound minimized their destruction in vitro. Although these effects were also noted in vivo with venous injections of microbubbles, they were not seen with aortic root or direct coronary artery injections. CONCLUSIONS: Ultrasound results in microbubble destruction that is more evident at lower frequencies and higher acoustic powers. Reducing the exposure of microbubbles to ultrasound minimizes their destruction. This effect is most marked in vivo with venous rather than aortic or direct coronary injections of microbubbles. These findings could lead to effective strategies for myocardial perfusion imaging with venous injections of microbubbles.

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Vasodilation of microvessels distal to a stenosis results in an increase in myocardial blood volume (MBV). The purpose of this study was to examine the changes in MBV induced by graded coronary artery stenoses by using myocardial contrast echocardiography (MCE). Accordingly, 21 dogs underwent progressive stenosis of a coronary artery in a random order, the severity of which was judged by the pressure distal to it. Total myocardial blood flow (MBF) to the bed distal to the artery (both anterograde and collateral) was measured by injection of radiolabeled microspheres into the left atrium. In seven dogs, anterograde and total MBF were measured at each stenosis stage by injection of different microspheres into the left atrium and directly into the coronary artery, respectively. MBV was calculated by dividing MBF by the mean transit rate of microbubbles injected directly into the coronary artery during MCE. The perfusion bed size of the artery was also measured by MCE. Our major findings are as follows: 1) there is a nonlinear increase in MBV with increasing degrees of coronary stenosis until the coronary stenosis becomes critical; 2) at moderate levels of coronary stenosis, MBV remains constant despite ongoing autoregulation because of reduction in the size of the perfusion bed supplied by the stenotic vessel; and 3) after exhaustion of autoregulation, a decrease in MBV is noted with increasing levels of stenosis. We conclude that assessment of MBV provides insights into myocardial perfusion distal to a coronary stenosis above and beyond that provided by the measurement of MBF alone.

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BACKGROUND: We hypothesized that microvascular reserve is a better indicator of the extent of viable myocardium postinfarction than contractile reserve, especially in the presence of a residual stenosis of the infarct-related artery. METHODS AND RESULTS: Fifteen dogs with various infarct sizes were studied after reperfusion. Contractile reserve, studied by use of dobutamine echocardiography, and microvascular reserve, studied by use of myocardial contrast echocardiography, were measured both before and after creation of a stenosis. In the absence of a stenosis, the relation between infarct size, expressed as percent of risk area, and wall thickening improved with increasing doses of dobutamine (r = .41, .71, and .90 for 5, 10, and 15 micrograms.kg-1.min-1, respectively; P < .01 for dobutamine 15 micrograms.kg-1.min-1). In the presence of a stenosis, however, the relation was poor for all doses of dobutamine (r = .22, .57, and .32 for 5, 10, and 15 micrograms.kg-1.min-1, respectively; P < .01 for 15 micrograms.kg-1.min-1 dobutamine in the absence of a stenosis). There was a fair correlation between infarct size and perfusion defect size on myocardial contrast echocardiography after reperfusion (r = .82), with the defect size underestimating infarct size by approximately 20%. This relationship improved (P < .01) during infusions of both adenosine (r = .99) and dobutamine (r = .94) in the absence of a stenosis. The correlations between infarct size and perfusion defect on myocardial contrast echocardiography also remained good in the presence of a stenosis (r = .95 and .81 for adenosine and dobutamine, respectively; P = NS compared with stenosis). CONCLUSIONS: Microvascular reserve is superior to contractile reserve for definition of the spatial topography of necrosis and hence the extent of viable myocardium within the infarct bed after reperfusion, particularly when a residual stenosis is present in the infarct-related artery.

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BACKGROUND: We have previously shown that the intravascular rheology of sonicated air-filled albumin microbubbles is similar to that of red blood cells (RBCs) and that their myocardial transit rate is also similar to that of RBCs in the beating canine heart. In the present study, we tested the hypothesis that the myocardial transit rates of these microbubbles reflect those of RBCs in humans at different coronary flow rates. METHODS AND RESULTS: RBC and microbubble transit rates were measured in 17 patients undergoing coronary angiography: in 8, measurements were made only at rest, whereas in 9, they were performed both at rest and during a pacing-induced increase in coronary blood flow. A gamma-variate function was used to derive mean RBC and microbubble transit rates from the time-activity and time-intensity plots after the left main injection of RBCs and microbubbles, respectively. There was linear correlation between the myocardial transit rates with both tracers with the slope of the correlation determined by the specific echocardiographic system that was used. Microbubble transit rate consistently overestimated RBC transit rate due to artificial narrowing of the time-intensity curves caused by chest wall attenuation of the echocardiographic signal, which was confirmed through in vitro experiments. CONCLUSIONS: There is close correlation between air-filled albumin microbubbles and RBC rheology in the human myocardium. The use of these microbubbles in the cardiac catheterization laboratory could, therefore, provide further insights into myocardial blood flow/myocardial blood volume relations in humans.

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The factors that influence the extent of mitral leaflet opening (MLO) and closure (MLC) have not been defined. We hypothesized that left ventricular (LV) systolic function determines the rate of increase of the early diastolic left atrial (LA)-LV pressure gradient, which is responsible for the extent of MLO, and also the rate of change of the early systolic LV-LA pressure gradient, which determines the degree of MLC. Accordingly, global LV function was changed by altering left main coronary artery flow with LA pressure held relatively constant. LV end-systolic dimension and peak positive LV rate of pressure development (dP/dt) correlated best with the degrees of MLO and MLC, with average correlation coefficients of 0.88 and 0.68, and 0.86 and 0.72, respectively. Although transsecting the submitral apparatus resulted in flailing of the mitral leaflets during normal LV systolic function, the extents of MLO and MLC during LV systolic dysfunction were still influenced by LV systolic function. It is concluded that LV systolic function determines the extent (both opening and closure) of mitral leaflet excursion.

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This study was designed to answer the question of whether, despite their theoretic superiority, integrated backscatter imaging (IBS) and digital data acquisition (DA) offer any advantage over conventional echocardiography (CE) during quantitative myocardial contrast echocardiography. In vitro experiments were performed (1) to determine the microbubble concentration versus videointensity relationships for CE and IBS and (2) to define the relationship between flow through and microbubble transit rates for CE and IBS. These data were stored on videotape. In vivo experiments were performed whereby microbubbles were injected into the left anterior descending artery at different flow rates in 14 dogs and IBS and CE data were stored both in digital format and on videotape. Although the level of compression did not affect the microbubble concentration versus videointensity plots during IBS compared with CE, in practical terms the mean transit rate, peak intensity, and area under the curve were not affected by the level of compression for both forms of imaging as long as the postprocessing used for CE imaging was linear and the microbubble dose was small. In addition, although DA resulted in higher peak intensity and area under the curve compared with storage on videotape because of its broader dynamic range, the correlation between these measurements was excellent with both forms of image storage. We conclude that, although differences exist between CE and IBS and between Da and analog acquisition, these differences do not significantly affect the derivation of parameters from time-intensity plots during myocardial contrast echocardiography when contrast material is injected into a coronary artery.

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Although retrograde cardioplegia (RC) is being increasingly used in clinical practice, its physiology is unclear. Because the microvascular architecture of the coronary venous system is different from that of the arterial system, we hypothesized that myocardial perfusion would be different during RC compared with anterograde cardioplegia (AC) delivery. To better understand these differences, three groups of dogs were studied during similar RC and AC flow rates. Radiolabeled microsphere-derived microvascular flow underestimated total cardioplegia flow by 66% during RC. For the same flows, the first-pass extraction fractions of 201Tl and 99mTc were significantly less during RC compared with AC despite adjusting for microsphere loss. Myocardial contrast echocardiography (MCE), however, provided an accurate estimation of AC and RC flow rates. In addition, the rate of myocardial cooling for most of the left ventricular myocardium was similar for AC and RC at the same flow rates, as long as the flow rates were brisk. It is concluded that microvascular and nutrient flows are significantly lower at the same flow rates during RC compared with AC due to loss of RC at different microvascular sites. Unlike microspheres and diffusible radioisotopes, MCE can provide a reliable measure of myocardial flow during RC delivery. Furthermore, myocardial cooling is similar in most of the myocardium during high-flow RC and AC, which suggests that the clinical benefits of RC are probably related to myocardial cooling and that substrate replenishment may be better achieved at the same flow rates and myocardial temperatures with AC rather than RC.

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The calculation of mean microbubble transit rate (MMTR) during contrast echocardiography provides information regarding the flow through and blood volume of a vascular system. Several technical factors can impact on the accuracy of MMTR determination. In this study, with computer simulation and in vitro and in vivo data, we systematically examined four such factors: the relationship between microbubble concentration versus videointensity, the size of the region of interest and the sampling rate used to derive time-intensity plots, and the method of deriving MMTR (direct numeric calculation vs use of a mathematic model). The results indicate that the effect of these technical factors on the estimation of MMTR can be significant.

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BACKGROUND: We hypothesized that the degree and spatial extent of blood flow mismatch in beds supplied by stenoses that are not flow-limiting at rest can be quantified with myocardial contrast echocardiography (MCE) using left atrial (LA) and right atrial (RA) injections of contrast during pharmacologically induced coronary hyperemia. METHODS AND RESULTS: In 12 open-chest dogs, MCE was performed and myocardial blood flow (MBF) was measured by use of radiolabeled microspheres at baseline and during phenylephrine-induced coronary hyperemia. In the presence of this drug, stenoses were placed during different stages on the left anterior descending (LAD) and left circumflex (LCx) coronary arteries, and MCE and MBF assessments were performed. LA injections of 2 mL of 0.5 billion/mL microbubbles (mean diameter, 4.3 microns) were performed at each stage in all 12 dogs, and RA injections of 10 mL of 6 billion/mL microbubbles (mean diameter, 3.7 to 5.3 microns) were administered in 7 dogs. MCE images in which the contrast disparity between the LAD and LCx beds was maximal were digitally subtracted from precontrast images, and mean videointensities in these beds were measured after the dynamic range of gray-scale intensities was increased in the subtracted image and the image was color coded. The region showing hypoperfusion during LAD stenosis was planimetered and expressed as a percentage of the myocardial area in the short-axis slice. There was an excellent correlation between the LAD/LCx bed videointensity ratio and LAD/LCx bed MBF ratio (y = 0.5x + 0.44, r = .91, P < .001) during 57 LA injections. There was also an excellent correlation between the hypoperfused bed size on MCE during LA injection of contrast in the presence of LAD stenosis and the hypoperfused myocardium as determined by radiolabeled microspheres (y = 0.8x + 4.2, r = .90, P < .001, SEE = 2.4, n = 11). The anterior myocardium was opacified in 6 dogs receiving RA injections of contrast, and the hypoperfused area during LAD stenosis correlated closely with that determined by radiolabeled microspheres (y = 0.86x + 3.4, r = .93, P < .01). CONCLUSIONS: Coronary stenoses, which are not flow limiting at rest, can be detected and the degree and spatial extent of blood flow mismatch during pharmacologically induced coronary hyperemia can be quantified with MCE using LA and RA injections of contrast. Thus, it is possible that the severity of coronary stenoses and the quantum of myocardium in jeopardy could be quantified in the future with MCE using venous injection of contrast.

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