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Noninvasive CardiologyFocused Review
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ontrast Echocardiography: Fulfillingts Promise
evin Wei, MD, FACC, Cardiac Imaging Center,ardiovascular Division, University of Virginia Schoolf Medicine, Charlottesville, Virginia
chocardiography has become an indispensable method forroviding an assessment of myocardial structure, function,nd flow within the cardiac chambers and major vessels. Itsbility to provide instantaneous information at the bedsideannot be matched by any other noninvasive imaging modal-ty.
In the last few years, increasing clinical data support these of microbubble contrast agents during echocardiogra-hy. This technology has been shown to improve left ven-ricular endocardial border delineation (LVEBD) in patientsith suboptimal acoustic windows—the only currently ap-roved indication for contrast echocardiography. The as-essment of LV function is the most common reason forrdering an echocardiogram, and its accurate assessmentnd quantification is critical for determining patient prog-osis and to help direct patient management, especiallyith current expanded indications for device therapies. These of contrast is important in situations where all myocar-ial segments must be adequately visualized, such as stresschocardiography. Moreover, LVEBD enhances quantifica-ion of LV volumes and ejection fraction (EF) and improveshe ability of automated border detection algorithms thatan aid in the assessment of LV function. Also, contrast canelp to delineate intracardiac masses or thrombi, aneu-ysms, and other structural abnormalities. Finally, contrastan be used to enhance Doppler signals to improve assess-ent of gradients or other hemodynamic variables.The development of contrast agents has also added perfu-
ion imaging to the diagnostic capabilities of echocardiogra-hy. As the field is currently perched on the cusp of havingyocardial perfusion imaging approved as a new clinical in-ication, it is an opportune time to review how myocardialontrast echocardiography (MCE) may fulfill its promise as theone-stop shop” of noninvasive cardiac imaging.
icrobubble Contrast Agentshe three agents currently approved to enhance LVEBD in thenited States include Optison (GE-Amersham, Princeton, NJ),efinity (Bristol-Myers Squibb Medical Imaging, North Bil-
erica, MA) and Imagent (IMCOR Pharmaceutical, San Diego,A), all of which are high molecular weight gases encapsulatedy a thin shell. The low solubility and diffusibility of these gases
ermit the agents to persist after intravenous (IV) administra- oACC CURRENT JOURNAL2005 by the American College of Cardiology Foundation
ublished by Elsevier Inc. 26
ion and to opacify the systemic circulation. Their size (smallerhan red blood cells) allows the microbubbles to transit theicrovasculature unimpeded.Unlike the tracers used with CT, MRI or SPECT, micro-
ubbles remain entirely intravascular, are hemodynami-ally inert, and have a microvascular rheology identical tohat of red blood cells. These properties make microbubblesnique perfusion agents, thus obviating the need for com-lex modeling required with many other technologies foruantifying myocardial blood flow (see below).
maging Modalities for Myocardial Contrastchocardiographyhe microbubble agents used during MCE are effectivecatterers of ultrasound because they are compressible andscillate within the sound field. In fact, at the acousticowers used clinically, microbubbles are easily destroyedy ultrasound. Thus, to successfully opacify the left ventric-lar cavity for LVEBD studies during high frame rate imag-
ng, the transmit power (as denoted by the mechanicalndex [MI] on the system) has to be reduced so as to
inimize microbubble destruction.Nonlinear oscillation and destruction of microbubbles
y ultrasound produce microbubble signals that are uniquerom myocardial tissue. These signals have been harnessedy novel imaging modalities designed specifically for MCE.he first MCE modality developed was harmonic imaging,here ultrasound at the fundamental frequency is transmit-
ed, and a high pass filter is used to selectively receiveignals at double the transmit frequency (second har-onic). Harmonic imaging is an excellent modality for
VEBD because it is available on all current systems androvides a high frame rate. As noted above, it is importanto reduce the MI (between 0.3 and 0.6) with harmonicmaging to avoid microbubble destruction in the cavity—specially at the apex. The associated reduction in signalan be accommodated by increasing the receive gain. Theains should be high enough to allow the epicardial bordero be seen, which allows assessment of wall thickening andot simply endocardial excursion, which can be affected byethering from adjacent segments. More recently, low MI
CE techniques (see below) that were designed for perfu-ion imaging have been used for LVEBD, but the frame ratesre invariably lower as all these techniques rely on theransmission of multiple ultrasound pulses per line (multi-ulse techniques).
For perfusion imaging, further refinements have beeneveloped. Although it is beyond the scope of this review toetail all the available imaging modalities, they essentiallytilize algorithms that incorporate various receive filtersnd also transmit sequential ultrasound pulses of differinghase and/or power, to both generate and detect uniquenonlinear” microbubble signals while suppressing tissueignals. The ultimate objective of these modalities is to fully
ptimize the signal (from microbubbles)-to-noise (fromREVIEW April 20051062-1458/05/$30.00
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issue) ratio. As shown in Figure 1, microbubble backscat-er signals (solid line, “a”) are of equal intensity to tissueignals (dotted line, “b”) with fundamental imaging, wherehe transmit and receive frequencies are identical (fo). Withecond harmonic imaging (transmit at fo with receive only atfo), improvement in the signal-to-noise ratio (“c” vs. “d”) ischieved, but strong tissue clutter (“d”) is still presentFigure 1). With the recent development of broader bandransducers, further improvement in the signal-to-noiseatio (“e” vs. “f”) has been accomplished with ultraharmonicmaging (transmit at fo with receive only at 5/2fo), whichakes advantage of low tissue noise (“f”) at the ultrahar-onic while microbubble destruction produces strong mi-
robubble signals (“e”) (Figure 1). Harmonic and ultrahar-onic imaging use B-mode processing techniques to
uppress tissue noise, but Doppler processing can also besed. With the latter, received signals from tissue show littlepectral decorrelation compared to the transmitted signal,hich can then be suppressed by an appropriate wall filter.onversely, microbubble destruction produces received
ignals that are markedly different from those transmitted;onsequently, only the power spectrum of microbubbles isisplayed (power harmonic Doppler).
Tissue clutter can also be suppressed using multipulsechemes where the amplitude (power modulation) or phasepulse inversion) of sequential pulses are altered. Withower modulation (Figure 2), pulses at half-height (“a”)nd full-height amplitude (“b”) are transmitted sequen-ially. The received signals from a linear scatterer such asissue (Panel A, Figure 2) are identical to the transmittedulses. Subsequently, the received echoes from the half-eight transmitted pulses are scaled and subtracted fromhe full-height signal, which results in effective removal ofissue clutter. Conversely, nonlinear scatterers such as mi-robubbles (Panel B, Figure 2) produce received signals thatre different from the transmitted pulses (especially theull-height pulse), resulting in residual microbubble signal
igure 1. Backscatter acoustic intensity from microbubbles (solid line) andtissue (dotted line) at the fundamental, harmonic, and ultraharmonicfrequencies. See text for details.
ven after subtraction.
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With pulse inversion (Figure 3), sequential pulses ofnverted phase are transmitted. Again, linear scatterersPanel A, Figure 3) produce received signals identical to theransmitted pulses, and summation of the received signalsesults in cancellation of tissue noise. Nonlinear scatterersPanel B, Figure 3), however, generate signals that cannote summed. Both power modulation and pulse inversionave also been combined into a single modality (contrastulse sequencing) where alternate ultrasound pulses haveiffering amplitude and phase. As noted above, the ability ofhese multipulse algorithms to suppress tissue depends on ainear response to the insonating ultrasound, which occurs
ainly at low MIs. At high MIs, nonlinear propagation ofltrasound through tissue generates harmonic signals.hus, these algorithms are incorporated mainly into low MI
maging modes.The wide array of imaging modalities provides the user
ith great range and flexibility, and if any particular mode
igure 2. Schema for imaging modalities using power modulation. See text fordetails.
igure 3. Schema for imaging modalities using pulse inversion. See text for
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s inadequate for a patient, a different one can be used. Achema is provided in Figure 4 to help organize the variousmaging modalities currently available on commercial sys-ems. Perfusion modalities can be grouped into those thattilize high or low MI. The former require imaging at a lowrame rate (triggered to the heart rate) because they destroy
icrobubbles, whereas the latter can be performed even atigh frame rates and therefore allow LV function and per-usion to be assessed simultaneously.
uantification of Capillary Blood Volumessessing the adequacy of myocardial perfusion requires anvaluation of both myocardial oxygen delivery and con-umption. Many techniques can address the former byuantifying myocardial blood flow (MBF), but becauseBF does not provide a measure of myocyte energy re-
uirements, its measurement alone may not be adequate forssessing myocardial perfusion in some disease states.
Use of MCE may provide a unique solution to thisroblem because both MBF velocity and myocardial bloodolume (MBV) can be determined independently. Micro-ubbles reside exclusively within the vascular space, so theyct as blood pool agents, and their concentration in theyocardium reflects the MBV, 90% of which is in capillar-
es. Thus, steady-state contrast enhancement provides anssessment of capillary blood volume. The ability to definehe spatial extent of capillary integrity underlies the assess-ent of myocardial viability on MCE. During acute myo-
ardial infarction, MCE can be used to noninvasively deter-ine the area at risk of necrosis, the degree of collateral flowithin the risk area, and therefore even ultimate infarct sizerior to reperfusion. The success of reperfusion strategiesn restoration of blood flow at the tissue level can also bessessed, and the extent of microvascular no-reflow pre-icts recovery of resting function and patient prognosis.he excellent spatial resolution of MCE (�1 mm axially)llows for detection of even subendocardial infarcts, andhe transmural extent of no-reflow on MCE has been showno correlate well with hyperenhancement on magnetic res-
igure 4. Organizational chart for commercially available perfusion imagingmodalities.
nance imaging (MRI). m
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MCE has defined the role of capillaries in the regulationf capillary hydrostatic pressure. At rest, the mean aorticressure is approximately 90 mm Hg, whereas the capillaryydrostatic pressure is only 30 mm Hg. A constant capillaryydrostatic pressure is essential for homeostasis and torevent development of interstitial or cellular edema. Al-hough myocytes can sustain fairly long periods of ischemiaup to 30 or 45 min), they are far more sensitive to fluctu-tions in capillary hydrostatic pressure, so tight control ofapillary hydrostatic pressure is an important function ofutoregulation. The aortic pressure is reduced to about 45m Hg at the proximal end of the capillaries owing to high
esistance in small-resistance arterioles, which contributebout 60% of the total myocardial vascular resistance atest. The capillaries contribute only 25% of total resistance,nd the veins about 15%.
As perfusion pressure decreases or increases, resistancerterioles respond respectively by dilating or constricting toodulate their tone and resistance to maintain normal
esting coronary blood flow and capillary hydrostatic pres-ure. This autoregulation is effective for coronary perfusionressures between about 45 mm Hg and 120 mm Hg. Inkeletal muscle, however, it has been shown that net trans-apillary fluid movement (a marker of capillary hydrostaticressure) remains remarkably stable even when perfusionressure is varied beyond the lower and upper limits of theutoregulatory range. Thus, MCE has demonstrated thathen coronary driving pressure was lowered below the
ower limits of the autoregulatory range with severe steno-es, capillaries themselves will participate in autoregulationo maintain capillary hydrostatic pressure. Therefore, ratherhan being passive conduits, capillary resistance can beynamically modulated. Because capillaries do not possessmooth muscle, they cannot constrict, so the only way theyan increase their resistance is by derecruitment. Moreover,ecause capillaries are laid in parallel, their total resistancearies inversely with their number. With critical stenoses,esting perfusion defects become evident on MCE fromapillary derecruitment. The same phenomenon occurshen IV infusions of phenylephrine increased driving pres-
ure above the upper limits of autoregulation.Capillaries are also involved in maintaining capillary
ydrostatic pressure in the presence of a coronary stenosisuring hyperemia. As shown in Figure 5, although arte-ioles contribute the greatest proportion of total coronaryascular resistance at rest (solid “Ra” bar), arteriolar resis-ance decreases about 85% during maximal hyperemiaopen “Ra” bar). In this setting, the capillaries contribute thereatest proportion (about 75%) of total coronary vascularesistance (open “Rc” bar). Capillary resistance, therefore,ictates the maximal possible increase in myocardial bloodow during hyperemia.
Owing to an imbalance between changes in coronaryriving pressure and flow during vasodilation in the pres-nce of a stenosis, capillaries have to derecruit in order to
aintain capillary hydrostatic pressure. Capillary dere-REVIEW April 2005
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ruitment in the stenosed bed during hyperemia results in aecrease in capillary volume, which produces perfusionefects on MCE. With more severe stenosis, there is greaterapillary derecruitment and more severe perfusion defects.gain, because capillaries are laid in parallel, the loss ofome capillaries results in increases in their resistance,hich decreases maximal hyperemic flow. Thus, the pro-ressive decrease in hyperemic flow with increasing levelsf stenosis is due to greater degrees of capillary derecruit-ent and higher resistance. Decreases in capillary blood
olume and increases in their resistance in the presence of atenosis during hyperemia are the most important factorsroducing regional differences in flow reserve and inducibleerfusion defects on MCE.
uantification of Myocardial Blood Flow Velocitypart from evaluating regional differences in capillary bloodolume, flow velocity mismatch between the stenosed andormal beds can be assessed with MCE because micro-ubbles have the same intravascular rheology as do redlood cells. Evaluating their transit through the microcir-ulation provides information regarding red blood cell ki-etics. At steady state during a continuous IV infusion oficrobubbles, the number of microbubbles entering or
eaving any microcirculatory unit is constant, and will de-end on the flow rate. By destroying microbubbles with anltrasound pulse, and then determining the rate of replen-
shment of microbubbles into tissue, microbubble (or redlood cell) velocity can be determined.
This concept is depicted in Figure 6. After microbubblesre destroyed by a pulse of ultrasound within the beamlevation (panel A), the degree of microbubble replenish-ent into the elevation increases as the pulsing interval is
ncreased as there is more time for replenishment to occuretween each destructive pulse of ultrasound (panels B–E).s long as the relation between microbubble concentrationnd myocardial acoustic intensity (AI) is linear, progres-ively higher tissue AI is seen at longer pulsing intervals
igure 5. Distribution of resistances through the coronary circulation at rest(filled bars) and after vasodilator stress (open bars) (reproducedwith permission from Wei et al., Cardiol Clin 2004;22:224).
panel F, Figure 6). When the pulsing interval is long i
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nough for the entire ultrasound beam elevation to beompletely replenished with microbubbles (panel E), fur-her increases in pulsing interval do not result in any furtherncreases in tissue AI, and the pulsing interval versus AIelation plateaus. Plateau myocardial AI represents myocar-ial (or capillary) blood volume. Because the normal restinglood flow velocity within the capillaries is very low (�1m · s�1), and the ultrasound beam elevation mea-
ures approximately 5 mm in thickness, more than 5 s areequired between pulses of ultrasound to allow completeeplenishment for estimation of capillary blood volume.he pulsing interval versus myocardial AI relation (panel F,igure 6) can be fitted to an exponential function: y �(1 � e��1), where A is the plateau AI representing capil-
ary blood volume, and � represents the mean microbubbleor red blood cell) velocity. Therefore, MCE can be used toetermine both specific components of MBF—flow velocity�) and blood volume (A, which is proportional to cross-ectional area).
The ability of MCE to assess regional differences inyperemic flow velocity are illustrated in Figure 7. Imagesere obtained from the apical 4-chamber view in a patientith a left anterior descending coronary artery stenosisuring dipyridamole stress at progressively longer pulsing
igure 6. Progressive replenishment of microbubbles into the ultrasound beamelevation (E) at increasing pulsing intervals (t1–t4) (Panels A–E).Pulsing interval versus myocardial acoustic intensity relation is fittedto an exponential function (Panel F). See text for details (reproducedwith permission from Tong KL, Wei K, Cardiol Clin 2004;22:235).
ntervals. The normal basal septum has a high MBF velocity
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uring hyperemia with rapid microbubble replenishment.ven at a short pulsing interval of 800 ms (every cardiacycle), the septum is already homogeneously replenishedith microbubbles, and no further increases in AI are seen
t longer intervals. The rate of replenishment in the apicalegion of the stenosed left anterior descending perfusioned is slower, especially in the subendocardial region, re-ulting in the appearance of a subendocardial perfusionefect. By 5000 ms (8 cardiac cycles), most of the apex haseplenished.
Delayed subendocardial replenishment during hyper-mia is a typical MCE finding of a coronary stenosis, andigure 7 illustrates how regional differences in MBF velocityeserve can be visually estimated. A semiquantitativeethod that can be used to visually determine abnormalBF velocity reserve is to note the pulsing interval at which
ubendocardial defects are seen. During hyperemia, normalncreases in MBF velocity should allow the myocardium toeplenish with microbubbles in 1 or 2 cardiac cycles. De-
igure 7. Images obtained at four different pulsing intervals (PI) from the api-cal 4-chamber view during dipyridamole stress. Pulsing interval ver-sus myocardial acoustic intensity curves from the septum and apexare shown below. See text for details.
able 1. Detection of CAD With MCE
tudy YearNo. of
Patients MCE ModeStressMethod
aul et al. 1997 30 High MI DPorter et al. 1997 28 High MI DPeinle et al. 2000 123 High MI Adwajg et al. 2000 45 Low MI Ex./Dbhimoni et al. 2001 100 Low MI Ex.himoni et al. 2001 44 Low MI Ex.orter et al. 2001 117 Low MI Dborter et al. 2001 40 Low MI Dbaluska et al. 2001 49 High MI DPraby et al. 2002 27 High MI DPraby et al. 2002 42 Low MI DPei et al. 2003 43 High MI DP
I � mechanical index, DP � dipyridamole, Ad � adenosine, Ex. � exercise, D
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ayed replenishment beyond this point would indicate ab-ormal hyperemic MBF velocity. Although the examplehows the use of a high MI-triggered perfusion modality,he same principle of replenishment can be applied to low
I techniques. With the latter, a few “impulse” high MIrames are transmitted to destroy myocardial microbubbles,nd replenishment can then be assessed from sequentialnd-systolic frames. The main advantage of low MI tech-iques is the rapidity with which replenishment curves cane attained.
Visual assessments of either regional differences in MBVr MBF velocity during exercise, vasodilator or inotropictress, using both low or high MI imaging from MCE, haveeen shown in studies involving more than 650 subjects toave excellent sensitivity, specificity, and concordanceompared to other noninvasive modalities and coronaryngiography for the detection of coronary artery diseaseCAD) (Table 1). The addition of myocardial perfusion alsoncreases the sensitivity and accuracy for detecting CADver evaluations of wall thickening alone during dobut-mine stress protocols.
Stenosis severity could be more precisely quantified bytting regional pulsing interval versus AI curves with thexponential function discussed above. As shown in Figure, the normal septum has high MBF velocity characterizedy the high rate constant �h, whereas that of the apex (�s) is
ower. Most ultrasound systems now provide off-line quan-ification packages for myocardial perfusion data. The ratio
s/�h provides a measure of relative MBF velocity reserve.ormalizing �h or �s to resting MBF velocity (�r) wouldrovide assessments of absolute regional MBF velocity re-erve. Quantification of MBF velocity reserve correlates wellith values derived using intracoronary Doppler flow wire,
nd can therefore be used to both detect and quantifytenosis severity with MCE.
Finally, coronary flow reserve may not specifically reflecthe severity of a coronary stenosis because it may be alteredy physiologic factors such as changes in aortic pressure,
Goldtandard
Sensitivity(%)
Specificity(%)
Concordance(%) Kappa
PECT – – 86 0.71PECT 92 84 84 –PECT – – 81 0.60ngio – – 80 0.61PECT – – 76 0.50ngio 75 100 – 0.67SE – – 91 0.70ngio – – 83 0.65PECT 83 55 – –PECT – – 82 0.49PECT – – 87 0.72PECT 96 63 84 0.63
dobutamine, SPECT � single-photon emission computed tomography, angio �
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eart rate, or contractility—factors that can alter both myo-ardial oxygen demand and flow. Figure 8 shows the rela-ion between %coronary stenosis severity and coronaryow reserve under normal physiologic conditions (openircles), when aortic pressure was increased with phenyl-phrine (closed circles), or decreased with nitroprussideclosed squares). There are striking differences in absoluteoronary flow reserve at all levels of stenosis, so the absolutealue alone is meaningless without some knowledge ofyocardial oxygen consumption. An assessment of capil-
ary blood volume can be used to provide insight intoyocardial oxygen consumption. It has been noted thathen myocardial oxygen consumption was increased withacing or dobutamine up to 200% of baseline levels, aroportional increase occurred in both coronary blood flownd MBV fraction. When myocardial oxygen consumptionas increased above 200%, the magnitude of increase inBV fraction outstripped that of coronary blood flow. So an
ssessment of MBV can again provide some insights into thehysiologic milieu that exists concurrently with changes inow.
ummaryhe development of microbubble contrast agents has im-roved the ability of echocardiography to qualitatively as-ess LV function and structural abnormalities, and it hasssentially removed the impediment of a suboptimal acous-ic window. Furthermore, the use of contrast significantlymproves the ability of echocardiography to provide quan-itative measures of LV volume and ejection fraction.
With the advent of myocardial perfusion imaging, echo-ardiography can be used to assess flow-function relations,valuate microvascular integrity in acute and chronic set-ings, and not only determine the presence of coronarytenoses but quantify their physiologic significance andeverity. Thus, MCE truly has the ability to be a one-stop
igure 8. Relation between %stenosis severity and absolute coronary flow re-serve at baseline (open circles), during phenylephrine (closed cir-cles), and nitroprusside (closed squares). See text for details (re-drawn with permission from Gould et al., J Am Coll Cardiol 1990;15:459 –74).
hop for noninvasive imaging.
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uestions and Answers
. During dobutamine stress echocardiography, LVEBDcould be accomplished using:A) Harmonic imagingB) Power harmonic Doppler imagingC) Power pulse inversion or power modulation imagingD) A or C
The answer is D. Both harmonic imaging and lowMI (mechanical index) modalities such as powerpulse inversion or power modulation imaging couldbe considered. However, the maximum frame ratesachievable with low MI modalities are lower, andassessment of wall thickening at high heart rates maybe compromised. Thus, these modalities are not asoptimal for young patients, or in situations whereimaging settings produce frame rates �20 Hz.Power harmonic Doppler is a poor choice for LVEBDbecause it is susceptible to motion artifacts during“real time” imaging.
. During a LVEBD study, contrast “swirling” is observed atthe apex and homogeneous opacification of the LV cav-ity cannot be achieved. Maneuvers to improve opacifi-cation include:A) Increasing the infusion rate or administering an-
other slow bolus of microbubblesB) Decreasing the MI and increasing the gainC) Decrease the frame rate by triggeringD) All of the the above
The answer is D. Inhomogeneous opacification dur-ing LVEBD studies is most commonly caused by inad-equate microbubble dose or excessive ultrasoundpower that destroys microbubbles in the LV cavity. Insituations where microbubbles have already been usedup, triggering the transmission of ultrasound to onlyend-diastole (peak of R wave on ECG) and end-systole(peak of T wave) would decrease destruction enough toopacify the cavity and still allow quantification ofLVEF.
. A patient with normal LV function is noted to have anapical perfusion defect during a resting MCE study. Thedefect represents:A) Severe myocardial ischemia in the left anterior de-
scending coronary artery territoryB) Prior apical infarctionC) Apical destruction artifactD) None of the above
The answer is C. It is not physiologically possibleto have a perfusion defect and normal thickening ofthe same segment at rest. Overlap of ultrasound linesin the near field often produces excessive micro-bubble destruction and an artefactual apical defect.The artefact is often more severe epicardially, which
is the reverse of true perfusion defects, which areREVIEW April 2005
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subendocardial in location. The artefact typicallyresolves by moving the transmit focus to the apex.
. After an evaluation of microbubble replenishment usinga low MI imaging modality, the pulsing interval versusmyocardial AI curve should be fitted to:A) Every frame acquired during real-time imaging after
the impulseB) Only sequential end-diastolic frames after the im-
pulseC) Only sequential end-systolic frames after the im-
pulseD) Alternate diastolic and systolic frames after the im-
pulseThe answer is C. Myocardial blood flow velocity
on MCE is assessed by evaluating the rate of micro-bubble replenishment into capillaries. MyocardialAI signals are derived exclusively from capillariesonly during systole, when large intramyocardial ves-sels are compressed. Pulsing interval versus AIcurves fitted to diastolic frames or all frames overes-timates MBF velocity by about 40% and 25%,respectively.
. A patient with globally reduced LV systolic functiondemonstrates homogeneous myocardial perfusion dur-ing power harmonic Doppler imaging. The myocardialcontrast enhancement represents:A) An intact microvasculature and extensive myocar-
dial viabilityB) Blooming artifact on power harmonic DopplerC) Tissue motion artifact on power harmonic Doppler
The answer is A. Unlike the situation in question3, resting myocardial perfusion may be normal inseverely hypokinetic or akinetic segments owing tostunning, or nonischemic cardiomyopathies. To dis-tinguish blooming or tissue motion artifacts fromtrue perfusion on power harmonic Doppler, somesystems provide a split screen that can display im-ages obtained from the first and last pulses transmit-ted during power Doppler imaging. With true per-fusion, the first image shows signals obtained frommicrobubbles, while the second image shows nomyocardial enhancement because all microbubbleswere destroyed during imaging.
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ayaweera AR, Wei K, Coggins M, Bin J-P, Goodman NC, Kaul S. Fateof capillaries distal to a stenosis. Their role in determining coro-
nary blood flow reserve. Am J Physiol 1999;46:H2363–72. VACC CURRENT JOURNAL
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e DE, Bin J-P, Coggins MP, Wei K, Kaul S. Relation betweenmyocardial oxygen consumption and myocardial blood vol-ume: a study using myocardial contrast echocardiography.J Am Soc Echocardiogr 2002;15:857–63.
e DE, Jayaweera AR, Wei K, Coggins MP, Lindner JR, Kaul S.Changes in myocardial volume over a wide range of coronarydriving pressures: role of capillaries in autoregulation. Heart2004;90:1199–205.
ei K, Kaul S. The coronary microcirculation in health anddisease. Cardiol Clin 2004;22:221–31.
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orter TR, Li S, Kricsfeld D, Armbruster RW. Detection of myo-cardial perfusion in multiple echocardiographic windowswith one intravenous injection of microbubbles using tran-sient response second harmonic imaging. J Am Coll Cardiol1997;29:791–9.
einle SK, Noblin J, Goree-Best P, et al. Assessment of myocardialperfusion by harmonic power Doppler imaging at rest andduring adenosine stress: comparison with (99m)Tc-sestamibiSPECT imaging. Circulation 2000;102:55–60.
wajg J, Xie F, O’Leary E, Kricsfeld D, Dittrich H, Porter TR.Detection of angiographically significant coronary artery dis-ease with accelerated intermittent imaging after intravenousadministration of ultrasound contrast material. Am Heart J2000;139:675–83.
himoni S, Zoghbi WA, Xie F, et al. Real-time assessment ofmyocardial perfusion and wall motion during bicycle andtreadmill exercise echocardiography: comparison with singlephoton emission computed tomography. J Am Coll Cardiol2001;37:741–7.
orter TR, Xie F, Silver M, Kricsfeld D, O’Leary E. Real-timeperfusion imaging with low mechanical index pulse inversionDoppler imaging. J Am Coll Cardiol 2001;37:748–53.
aluska B, Case C, Short L, Anderson J, Marwick TH. Effect ofpower Doppler and digital subtraction techniques on thecomparison of myocardial contrast echocardiography withSPECT. Heart 2001;85:549–55.
raby MA, Hays J, Maklady FA, El-Hawary AA, Zabalgoitia M.Assessment of myocardial perfusion during pharmacologic con-trast stress echocardiography. Am J Cardiol 2002;89:640–4.
raby MA, Hays J, Maklady FA, El-Hawary AA, Yaneza LO,Zabalgoitia M. Comparison of real-time coherent contrastimaging to dipyridamole thallium-201 single-photon emis-sion computed tomography for assessment of myocardialperfusion and left ventricular wall motion. Am J Cardiol2002;90:449–54.
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Address correspondence and reprint requests to Kevin Wei,D, P.O. Box 800158, Cardiovascular Division, University of
irginia, Charlottesville, VA 22908-0158.REVIEW April 2005
