Copyright © 2004, The European Society of Cardiology
Usefulness of quantitative intravenous myocardial contrast echocardiography to analyze microvasculature perfusion in patients with a recent myocardial infarction and an open infarct-related artery: comparison with intracoronary myocardial contrast echocardiography
a Cardiology Department, Hospital Clínic i Universitari, Blasco Ibáñez Avenue 17, 46010 Valencia, Spain
b ERESA, Blasco Ibáñez Avenue 17, 46010 Valencia, Spain
Received 14 April 2004; received in revised form 6 August 2004; accepted after revision 6 August 2004.
* This work was supported by the ‘Instituto de Salud Carlos III’ (Spanish Public Health System) with grant no. PI030013 and by the Spanish Society of Cardiology with the grant ‘Bayer’ 2004.
* Corresponding author. Tel./fax: +34 96 3862658. vicentbodi{at}hotmail.com
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
Aims: We analyzed the usefulness of quantitative intravenous myocardial contrast echocardiography to study microvasculature perfusion after infarction in comparison with intracoronary myocardial contrast echocardiography.
Methods and results: Thirty-two patients with a first ST elevation myocardial infarction, single-vessel disease and an open artery (TIMI 3) were studied before discharge. Myocardial perfusion in the risk area was quantified with intracoronary and intravenous myocardial contrast echocardiography. Perfusion was normal (intracoronary contrast echocardiography normalized videointensity > 0.75) in 78 out of 97 dysfunctional segments (80%). Sensitivity and specificity of intravenous contrast echocardiography to predict normal perfusion were 87% and 63% for ‘first-pass myocardial blood flow’ (upslope of contrast arrivalxpeak intensity after intravenous bolus injection of contrast) and 91% and 89% for end-systolic single-triggered images captured every 6 cycles, respectively. In an analysis per patients, normal perfusion (0 or 1 hypoperfused segments with intracoronary contrast echocardiography) was observed in 22 cases (69%). End-systolic single-triggered images showed a strong correlation with intracoronary contrast echocardiography (R2=0.82, p = 0.0001).
Conclusions: Intravenous contrast echocardiography is a useful technique to analyze microvasculature perfusion soon after infarction. A quantitative analysis of single-triggered images is an easy-to-obtain and reliable method to define perfusion when compared with intracoronary contrast echocardiography.
Keywords: Microcirculation; Myocardial contrast echocardiography; Perfusion
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
The primary objective of therapy after myocardial infarction is to restore tissue perfusion.1 Lack of perfusion either at the epicardial vessel2–4 level or at the microvasculature5–14 is related to a more depressed systolic function and to a worse outcome.1–15 At present, the ideal diagnostic method to analyze myocardial microcirculation is unclear.1,5,6,16
Intracoronary myocardial contrast echocardiography demonstrated more than a decade ago that Thrombolysis in Myocardial Infarction (TIMI) grade 3 is necessary but does not guarantee optimum reperfusion.3,5 Therefore, intracoronary contrast echocardiography may represent a clinical standard of perfusion16 but it has all the limitations of an invasive method. During the last few years myocardial contrast echocardiography with intravenous injection of contrast has gained a place for analyzing myocardial perfusion.5,6,16–23 Quantification of intravenous contrast echocardiography has added reliability to this technique.17–19 Although the initial results have been promising,18–23 a direct comparison between quantitative intravenous and intracoronary myocardial contrast echocardiography has not been performed.
In the present study, we aimed to elucidate the ability of quantitative intravenous myocardial contrast echocardiography to detect normal perfusion in the coronary microcirculation when compared with intracoronary contrast echocardiography (as the reference method) in a homogeneous series of patients with a first myocardial infarction, single-vessel disease and an open infarct-related artery (TIMI 3).
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
Study group
We prospectively screened consecutive patients admitted in our institution because of a first Q wave myocardial infarction diagnosed on the basis of typical chest pain lasting > 30min, ST elevation > 0.1mV in at least 2 leads and an increase in troponin I > twice maximum normal limit in our institution. Patients were eligible for inclusion if they fulfilled the following inclusion criteria: (1) stable clinical course without complications, (2) absence of clinical history suggesting any prior heart disease, (3) single-vessel disease and a patent (TIMI 3 flow and a residual lesion <50%) infarct-related artery at the end of the cardiac catheterization performed before discharge, (4) adequate thoracic window for echocardiography, and (5) stable sinusal rhythm at the moment of echocardiography.
Twenty-three patients received reperfusion therapy within the first six hours after chest pain onset: thrombolysis in 19 cases and primary angioplasty in 4 cases. In 9 patients, early reperfusion was not attempted because of arrival > 12h after chest pain onset (6 cases) or contraindication to thrombolysis (3 cases).
The study complies with the declaration of Helsinki. Our local ethics committee approved the research protocol and informed consent was obtained from all subjects participating in the study. Clinical and baseline characteristics were prospectively recorded (Table 1).
|
Cardiac catheterization
Cardiac catheterization was performed 5±1 days (range 3–7 days) after myocardial infarction. Percutaneous coronary revascularization (28 patients: 4 cases during primary angioplasty and 24 cases at pre-discharge catheterization, stent in all patients) was performed if the lumen narrowing in the IRA was > 50%. At the end of the pre-discharge study all patients showed a patent infarct-related artery (TIMI 3) and a residual lesion <50%. In those 4 patients in whom primary angioplasty was performed, cardiac catheterization was repeated before discharge (at least 3 days after infarction) and angiographic and intracoronary myocardial contrast echocardiography data were recorded at this moment. TIMI 3 flow was confirmed in a core laboratory (ICICOR, Valladolid, Spain).
Intracoronary myocardial contrast echocardiography
At the end of cardiac catheterization, intracoronary myocardial contrast echocardiography (apical 4-chamber and 2-chamber views) was performed in all cases by injecting a bolus of 1ml (concentration, 350mg/ml) of Levovist (Schering AG, Germany) followed by a 5ml saline flush through the catheter situated in the infarct-related artery. Boluses of contrast were repeated if necessary. No side effect was observed. Myocardial perfusion was registered in real time and second harmonic mode using the echocardiograph Agilent Sonos 5500 (Philips, Netherlands); gain and compression settings were optimized and unchanged during the study. Images were digitized and analyzed on separate days by 2 experienced observers unaware of the results of the other explorations.
For analysis of contrast images, we digitally captured the end-systolic frames with maximum contrast intensity and for all purposes in the present study, the risk area was considered as those dysfunctional segments included in the infarct-related artery territory and visualized in the apical 4-chamber and 2-chamber views (13 segments using the 17-segment model).24 Quantification of echocardiographic images was performed in all cases using the possibilities derived from the MATLAB 6.5 (The Mathworks Inc., Natick, Massachusetts, USA) software package. A region of interest was sampled in each segment (avoiding the inner and outer 20% borders); the mean myocardial intensity value of a 4x4 pixel matrix placed at the middle of segments was quantified. Using this relatively small matrix, we aimed to prevent misidentification of left ventricular cavity or the neighbouring segment as the region of interest.
In order to correct the inherently non-linear relation between videointensity and the underlying acoustical signal, as well as to obtain values of myocardial contrast intensity which could be comparable between segments and patients, a normalized scale (non-numeric, range from 0 to 1) was applied for all purposes of perfusion quantification. Background-subtracted contrast intensity of each segment (units of digitized videointensity) was normalized to the segment showing normal contractility and maximum contrast intensity (units of digitized videointensity), resulting in all segments having a non-numeric normalized range of perfusion between 0 and 1.
The mean perfusion score in the risk area (sum of scores of each segment divided by the number of segments in the risk area) was calculated as previously described.20 According to our previous experience,25 normal perfusion in an individual segment was considered in the case of an intracoronary contrast echocardiography normalized videointensity > 0.75. A patient was considered to have normal perfusion in the case of 0 or 1 segment with abnormal intracoronary contrast echocardiography (<0.75) in the risk area. Inter-observer discrepancies regarding the presence or absence of normal perfusion took place in 2 cases (6%) solved by consensus.
Intravenous myocardial contrast echocardiography
Intravenous myocardial contrast echocardiography was performed 8±2 days (range 6–12 days) after infarction, at least 48h after cardiac catheterization and intracoronary contrast echocardiography (due to logistical reasons and to avoid the possible acute changes in microcirculation after angioplasty). Apical 4-chamber and 2-chamber views were obtained and the same 17-segment model used in the case of intracoronary contrast echocardiography was applied.24 Machine settings were decided during our learning curve. Using the echocardiograph Agilent Sonos 5500 and the contrast SonoVue (Bracco International B.V., Netherlands), 2 perfusion indexes were quantified:
(a) First-pass myocardial blood flow. A low mechanical index (0.3), an S3 transducer (1.6–3.2MHz), 25Hz frame rate and grey-scale images were used. Gain (around 65) and compression (around 88) settings were optimized and unchanged throughout the studies. A bolus of 1.5ml of SonoVue was injected intravenously followed by a 5ml saline flush. Off-line, end-systolic images were digitally captured every cardiac cycle from contrast arrival to the left atrium and during the following 45s. Background-subtracted myocardial contrast intensity was measured at each cycle in each segment and normalized to that of the left ventricular cavity as recommended.5 Plots of myocardial contrast intensity were constructed and fitted to an exponential function y=A(1+e–Bx) as described by Wei et al. for a steady-state context.17 The derived plateau and the slope of the ascending curve were calculated. Finally, the product of slope and peak myocardial contrast intensity in each segment was considered as a surrogate of perfusion. According to the receiver operator characteristics curve to predict normal perfusion with intracoronary contrast echocardiography, a cut-off value of 0.06 was established for myocardial blood flow. An individual patient was considered to have normal perfusion as derived from myocardial blood flow in the case of 0 or 1 segment with abnormal (<0.06) perfusion in the risk area.
(b) Single-triggered images. After performing first-pass studies, a continuous infusion of SonoVue was administered. The infusion rate was adjusted to minimize attenuation, confining it to beyond the mitral valve plane. The focus was set at the mitral valve level but if there was any concern about a possible apical defect, the focus was moved up towards the apex. A high mechanical index (1.6), an S3 transducer (1.6–3.2MHz) and ultraharmonic imaging were used. Gain (around 65) and compression (around 88) settings were optimized and unchanged throughout the studies. Images from the apical 4-chamber and 2-chamber views were obtained. Once a steady-state of contrast infusion was achieved, single frame images were captured using an electrocardiogram trigger set at end-systole; images were captured every 6 cycles. Background-subtracted contrast intensity was quantified in each segment and normalized to that from the left ventricular cavity.5 According to the receiver operator characteristics curve to predict normal perfusion with intracoronary contrast echocardiography, a cut-off value of 0.9 was established for triggered images. An individual patient was considered to have normal perfusion as derived from triggered images in the case of 0 or 1 segment with abnormal (<0.9) perfusion in the risk area. The mean perfusion score in the risk area (sum of scores of each segment divided by the number of segments in the risk area) was also calculated for myocardial blood flow and triggered images.20
Intravenous contrast echocardiography images were digitized and analyzed on separate days by 2 experienced observers unaware of the results of the other explorations. Inter-observer discrepancies regarding the presence or absence of normal perfusion, either with myocardial blood flow or with triggered images took place in 3 cases (9%) solved by consensus.
Cardiac magnetic resonance
We used cardiac magnetic resonance for evaluating systolic function and the transmural extent of necrosis because of its well-established high accuracy for these purposes.26 Studies (Magnetom Sonata, Siemens Medical Solutions, Germany) were performed 190±23 days after infarction. All images were acquired by use of a phased-array body surface coil with 4–12 elements during breath-holds. Cine images with a slice thickness of 6mm were acquired throughout the entire left ventricle by use of contiguous 2D true fast imaging in steady-state precession sequences. Ejection fraction (%; Simpson's method) and regional wall motion (%; mean systolic wall thickening in the risk area) were quantitatively calculated. The same 17-segment model applied in the case of myocardial contrast echocardiography was used for defining the risk area with cardiac magnetic resonance.24
Afterwards, intravenous gadolinium–DTPA was administered (0.1mmol/kg). In order to determine the transmural extent of necrosis, imaging was performed with a delay time of 15min and, as a surrogate for nonviable-necrotic myocardium,13 the percentage extent of transmural late enhancement of each segment in the risk area was quantified and the average of all segments was calculated.
Cardiac magnetic resonance data were analyzed on separate days by 2 experienced observers unaware of the results of the other explorations. Mean inter-observer variability with regard to left ventricular systolic function and transmural late enhancement (as continuous parameters) was <3%.
Statistical analysis
Continuous variables were expressed as mean±standard deviation and compared by means of 2-tailed unpaired t-test. Discrete variables were expressed as percentages of the study population and compared by the chi-square test or Fisher's exact test. Sensitivity, specificity, predictive values and likelihood ratios of intravenous contrast echocardiography to predict normal perfusion as derived from intracoronary contrast echocardiography were determined. Receiver operator characteristics curves analyses were used to define the best cut-off values of myocardial blood flow and triggered images (as continuous parameters) to predict normal perfusion as derived from intracoronary contrast echocardiography. Regression lines were obtained by least squares regression method. Statistical significance was assumed if p<0.05. All statistical analysis was performed with SPSS software (version 9.0, SPSS Inc., Chicago, Illinois, USA).
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
Characteristics of the 32 patients included in the study group are expressed in Table 1.
Analysis per segments
Adequate intracoronary contrast echocardiography images were achieved in 105 (95%) of the 110 dysfunctional segments. Intracoronary contrast echocardiography prolonged 6±1min, the cardiac catheterization procedure and quantification took 5±1min.
Adequate intravenous contrast echocardiography was achieved in 97 (88%) of the 110 dysfunctional segments. Quantification took longer in the case of myocardial blood flow (9±2min vs. 5±1min with triggered images, p=0.01). Artefacts preventing assessment of intravenous contrast echocardiography occurred more frequently in the lateral wall (21% vs. 6% in non-lateral walls, p<0.0001).
Study results were focused on those 97 dysfunctional segments properly evaluated and quantified with both intracoronary and intravenous contrast echocardiography. Perfusion was normal (intracoronary contrast echocardiography > 0.75) in 78 segments (80%) and abnormal (intracoronary contrast echocardiography <0.75) in 19 segments (20%).
Segments with myocardial blood flow > 0.06 and with triggered images > 0.9 showed a higher percentage of cases with normal perfusion (intracoronary contrast echocardiography > 0.75) than those with myocardial blood flow <0.06 and with triggered images <0.9 (Fig. 1). Predictive values and likelihood ratios of myocardial blood flow and triggered images for detecting normal perfusion in a ‘per segments’ analysis are expressed in Table 2.
|
|
Analysis per patients
Twenty-two patients (69%) showed normal perfusion (0 or 1 segment with intracoronary contrast echocardiography <0.75) and 10 patients (31%) had abnormal perfusion in the risk area (2 or more segments with intracoronary contrast echocardiography <0.75).
Patients with normal triggered images (0 or 1 segment with perfusion <0.9) showed a higher percentage of cases with normal intracoronary contrast echocardiography than those with abnormal triggered images (Fig. 1). A similar but not significant trend was observed in the case of normal myocardial blood flow (0 or 1 segment with myocardial blood flow <0.06) (Fig. 1). Predictive values and likelihood ratios of myocardial blood flow and triggered images for detecting normal perfusion in a ‘per patients’ analysis are expressed inTable 2.
Finally, when perfusion indexes were analyzed as continuous variables, mean intracoronary contrast echocardiography score in the risk area showed a strong correlation with mean triggered images score in the risk area (R2=0.82, p=0.0001) (Fig. 2) and a borderline correlation with myocardial blood flow (R2=0.11, p=0.07).
|
Systolic function and transmural extent of necrosis
A more preserved perfusion in the risk area predicted a better late systolic function. Ejection fraction and regional wall motion at sixth month were related to mean intracoronary contrast echocardiography score and mean triggered images score in the risk area (Table 3). Mean intracoronary contrast echocardiography score R2=0.25, p=0.004) and mean triggered images score in the risk area (R2=0.34, p=0.001) were inversely related to the transmural extent of necrosis.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
The present study demonstrates that in patients with a first myocardial infarction, single-vessel disease and an open infarct-related artery, a quantitative analysis of myocardial contrast echocardiography performed with intravenous injection of contrast can be useful to evaluate coronary microcirculation—myocardial contrast echocardiography with intracoronary injection of contrast being the reference.
Intracoronary myocardial contrast echocardiography
Following the classical observations of Ito et al.3,27 intracoronary contrast echocardiography has become a standard for analyzing myocardial perfusion after myocardial infarction.16 These authors and others have demonstrated that about one fifth to one third of patients with TIMI grade 3 have evidence of microvasculature damage.3,5,6,14,25 In agreement with these observations we detected microvasculature damage in 20% of segments and in 31% of patients. Intracoronary contrast echocardiography showed the best correlation with sixth month systolic function. Ito et al. obtained identical results when they compared systolic function and intracoronary contrast echocardiography one month after infarction in a series of patients similar to ours.27
Intracoronary contrast echocardiography (as a consequence of the great amount of contrast directly arriving to the microcirculation) offers high-quality and easily-interpretable images (Figs. 3 and 4
). In our experience, intracoronary contrast echocardiography prolonged minimally the procedures and no side effects were observed. Taking into account all the considerations mentioned above, it is understandable that intracoronary contrast echocardiography (although not applicable in daily practice to all cases because of its invasive profile) has become a standard of perfusion16 and it was the reference method in the present study.
|
|
Comparison between intracoronary and intravenous contrast echocardiography
New non-invasive methods are needed in order to identify those cases with a totally open epicardial vessel and concomitant microcirculation obstruction. Intravenous contrast echocardiography has made significant advances in the recent years due to the development of contrast agents and ultrasonic modalities.16–23 In general, a qualitative or semi-quantitative assessment of perfusion images was performed20–23 and results were focused on viability or systolic function recovery18–23 rather than on validation of intravenous contrast echocardiography results with a clinical standard method.18–23
Although the qualitative analysis still plays a significant role in the daily practice evaluation of intravenous myocardial contrast echocardiography, a quantitative assessment is strongly recommended;16 therefore, for all purposes in the present study we used only a quantitative approach. Before this technique is ready for widespread application in the assessment of microcirculation in clinical practice, a number of hurdles have to be overcome such as optimal echocardiographic machine settings, optimal and clinically applicable study protocols, use of quantitative contrast image interpretation and especially analysis of whether the results obtained after intracoronary and intravenous injection are comparable.16
We used different contrast agents in the case of intracoronary and intravenous contrast echocardiography. The rationale for these choices was based on the previous experience of other groups with these agents28 and on our own experience during the learning curve.25 According to the different kinetics of bubbles during both techniques, we do not believe that the use of different agents plays a definitive role in results. It seems more important to obtain a sufficient amount of bubbles and a good image quality and in our experience this was obtained with different agents in the case of intracoronary and intravenous contrast echocardiography.
Few studies have been performed using quantitative methods for analyzing intravenous contrast echocardiography images. Shimoni et al.,18,19 in a group of 20 patients with chronic, stable ischemic heart disease and left ventricular dysfunction, demonstrated that a quantitative assessment of myocardial blood flow correlated with microvascular density, predicted systolic function recovery, improved accuracy compared with qualitative studies and showed a moderate agreement with thallium 201 scintigraphy and dobutamine echocardiography.
No previous data regarding the accuracy of a quantitative assessment of intravenous contrast echocardiography to analyze microvasculature early after myocardial infarction in comparison with intracoronary contrast echocardiography in a homogeneous series of patients like ours have been reported. Summarizing, we used 2 intravenous myocardial contrast echocardiography methods to analyze microvascular volume:
(a) In the first step, we analyzed myocardial blood flow as derived from analysis of curves of contrast arrival in a similar way to those obtained with cardiac magnetic resonance11–13 (Figs. 3 and 4
). Kinetics of contrast in magnetic resonance and echocardiography imaging are different and the model of quantification proposed by Wei et al.17 was described for a steady-state context. However, we tested this model to quantify first-pass myocardial blood flow. This method showed a high positive predictive value but a low negative predictive value to detect normal perfusion: a normal result almost assured normal perfusion but a negative result did not immediately indicate microcirculation damage, suggesting the possibility of some false negative results because of not enough contrast arrival, attenuation or inherent drawbacks with this method.
(b) In the second step, we analyzed normalized peak videointensity in triggered images as a surrogate of microvascular volume. Quantification of contrast intensity in a single end-systolic image captured 1 of each 6 cycles (in order to allow full replenishment after ultrasound pulses) showed a good correlation with late ejection fraction and with the transmural extent of necrosis. Moreover, normal perfusion (as derived from intracoronary contrast echocardiography) was accurately predicted with this method. Taking into account its high reliability as well as quantification of single-triggered images not being time-consuming and being easily-interpretable (Figs. 3 and 4), this method could be currently applicable in daily echo labs practice for assessment of post-infarction perfusion until new equipment, contrasts and quantification methods are available.
|
Limitations |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
The presented findings are only applicable to the agents and techniques used and to the clinical scenario of the present study and the results may be different when other modalities are employed or other clinical situations are evaluated. A time interval of at least 48h was set between intracoronary and intravenous contrast echocardiography; a shorter time interval could improve the correlation between both techniques. Perfusion of segments with normal contractility was not quantified; although inclusion of all segments could improve the results, we considered that the analysis of perfusion in those segments with a totally normal contractility is not of great interest (in general, it is normal).
|
Conclusions |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
Quantitative intravenous myocardial contrast echocardiography is useful to assess microvasculature perfusion early after myocardial infarction in patients with TIMI 3 flow when compared with intracoronary myocardial contrast echocardiography. The product of upslope of contrast arrival and peak myocardial intensity after a single intravenous bolus injection of contrast allows a fast and first approach to perfusion. The quantitative analysis of single end-systolic triggered images is a highly accurate and easy-to-obtain method to study microvasculature damage.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionLimitationsConclusionsReferences |
|---|
- Braunwald E. Reperfusion therapy for acute myocardial infarction: historical context and future promise. Eur Heart J (2002) 4:E10–E14.[CrossRef]
- Cannon C.P. Importance of TIMI 3 flow. Circulation (2001) 104:624–626.
[Free Full Text] - Ito H., Tomooka T., Sakai N., Yu H., Higashino Y., Fujii K., et al. Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction. Circulation (1992) 85:1699–1705.
[Abstract/Free Full Text] - Kim C.B., Braunwald E. Potential benefits of late reperfusion of infarcted myocardium. The open artery hypothesis. Circulation (1993) 88:2426–2436.
[Free Full Text] - Kaul S., Ito H. Microvasculature in acute myocardial ischemia: part I. Evolving concepts in pathophysiology, diagnosis and treatment. Circulation (2004) 109:146–149.
[Free Full Text] - Kaul S., Ito H. Microvasculature in acute myocardial ischemia: part II. Evolving concepts in pathophysiology, diagnosis and treatment. Circulation (2004) 109:310–315.
[Free Full Text] - Reffelmann T., Hale S.L., Dow J.S., Kloner R.A. No-reflow phenomenon persists long-term after ischemia/reperfusion in the rat and predicts infarct expansion. Circulation (2003) 108:2911–2917.
[Abstract/Free Full Text] - Haager P.K., Christott P., Lepper W., Hanrath P., Hoffmann R. Prediction of clinical outcome after mechanical revascularization in acute myocardial infarction by markers of myocardial reperfusion. J Am Coll Cardiol (2003) 41:532–538.
[Abstract/Free Full Text] - Henriques J.P., Zijlstra F., van't Hof A.W., de Boer M.-J., Dambrink J., Gosselink M., et al. Angiographic assessment of reperfusion in acute myocardial infarction by myocardial blush grade. Circulation (2003) 107:2115–2119.
[Abstract/Free Full Text] - Bax M., de Winter R.J., Schotborgh C.E., Koch K.T., Meuwissen M., Voskuil M., et al. Short- and long-term recovery of left ventricular function predicted at the time of primary percutaneous coronary intervention in anterior myocardial infarction. J Am Coll Cardiol (2004) 43:534–541.
[Abstract/Free Full Text] - Nagel E., Klein C., Paetsch I., Hettwer S., Schnockenburg B., Wegscheider K., et al. Magnetic resonance perfusion measurements for the non-invasive detection of coronary artery disease. Circulation (2003) 108:432–437.
[Abstract/Free Full Text] - Bello D., Shah D., Farah G., S. Di Luzio, Parker M., Johnson M., et al. Gadolinium cardiovascular magnetic resonance predicts reversible myocardial dysfunction and remodeling in patients with heart failure undergoing beta-blocker therapy. Circulation (2003) 108:1945–1953.
[Abstract/Free Full Text] - Wu K.C. Myocardial perfusion imaging by magnetic resonance imaging. Curr Cardiol Rep (2003) 5:63–68.[Medline]
- Wu K.C., Zerhouni E.A., Judd R.M., Lugo-Olivieri C., Barouch L., Schulman S., et al. Prognostic significance of microvascular obstruction by magnetic resonance imaging in patients with acute myocardial infarction. Circulation (1998) 97:765–772.
[Abstract/Free Full Text] - De Luca G., van't Hof A.W., de Boer M.J., Hoorntje J.C., Gosselink M., Dambrink E., et al. Impaired myocardial perfusion is a major explanation of the poor outcome observed in patients undergoing primary angioplasty for ST-segment-elevation myocardial infarction and signs of heart failure. Circulation (2004) 109:958–961.
[Abstract/Free Full Text] - Marques K.M.J., Visser C.A. Myocardial contrast echocardiography in the assessment of pharmacologic intervention of the reperfusion injury. Eur Heart J (2003) 24:19–20.
[Free Full Text] - Wei K., Jayaweera A.R., Firoozan S., Linka A., Skyba D.M., Kaul S. Quantification of myocardial blood flow with ultrasound-induced destruction of microbubbles administered as a constant venous infusion. Circulation (1998) 97:473–483.
[Abstract/Free Full Text] - Shimoni S., Frangogiannis N.G., Aggeli C.J., Shan K., Verani M.S., Quinones M.A., et al. Identification of hibernating myocardium with quantitative intravenous myocardial contrast echocardiography. Comparison with dobutamine echocardiography and thallium-201 scintigraphy. Circulation (2003) 107:538–544.
[Abstract/Free Full Text] - Shimoni S., Frangogiannis N.G., Aggeli C.J., Shan K., Quinones M.A., Espada R., et al. Microvascular structural correlates of myocardial contrast echocardiography in patients with coronary artery disease and left ventricular dysfunction. Implications for the assessment of myocardial hibernation. Circulation (2002) 106:950–956.
[Abstract/Free Full Text] - Balcells E., Powers E.R., Lepper W. Detection of myocardial viability by contrast echocardiography in acute infarction predicts recovery of resting function and contractile reserve. J Am Coll Cardiol (2003) 41:827–833.
[Abstract/Free Full Text] - Senior R., Swinburn J.M. Incremental value of myocardial contrast echocardiography for the prediction of recovery of function in dobutamine nonresponsive myocardium early after myocardial infarction. Am J Cardiol (2003) 91:397–402.[CrossRef][Web of Science][Medline]
- Swinburn J.M., Lahiri A., Senior R. Intravenous myocardial contrast echocardiography predicts recovery of dysfunctional myocardium early after acute myocardial infarction. J Am Coll Cardiol (2001) 38:19–25.
[Abstract/Free Full Text] - Mengozzi G., Rossini R., Palagi C., Musumeci G., Petronio A., Limbruno U., et al. Usefulness of intravenous myocardial contrast echocardiography in the early left ventricular remodeling in acute myocardial infarction. Am J Cardiol (2002) 90:713–719.[CrossRef][Web of Science][Medline]
- Cerqueira M.D., Weissman N.J., Dilsizian V., Jacobs A.K., Kaul S., Laskey W.K., et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the heart. Circulation (2002) 105:539–542.
[Free Full Text] - Bodí V., Sanchis J., López-Lereu M.P., Llácer A., Pellicer M., Losada A., et al. Study of the perfusion in post-infarction patients by means of myocardial echocardiography with intracoronary injection of contrast. Implications and relationship with angiography and magnetic resonance imaging. Rev Esp Cardiol (2004) 57:20–28.[CrossRef][Web of Science][Medline]
- Grothues F., Smith G.C., Moon J.C., Bellenger N.G., Collins P., Klein H.U., et al. Comparison of interstudy reproducibility of cardiovascular magnetic resonance imaging with two-dimensional echocardiography in normal subjects and in patients with heart failure or left ventricular hypertrophy. Am J Cardiol (2002) 90:29–34.[CrossRef][Web of Science][Medline]
- Ito H., Iwakura K., Oh H. Temporal changes in myocardial perfusion patterns in patients with reperfused anterior wall myocardial infarction. Their relation to myocardial viability. Circulation (1995) 91:656–662.
[Abstract/Free Full Text] - Seggewiss H. Medical therapy versus interventional therapy in hypertrophic obstructive cardiomyopathy. Curr Control Trials Cardiovasc Med (2000) 1:115–119.[Medline]
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  V Bodi, J Sanchis, M P Lopez-Lereu, J Nunez, R Sanz, P Palau, C Gomez, D Moratal, F J Chorro, and A Llacer Microvascular perfusion 1 week and 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging Heart, December 1, 2006; 92(12): 1801 - 1807. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||