Quantitative assessment of myocardial perfusion during graded coronary stenosis by real-time myocardial contrast echo refilling curves

OBJECTIVES: The present study examined the ability of real-time myocardial contrast echocardiography (MCE) to delineate abnormalities produced by graded coronary stenoses and to correlate signal intensity (SI) parameters derived from destruction/refilling curves with regional myocardial blood flow (MBF) and contractile function. BACKGROUND: Recent technological advances have enabled myocardial opacification by MCE to be achieved during real-time imaging. METHODS: In eight open-chest dogs, we created LAD occlusion and graded stenoses that were either flow-limiting at rest (FLS) or reduced adenosine hyperemia (non-flow-limiting at rest = NFLS). Myocardial contrast echo used Optison infusion and low-energy real-time power pulse inversion imaging. High-energy FLASH frames destroyed bubbles every 15 cardiac cycles. Myocardial SI-versus-time plots were fitted to a one-exponential function to obtain the rate of SI rise (b) and peak SI in the last frame. RESULTS: Dyssynergy was not observed during any NFLS, but perfusion abnormalities were. Visual detection of decreased opacification was possible with severe NFLS and FLS. b demonstrated a significant reduction with severe NFLS and near significant with moderate NFLS; peak SI did not. All exponential parameters were significantly decreased with FL stenosis and occlusion. The MBF ratio in LAD/LCx beds (fluorescent microspheres) correlated with b (r = 0.79) and the product of the peak SI and b (r = 0.80). CONCLUSIONS: In an open-chest dog model, parameters derived from microbubble refilling of the imaging field by real-time MCE correlate well with myocardial blood flow and can identify coronary stenosis.     

Assessment of adenosine-induced coronary steal in the setting of coronary occlusion based on the extent of opacification defects by myocardial contrast echocardiography

The authors examined the ability of real-time myocardial contrast echocardiography (MCE) to assess adenosine-induced coronary steal in the setting of coronary artery occlusion. The left anterior descending (LAD) coronary artery was occluded in 8 open-chest dogs. Real-time MCE was performed during LAD occlusion, and the extent of opacification defects from MCE was measured without and with adenosine infusion. Microsphere-derived myocardial blood flow (MBF) was measured in the LAD and left circumflex (LCx) coronary artery beds, and the LAD/LCx ratio of MBF was calculated. The LAD/LCx ratio of MBF decreased in response to adenosine administration (without adenosine: 0.66, with adenosine: 0.43, p < 0.01). The extent of opacification defects from MCE increased in response to adenosine administration (without adenosine: 18%, with adenosine: 22%, p < 0.01). Thus, real-time MCE allows for the detection of adenosine-induced coronary steal as changes in the extent of opacification defects in the setting of occlusion of 1 coronary artery accompanying another normally patent coronary artery.     

A novel hydrodynamic approach to the treatment of coronary artery disease.

AIMS: During severe coronary stenosis, capillary resistance increases. Drag-reducing polymers (DRPs) are blood-soluble macromolecules that reduce vascular resistance, possibly by altering blood hydrodynamics and rheology. Thus, we hypothesized that DRPs would enhance myocardial perfusion distal to a severe coronary stenosis. METHODS AND RESULTS: A flow-limiting left anterior descending (LAD) coronary artery stenosis was created in 12 open chest dogs. Coronary driving pressure, flow, trans-stenotic gradient, and radiolabelled microsphere myocardial perfusion were measured. Myocardial contrast echocardiography was performed and videointensity vs. pulsing interval data in the LAD and left circumflex beds were used to derive red cell velocity and capillary volume. Relative to baseline, the stenosis decreased LAD bed capillary volume (P = 0.019) and red blood cell velocity (P = 0.010). Intravenous DRP (polyethylene oxide, 2.5 ppm) decreased LAD microvascular resistance (P = 0.003) and increased microsphere flow (P = 0.009), capillary volume (P = 0.0006), and red cell velocity (P = 0.007) despite the presence of a severe stenosis. DRP did not alter blood viscosity. CONCLUSIONS: DRPs improve perfusion to myocardium subserved by a flow-limiting coronary stenosis by decreasing microvascular resistance through an increase in capillary volume. Primary modulation of blood hydrodynamics and rheology to reduce microvascular resistance offers a novel approach to the treatment of ischaemic coronary syndromes.     

不同程度狭窄病变冠心病患者介入治疗后心肌灌注变化及临床意义

目的利用经冠状动脉超声心肌声学造影（MCE）比较单支血管不同程度狭窄病变冠心病患者经皮冠状动脉介入术（PCI）后心肌灌注的变化,并探讨其临床意义。方法62例进行PCI治疗的住院患者根据选择性冠状动脉造影结果,按血管狭窄程度分组:A组,血管狭窄75%95%;B组,血管狭窄>95%;C组,急性血管闭塞。PCI前及术后15 min进行经冠状动脉MCE,检测心肌灌注状况。其中,MCE有关定量参数分别为:造影剂峰值密度反映心肌血容量;峰值时间反映心肌灌注速度;曲线下面积反映心肌血流量。结果所有患者PC I后均达到TIMIⅢ级血流;A组术后心肌血流量较术前增加（P<0.05）;B组心肌血容量及血流量也较术前增加（P<0.05）;而C组心肌血容量、血流量及灌注速度较术前增加更显著（P<0.01）。结论不同狭窄程度病变冠心病患者,PCI后心肌灌注均得到不同程度改善,其中,以急性闭塞病变改善最明显,该类患者为PCI治疗的最大获益者。     

Proximal coronary hemodynamic changes evaluated by intracardiac echocardiography during myocardial ischemia and reperfusion in a canine model

BACKGROUND: The purpose of this study was to assess whether the dynamic changes in coronary flow velocity and coronary flow velocity reserve (CFVR) by intracardiac echocardiography (ICE) within proximal coronary arteries are related to myocardial perfusion status and infarct size in a myocardial ischemia-reperfusion injury model. METHODS: In 14 dogs, left anterior descending coronary artery (LAD) was ligated for 2 hours followed by 2 hours reperfusion. Coronary flow velocity was obtained by ICE within coronary arteries at baseline, and at the end of both occlusion and reperfusion period. The CFVR was calculated as the ratio of hyperemic to resting peak diastolic velocity (PDV). Myocardial perfusion was evaluated by real time myocardial contrast echocardiography (MCE). The infarct area was detected by triphenyltetrazolium chloride (TTC) staining and expressed as the percentage of the whole left ventricular (LV) area. RESULTS: CFVR significantly decreased both in proximal LAD and left circumflex (LCx) artery at the end of occlusion, and did not recover at the end of reperfusion. However, no significant difference in flow parameters was observed between dogs with myocardial perfusion defect and those without. CFVR in LAD at the end of reperfusion did not correlate with the infarct size (r =-0.182, P = NS) either. CONCLUSIONS: Decreased CFVR detected by ICE occurs both in ischemic and in nonischemic proximal arteries during myocardial ischemia and early stage of reperfusion. This change in CFVR has poor correlation with the extent of microvascular impairment and cannot be used to predict infarct size.     

The effect of coronary artery lesions on the relationship between coronary perfusion pressure and myocardial blood flow during cardiopulmonary resuscitation in pigs

In subjects without coronary disease, coronary perfusion pressure generated with closed-chest cardiopulmonary resuscitation (CPR) bears a direct relationship to myocardial blood flow. The effect of coronary lesions on this relationship was studied in an experimental porcine model not requiring thoracotomy. Coronary stenoses (a 50% reduction in coronary cross-sectional area) or total coronary occlusions were created by percutaneous, transarterial catheter placement of a Teflon cylinder in the left anterior descending artery of 21 swine (30 to 60 kg). Coronary perfusion pressure, defined as the aortic diastolic pressure minus right atrial diastolic pressure, was correlated with myocardial blood flow measured with nonradioactive, colored microspheres during external chest compression CPR. Complete occlusion of the left anterior coronary artery resulted in essentially no CPR-generated blood flow to the anterior myocardium distal to the site of occlusion. Coronary perfusion pressure showed a positive correlation with myocardial blood flow above the area of occlusion (r = 0.783; p less than 0.01) but did not correlate with myocardial blood flow below the occlusion site (r = 0.239). In the presence of a patent coronary artery stenosis, coronary perfusion pressure correlated with myocardial blood flow both above (r = 0.841; p less than 0.001) and below (r = 0.508; p less than 0.05) the stenosis. During closed-chest CPR producing coronary perfusion pressures between 30 and 60 mm Hg, anterior myocardial blood flow was 109 +/- 16 ml/min/100 gm above a patent stenosis and 66 +/- 13 ml/min/100 gm below the stenosis (p less than 0.005). Over a wide range of coronary perfusion pressures, myocardial blood flow below a coronary lesion was significantly less than that above the lesion. Coronary occlusions and stenoses can substantially affect the amount of CPR-generated coronary perfusion pressure needed to produce distal myocardial blood flow.     

Alterations in transmural blood flow and body surface ST segment abnormalities produced by ischemia in the circumflex and left anterior descending coronary arterial beds of the dog

Previous studies have documented a quantitative relation between alterations in transmural myocardial blood flow and body surface electrocardiographic distributions during rapid atrial pacing after chronic occlusion of the left circumflex coronary artery (LCx). Because other studies have described functional differences between the left anterior descending (LAD) and the LCx perfusion beds, we tested the hypothesis that these two territories exhibit quantitative differences in their responses to demand-dependent myocardial ischemia. To do so, 25 sedated dogs were studied 3 weeks after implantation of an ameroid constrictor around the proximal LCx (15 dogs, group I) or the LAD (group II). Oxygen demand was increased by rapid atrial pacing at rates of 90 to 210 beats/min, myocardial blood flow was measured by serial injections of radiolabeled microspheres, and the electrocardiographic consequences were evaluated by isopotential body surface mapping. Endocardial flows and the endocardial/epicardial flow ratio fell to significantly lower levels during atrial pacing in the ischemic LAD bed than in the LCx perfusion zone. Electrocardiographic patterns indicative of subendocardial ischemia also developed with lesser abnormalities in endocardial/epicardial ratios as determined by logistic regression models, in the LAD than in the LCx bed. Thus the LAD bed is more susceptible to ischemia than the LCx region because of differences in collateral blood flow patterns. In addition, the intensity of the surface electrocardiographic potentials during ischemia was significantly greater, as measured by linear regression, after LAD than after LCx obstruction. These data thus demonstrate significant differences between the two cardiac regions as electrocardiographic potential sources during ischemia.     

Visualization of risk-area myocardium as a high-intensity,hyperenhanced "hot spot" by myocardial contrast echocardiography following coronary reperfusion: quantitative analysis

OBJECTIVES: We examined whether delayed post-injection imaging of a new ultrasound contrast agent (BR-14) could produce prolonged opacification and hyperenhancement of myocardium subjected to coronary occlusion/reperfusion. BACKGROUND: We hypothesized that ultrasound exposure destroyed BR-14 and eliminated visualization of sustained myocardial opacification from retained microbubbles. METHODS: We studied eight open-chest dogs with 3 h of left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Myocardial contrast echocardiography (MCE) was performed before occlusion and 120 min after the onset of both occlusion and reperfusion. Ultrasound imaging was initiated 15 min after injection. Myocardial blood flow (MBF) was assessed by microspheres. RESULTS: Pre-occlusion images revealed uniform opacification of left ventricular myocardium greater than that of the cavity, with a mean intensity of the LAD bed of 8.66 +/- 1.38 dB. During occlusion, MCE resulted in the appearance of a perfusion defect in the LAD risk area (intensity 2.08 +/- 1.10 dB). After 120 min of reperfusion, the LAD risk-area myocardium manifested dense opacification of a higher intensity ("hot spot") than baseline (13.7 vs. 8.7 dB), but with reduced MBF consistent with accumulation of a high concentration of microbubbles. Increased MCE intensity was associated with a greater myeloperoxidase score. CONCLUSIONS: These data establish that contrast opacification by BR-14 may be selectively retained within the perfusion bed of a coronary artery subjected to occlusion/reperfusion. Such opacification exhibits defects with occlusion, manifests hyperenhanced intensity (hot spot) with reperfusion, is associated with the level of myeloperoxidase activity, and conforms to the area of myocardium subjected to altered flow.     

Real-time assessment of myocardial perfusion during balloon angioplasty of the left anterior descending coronary artery

Balloon occlusion and release during elective percutaneous coronary intervention (PCI) provides a unique opportunity to study dynamic temporal alterations in myocardial perfusion in a controlled setting. These changes in flow and volume mimic those that occur during presentation with, and successful therapy of, ST-segment elevation acute myocardial infarction (AMI). Eleven patients underwent myocardial contrast echocardiography (MCE) using a continuous infusion of Definity at baseline, during coronary occlusion, and during reactive hyperemia immediately after balloon deflation. Fifty separate flow state sequences were acquired, and off-line analysis was performed to determine myocardial contrast intensity within a region of interest in the distribution of the left anterior descending artery (LAD). A reader blinded to flow state also performed qualitative evaluation (perfusion or lack of perfusion). Quantitative analysis demonstrated significant differences in myocardial contrast intensity by flow state (p = 0.0001 for occlusion vs reperfusion). Qualitative assessment demonstrated a high rate of correct classification (92%). Real-time myocardial perfusion assessment using MCE accurately differentiates coronary occlusion and reactive hyperemia in humans by qualitative and quantitative assessment. This technique may be clinically useful in assessing the efficacy of thrombolytic therapy in ST-segment elevation AMI and in clinical trial assessment of new drugs and devices aimed at limitation of infarct size.     

Detection and quantification of coronary stenosis severity with myocardial contrast echocardiography

The development of microbubble contrast agents and new imaging modalities now allows the assessment of myocardial perfusion during echocardiography. These microbubbles are excellent tracers of red blood cell kinetics. Apart from providing a spatial assessment of myocardial perfusion, myocardial contrast echocardiography (MCE) can also be used to quantify the 2 specific components of myocardial blood flow-flow velocity and myocardial blood volume. The method to quantify myocardial blood flow velocity is based on rapid destruction of microbubbles by ultrasound, and subsequent assessment of the rate of replenishment of microbubbles into the myocardial microcirculation within the ultrasound beam elevation. Assessment of steady state myocardial video intensity (VI) provides a measure of myocardial or capillary blood volume. Perfusion defects that develop distal to a stenosis during hyperemia are therefore due to capillary derecruitment. We have shown that the degree of derecruitment (and therefore the severity of a perfusion defect) is proportional to stenosis severity. Because the capillary bed also provides the greatest resistance to hyperemic flow, decreases in capillary blood volume distal to a stenosis during hyperemia result in increases in microvascular resistance, which is the mechanism underlying the progressive decrease in flow reserve in the presence of a stenosis. Consequently, both the severity of a perfusion defect and quantification of abnormal myocardial blood flow reserve on MCE can be used to determine stenosis severity. As imaging methods with MCE continue to be refined, the optimal imaging algorithms for clinical practice still need to be determined. MCE, however, holds promise as a noninvasive, instantaneous, on-line method for the detection and quantification of coronary artery disease.     

Can myocardial contrast echo determine coronary flow reserve?

OBJECTIVE: The aim was to evaluate the applicability of myocardial contrast echocardiography in the measurement of coronary flow reserve. METHODS: Eleven anaesthetised open chest pigs were studied, in which coronary atherosclerosis had been induced by abrasion of the left anterior descending coronary artery at one month, followed by an atherogenic diet for eight months. Coronary flow reserve was determined by electromagnetic flow measurement and contrast echocardiography before and after partial occlusion of the left anterior descending coronary artery, using papaverine as a coronary vasodilator. Coronary blood flow was reduced by tightening a clamp placed around the coronary artery. Systemic haemodynamics and myocardial wall thickness (epicardial ultrasound 5 MHz transducer) were recorded simultaneously. Echocardiograms were recorded on VHS tape and analysed by digitised videodensitometry off line for construction of the time v videointensity curve (time-intensity curves). From these curves washout time (T50), area under the curve, peak contrast intensity, and time to peak intensity were calculated. RESULTS: Following papaverine, coronary blood flow increased significantly from 47 (SD 23) ml.min-1 at baseline to 88(39) ml.min-1 (p less than 0.05). During the stenosis, flow decreased to 19(16) ml.min-1 (p less than 0.01), and increased to 38(29) ml.min-1 (p less than 0.05 v stenosis) after administration of papaverine. Correlations between coronary blood flow and indices calculated from the quantitative videodensitometric analysis were poor, varying between r = 0.03 for area at control flow to r = 0.62 for T50 during stenosis. The same was true for coronary flow reserve: r = 0.09 for peak to r = 0.75 (p less than 0.05) for time to peak without the stenosis. CONCLUSIONS: Current limitations in injection, imaging, and analysis techniques cause variability in data from time-intensity curves, which precludes accurate quantification of coronary flow (reserve) by myocardial contrast echocardiography.     

Detection of coronary stenosis and myocardial viability using a single intravenous bolus injection of BR14

OBJECTIVES: The aim of the study was to determine whether coronary stenosis can be detected and myocardial viability assessed after myocardial infarction from a single venous bolus injection of BR14, a new ultrasound contrast agent. BACKGROUND: BR14 is an ultrasound contrast agent that, like (201)Tl, demonstrates redistribution. Whether this principle can be used to determine myocardial viability is not known. METHODS: Non-critical (n = 6) or flow-limiting (n = 4) stenoses were placed on coronary arteries of 10 open-chest dogs, which then underwent 2 h of coronary occlusion followed by reperfusion through the stenosis. Hyperemia was induced to create flow mismatch in the dogs with non-critical stenosis. Hyperemia was not induced in dogs with reduced resting coronary blood flow. All dogs were given 2 ml of BR14 as a bolus injection and serial images were obtained. Myocardial blood flow (MBF) was measured using radiolabeled microspheres. At the end of the experiment, tissue staining was performed to determine infarct size and topography. RESULTS: Initial images demonstrated flow mismatch between the normal bed and that subtended by the stenosis (during hyperemia in dogs without critical stenosis and during rest in those with reduced resting MBF). The perfusion defect size correlated well with radiolabeled microsphere-derived hypoperfused zone (r = 0.89). Regions within the hypoperfused zone that had not undergone necrosis showed redistribution, whereas the necrotic regions showed a persistent defect, the size of which correlated well with infarct size (r = 0.80). CONCLUSIONS: Because of its ability to redistribute, BR14 can define regions of relative hypoperfusion and also discriminate between infarcted and viable tissue within the hypoperfused zone after a single venous injection. This property lends itself to assessing myocardial perfusion during exercise stress.     

Differential value of adenosine myocardial contrast echocardiography and dobutamine stress echocardiography in evaluating functional significance of coronary artery stenosis in a porcine model

Aim Myocardial contrast echocardiography (MCE) during adenosine induced hyperemia is an experimental method that detects flow limiting coronary artery stenosis by visualizing myocardial perfusion defects. Noninvasive detection of flow limiting coronary artery stenosis in clinical routine is a frequent domaine of dobutamine stress echocardiography (DSE) visualizing ischemia related regional wall motion abnormalities. This study investigated the values of adenosine MCE and DSE in the detection of functionally significant coronary artery stenosis in an experimental open chest pig model. Methods A total of 28 proximal LAD stenoses were instrumented in 12 animals. Reduction of coronary blood flow reserve (Δ CFR [%]) was calculated as a marker of functional significance of coronary artery stenosis (mild to moderate stenosis: Δ CRF ≤ 50%; severe stenosis: Δ CFR > 50%). Fractional area shortening (FAS) and wall thickening (WT) were calculated to evaluate regional wall motion. Peak myocardial contrast intensities (PCI) were measured following aortic root injections of Levovist' to detect myocardial perfusion defects. Results As a group, severe stenosis significantly reduced wall motion response to dobutamine (Δ FAS: 12.0 ± 3.0%, vs. 20 ± 3.0% without stenosis, p < 0.05; Δ WT: 2.2 ± 0.9 mm vs. 0.0 ± 0.8 mm without stenosis, p < 0.05) and diminished myocardial opacification during hyperemia (PCI: 59 ± 8 units vs. 143 ± 16 units without stenosis, p < 0.05). Mild to moderate stenosis did not influence wall motion but reduced myocardial opacification (PCI 89 ± 14 units vs. 143 ± 16 units). PCI correlated more closely with alterations in CFR (r = −0.7, p < 0.0001) than did FAS (r = −0.5, p < 0.002) or WT (r = −0.2, p = 0.3). Conclusion Adenosine myocardial contrast echocardiography detects flow limiting coronary artery stenosis and compares favorably to regional wall motion analysis during dobutamine infusion. Received: 22 May 2000 / Returned for 1. revision: 26 June 2000 / 1. Revision returned: 11 September 2000 / Returned for 2. revision: 11 October 2000 / 2. Revision returned: 21 December 2000 / Accepted: 15 January 2001     

Relation of perfusion defects observed with myocardial contrast echocardiography to the severity of coronary stenosis: correlation with thallium-201 single-photon emission tomography.

It has been previously shown that myocardial contrast echocardiography is a valuable technique for delineating regions of myocardial underperfusion secondary to coronary occlusion and to critical coronary stenoses in the presence of hyperemic stimulation. The aim of this study was to determine whether myocardial contrast echocardiography performed with a stable solution of sonicated albumin could detect regions of myocardial underperfusion resulting from various degrees of coronary stenosis. The perfusion defect produced in 16 open chest dogs was compared with the anatomic area at risk measured by the postmortem dual-perfusion technique and with thallium-201 single-photon emission tomography (SPECT). During a transient (20-s) coronary occlusion, a perfusion defect was observed with contrast echocardiography in 14 of the 15 dogs in which the occlusion was produced. The perfusion defect correlated significantly with the anatomic area at risk (r = 0.74; p less than 0.002). During dipyridamole-induced hyperemia, 12 of the 16 dogs with a partial coronary stenosis had a visible area of hypoperfusion by contrast echocardiography. The four dogs without a perfusion defect had a stenosis that resulted in a mild (0% to 50%) reduction in dipyridamole-induced hyperemia. The size of the perfusion defect during stenosis correlated significantly with the anatomic area at risk (r = 0.61; p = 0.02). Thallium-201 SPECT demonstrated a perfusion defect in all 14 dogs analyzed during dipyridamole-induced hyperemia; the size of the perfusion defect correlated with the anatomic area at risk (r = 0.58; p less than 0.03) and with the perfusion defect by contrast echocardiography (r = 0.58; p less than 0.03). Thus, myocardial contrast echocardiography can be used to visualize and quantitate the amount of jeopardized myocardium during moderate to severe degrees of coronary stenosis. The results obtained show a correlation with the anatomic area at risk similar to that obtained with thallium-201 SPECT.     

Effects of glycoprotein IIb/IIIa inhibition on microvascular flow after coronary reperfusion. A quantitative myocardial contrast echocardiography study

OBJECTIVES: We assessed the effect of glycoprotein IIb/IIIa inhibition (GPI) on microvascular flow after coronary occlusion/reperfusion using quantitative myocardial contrast echocardiography (QMCE). BACKGROUND: Platelets may play a major role in the dissociation of epicardial artery recanalization and tissue-level reperfusion, referred to as the "no-reflow phenomenon." Therefore, GPI might improve myocardial reperfusion, distinct from its effects on epicardial patency.T METHOD: hree-hour occlusion of the left anterior descending coronary artery (LAD) was followed by 3-h reperfusion in 16 open-chest dogs: 8 controls and 8 given a continuous infusion of the GPI tirofiban, starting 45 min before LAD reopening. Perfusion of the LAD bed was quantified by the rate of intensity rise (b) by QMCE; myocardial blood flow (MBF) was assessed by fluorescent microspheres. RESULTS: No differences in b or MBF were observed within the risk area between the control and GPI groups at baseline or occlusion. However, b and MBF were higher in GPI dogs than in controls during reperfusion, despite similar epicardial flow (p < 0.05 at 30, 60, and 90 min; p = NS at 180 min). Infarct area size was significantly reduced in GPI dogs compared with non-treated dogs (26.9 +/- 10.5% vs. 49.0 +/- 11.1% of at-risk area, respectively). CONCLUSIONS: As demonstrated by QMCE, GPI improves microvascular flow and reduces the infarct area after coronary occlusion/reperfusion, independent of epicardial flow. These data demonstrate the usefulness of QMCE in assessing microvascular flow, provide novel evidence for the role of platelets in the early phase of reperfusion injury, and show that GPI is of value in preserving microvascular perfusion after coronary reperfusion.     

Quantitative assessment of harmonic power Doppler myocardial perfusion imaging with intravenous Levovist in patients with myocardial infarction: comparison with myocardial viability evaluated by thallium-201 single-photon emission computed tomography and coronary flow reserve.

BACKGROUND: Intravenous myocardial contrast echocardiography with harmonic power Doppler imaging is a novel technique for assessing myocardial perfusion. AIMS: The aim of this study was to quantitatively assess myocardial perfusion by harmonic power Doppler imaging in patients with a previous myocardial infarction and compare myocardial contrast echocardiography results with myocardial viability evaluated by thallium-201 single-photon emission computed tomography ((201)Tl-SPECT) and the results of Doppler flow measurement of coronary flow velocity reserve. METHODS: Twenty-three patients with anterior myocardial infarction who were scheduled for adenosine stress (201)Tl-SPECT underwent myocardial contrast echocardiography with harmonic power Doppler imaging. Harmonic power Doppler imaging was performed at rest and during adenosine infusion (0.15 mg/kg/min) using an intravenous infusion of Levovist. The peak colour pixel intensity ratios of the risk area to the control area were used for quantitative analysis of myocardial perfusion by harmonic power Doppler imaging. Coronary blood flow velocity was measured using Doppler-tipped guidewire in the distal portion of left anterior descending artery and coronary flow velocity reserve was calculated. RESULTS: In patients with myocardial viability assessed by (201)Tl-SPECT, pixel intensity ratios both at rest and during hyperaemia were significantly higher compared with those in patients without myocardial viability (at rest: 0.62 +/- 0.28 vs 0.37 +/- 0.17, P=0.038, during hyperaemia 0.72 +/- 0.19 vs 0.40 +/- 0.18, P=0.003). Coronary flow velocity reserve was significantly different between two groups (2.35 +/- 0.43 vs 1.49 +/- 0.53, P <0.01). CONCLUSIONS: Quantitative assessment of microvascular integrity by harmonic power Doppler imaging corresponds to the evaluation of the microcirculation by coronary flow velocity reserve.     

Comparative effects of nitroglycerin and nifedipine on myocardial blood flow and contraction during flow-limiting coronary stenosis in the dog

Both nifedipine and nitroglycerin are used to treat angina pectoris. The comparative effects of these agents on myocardial blood flow and contraction in the setting of flow-limiting coronary stenosis are poorly understood. Thus 24 open chest dogs underwent carotid to left anterior descending coronary arterial perfusion with coronary flow probe and perfusion pressure monitoring. Segment length was measured with ultrasonic crystals in the subendocardial ischemic and nonischemic zones. Myocardial blood flow was measured with radioactive microspheres. Partial coronary occlusion was performed to attain a diastolic perfusion pressure of 40 mm Hg. Twelve dogs received intravenous nifedipine, 3 μg/kg per min, and 12 received intravenous nitroglycerin to reduce aortic pressure by 20 mm Hg. Partial occlusion resulted in a slight but significant decrease in segment shortening in the ischemic zone. Neither nitroglycerin nor nifedipine affected shortening in the ischemic zone. After occlusion, blood flow decreased in the subendocardial ischemic zone but was unchanged in the subepicardium. Nifedipine increased subendocardial blood flow in the nonischemic zone and decreased it in the ischemic zone but caused no change in subepicardial flow in the ischemic zone. In contrast, nitroglycerin decreased subendocardial and subepicardial blood flow in both the ischemic and nonischemic zones. In the setting of coronary stenosis, different classes of vasodilators may have varying effects on myocardial blood flow, suggesting different sites and mechanisms of action. In addition, segment function may not always reflect changes in myocardial blood flow.     

Intravenous myocardial contrast echocardiography for the diagnosis of coronary artery disease

PURPOSE OF REVIEW: Myocardial contrast echocardiography is a recently developed technique that permits the noninvasive assessment of myocardial perfusion. Myocardial contrast enhancement from microbubbles characteristically reflects the myocardial blood volume. The analysis of microbubble kinetics using quantitative myocardial contrast echocardiography permits the evaluation of myocardial blood flow both at rest and during pharmacological stress. RECENT FINDINGS: Myocardial contrast echocardiography has been shown to have good concordance with single photon emission computed tomography for the localization of perfusion abnormalities. As a result of its better spatial resolution and the fact that it tracks myocardial blood flow changes, it seems to have higher sensitivity for the detection of angiographically significant coronary artery disease, while maintaining similar specificity to single photon emission computed tomography. Low mechanical index imaging techniques (real-time myocardial contrast echocardiography) have the advantage of permitting simultaneous analysis of wall motion and perfusion, which is particularly important during dobutamine stress. Myocardial perfusion analysis using real-time myocardial contrast echocardiography has been shown to have higher sensitivity and diagnostic accuracy than wall motion analysis for the detection of coronary artery disease. Quantitative myocardial contrast echocardiography seems to overcome the expertise requirements for appropriate interpretation of myocardial perfusion images, and may have been demonstrated to be an accurate supplemental technique for estimating the severity of coronary artery disease. SUMMARY: Recent technological advances have positioned myocardial contrast echocardiography as a safe and feasible technique for the evaluation of myocardial perfusion. The analysis of myocardial perfusion using myocardial contrast echocardiography has higher diagnostic accuracy than wall motion analysis for detecting coronary artery disease.     

经皮冠状动脉介入术后心肌灌注评价方法的比较

目的比较经冠状动脉超声心肌声学造影(MCE)与校正的心肌梗死溶栓临床试验(TIMI)帧数计数(CTFC)及冠状动脉血流速度方法对经皮冠状动脉介入术(PCI)后心肌灌注的评价,并探讨相关临床意义。方法68例住院患者根据选择性冠状动脉造影结果,按血管狭窄程度分组A组,正常对照组;B组,血管狭窄75%~95%;C组,血管狭窄>95%;D组,急性血管闭塞。对各病变血管均进行PCI治疗,并恢复TIMI3级血流。采用定量经冠状动脉MCE、CTFC及冠状动脉血流速度方法对术后心肌灌注状况进行检测。其中,经冠状动脉MCE有关定量参数分别为造影剂峰值密度(A)反映心肌血容量;峰值时间(TP)反映心肌灌注速度;曲线下面积(AUC)反映心肌血流量。结果PCI后心外膜血管恢复正常血流的前提下,各狭窄病变血管组CTFC与对照组差异无统计学意义;而闭塞血管组冠状动脉血流速度较对照组低;在MCE检测中,C组的心肌血容量及血流量较对照组低,而D组反映心肌灌注的3个参数值均较对照组差异均有统计学意义。结论经冠状动脉MCE通过多个参数进行定量分析,较其他两种方法能更精确地评价PCI后心肌灌注状况。     

Physiological assessment of coronary artery disease and myocardial viability in ischemic syndromes using adenosine echocardiography

We hypothesized that it would be feasible and safe to use adenosine echocardiography to assess the physiological significance of coronary stenoses, detect ischemic myocardium, and assess myocardial viability in a high risk group of patients with coronary artery disease (CAD). Therefore, in 40 patients with either unstable angina, non-Q myocardial infarction, or myocardial infarction treated with thrombolytic therapy, we performed adenosine echocardiography (140 mug/kg per min for 5 mins with a 16 segment model for analysis) and compared the findings with quantitative planar thallium-201 scintigraphy, and (in 26 patients) coronary angiography. The technique was safe, and there were no serious complications. Adenosine resulted in a significant increase in heart rate and decrease in blood pressure. The sensitivity of adenosine echocardiography and thallium scintigraphy were 96% and 88%, respectively, for detecting greater than 75% stenosis. The change in echo score from baseline during adenosine infusion was significantly higher with more severe coronary disease (single vessel right coronary artery {RCA} or left circumflex {LCX} disease = 0.125 +/- 0.15, proximal left anterior descending coronary artery {LAD} disease = 0.23 +/- 0.15, RCA and LCX disease = 0.30 +/- 0.14, LAD and RCA and/or LCX disease = 0.62 +/- 0.13). Likewise, the echo score during adenosine infusion was significantly higher in patients with high risk thallium scans (low risk = 1.29 +/- 0.26, medium risk = 1.74 +/- 0.22, and high risk = 2.21 +/- 0.37). In 13 patients receiving thrombolytic therapy, adenosine echocardiography identified 12 with viable myocardium as defined by quantitative thallium criteria. Furthermore, the wall-motion response of the viable segment was indicative of the degree of stenosis of the artery subtending the segment. Regional function deteriorated in patients with high grade (95 +/- 2%) stenoses and improved in those with nonflow limiting stenoses (66 +/- 25%, P = 0.03). Therefore, we conclude that adenosine echocardiography can detect significant coronary stenoses, has a high degree of concordance with thallium in detecting cardiac perfusion abnormalities, and can assess myocardial viability following thrombolytic therapy.