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J Am Coll Cardiol, 2007; 49:1178-1185, doi:10.1016/j.jacc.2006.12.032 (Published online 5 March 2007).
© 2007 by the American College of Cardiology Foundation
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CLINICAL RESEARCH: CARDIAC IMAGING

Acute Myocardial Infarction Early Viability Assessment by 64-Slice Computed Tomography Immediately After Coronary Angiography

Comparison With Low-Dose Dobutamine Echocardiography

Michel Habis, MD*,*, André Capderou, MD, PhD{dagger}, Saïd Ghostine, MD*, Béatrice Daoud, MD{ddagger}, Christophe Caussin, MD*, Jean-Yves Riou, MD{ddagger}, Philippe Brenot, MD{ddagger}, Claude Yves Angel, MD{ddagger}, Bernard Lancelin, MD* and Jean-François Paul, MD{ddagger}

* Department of Cardiology, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson, France
{dagger} Department of Physiology, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson, France
{ddagger} Department of Radiology, Centre Chirurgical Marie Lannelongue, Le Plessis Robinson, France.

Manuscript received September 19, 2006; revised manuscript received November 28, 2006, accepted December 21, 2006.

* Reprint requests and correspondence: Dr. Michel Habis, Centre Chirurgical Marie Lannelongue, 133 avenue de la Resistance, 92350 Le Plessis Robinson, France. (Email: mhabis{at}ccml.fr).


   Abstract
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Objectives: Early evaluation of myocardial viability in acute myocardial infarction is useful to guide therapy. Therefore, we assessed 64-slice computed tomography (CT) immediately after coronary angiography in this setting.

Background: Recent preliminary studies have shown the promising usefulness of late hyperenhancement multislice computed tomography (MSCT) for non-viability assessment.

Methods: Thirty-six patients admitted for a first acute myocardial infarction had a coronary angiogram early after admission followed by 64-slice CT without iodine reinjection. The 16 segments of the left ventricle depicted by the American Society of Echocardiography were graded: no, subendocardial, or transmural hyperenhancement. No or subendocardial hyperenhancement were expected to reflect viability. Two to 4 weeks later, the same segments’ contractility was evaluated at rest. Low-dose dobutamine echocardiography was performed in case of akinetic segment at rest.

Results: Mean delay between coronary angiography and MSCT was 24 ± 11 min (range 7 to 51 min). We compared 576 segments evaluated by each method. Agreement was noted for 560 segments (97%) and disagreement for 16 segments (3%). Thus, 64-slice CT after coronary angiography for an acute myocardial infarction had 98% sensitivity, 94% specificity, 97% accuracy, and 99% positive and 79% negative predictive values for detecting viable myocardial segments at a very early stage of an acute myocardial infarction. On a per-patient analysis, sensitivity, specificity, accuracy, and positive and negative predictive values were 92%, 100%, 94%, and 100% and 85%, respectively.

Conclusions: A 64-slice CT after coronary angiography for an acute myocardial infarction is a promising method for early evaluation of viable myocardium.

Abbreviations and Acronyms
  AMI = acute myocardial infarction
  CT = computed tomography
  MRI = magnetic resonance imaging
  MSCT = multislice computed tomography
  WMSI = wall motion score index

After a coronary occlusion, myocardial necrosis progresses in a wave front extending from subendocardium to subepicardium (1). At the same time, as much as 58% of the left ventricle wall thickening relies on the endocardium, 25% on the middle, and 17% on the subepicardial layer (2). Infarct size and ejection fraction are important prognostic predictors after myocardial infarction (3). However, ejection fraction is load-dependent and could be unaltered in case of akinetic area with a hyperkinetic remote myocardium. Distinction between stunned and irreversibly damaged myocardium is a major concern in the setting of an acute myocardial infarction (AMI). A previous study using positron emission tomography showed that as much as 40% of the myocardial area at risk identified after a myocardial infarction is stunned (4). Identification of stunned myocardium is essential in helping the revascularization decision when a successful thrombolysis leaves a significant stenosis of the culprit coronary artery. Prognosis is better, even without revascularization, when stunned myocardium is identified in a post-infarction dysfunctional left ventricle (5). On the other hand, remodeling depends on the transmural extent of the myocardial infarction (6) and the reflow downstream the culprit coronary artery (7–9). Thallium imaging offers a good level of sensitivity but a specificity below 60% (10,11) for viability assessment. Dobutamine echocardiography, although providing a better specificity (83% to 86%) (10,11) and a similar sensitivity, could be hazardous in cases of severe dysfunctional left ventricle or critical stenosis with limited flow at rest or in case of ventricular arrhythmia. Delayed enhancement magnetic resonance imaging (MRI) has been widely validated for non-viability assessment (12,13), and very recently electrocardiogram (ECG)-gated multislice computed tomography (MSCT) has shown comparable results as an alternative technique (14–16). As CT is quicker and easier than MRI and available in an emergency setting, we wanted to evaluate the usefulness of 64-slice CT delayed enhancement without iodine reinjection immediately after coronary angiography. Computed tomography findings were compared with a previously validated technique: low-dose dobutamine echocardiography.


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For 6 consecutive months, patients were admitted in our hospital and enrolled in our study at daytime hours only (from December 2005 to June 2006). Inclusion criteria were ST-segment elevation, and/or long-lasting spontaneous chest pain within the preceding 5 days, and/or acute coronary occlusion with more than 2 times normal creatine phosphokinase release. Exclusion criteria were previous myocardial infarction, renal impairment (creatinine above 200 µmol·l–1). Coronary angiography was performed as soon as the patient arrived at hospital in case of unrelieved chest pain. Contrast media used was Iomeprol (Bracco, Milan, Italy). When thrombolytic agent was perfused, coronary angiography was performed 90 min later with continuing chest pain or the following day in case of relieved chest pain. The culprit coronary artery was defined on the combination of ECG at admission and the angiographic result. Angioplasty was immediately attempted when unrelieved chest pain and/or Thrombolysis In Myocardial Infarction flow grade 2 or less downstream the culprit stenosis. All patients underwent 64-slice CT immediately after coronary angiography. Iodine volume and time lasting from the last coronary injection to 64-slice CT scanning were measured. The study was approved by our institution committee, and all the patients enrolled gave their informed consent.


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64-slice CT.   A 64-slice CT is next to the catheterization laboratory in our institution. All images were acquired without contrast medium reinjection. Images were performed on a 64-slice CT (Sensation 64, Siemens, Erlangen, Germany) using ECG-gated acquisition with ECG-tube current modulation. Low kilovoltage setting was applied (80 kV in patients below 70 kg, 100 kV above) with a tube current of 700 mAs in both cases. Mean dose length product was 240 mGyxcm corresponding to an approximate mean radiation dose of 4 mSv.

Images were reconstructed at the mid-diastolic phase with an initial slice thickness of 3 mm. Sections of the left ventricle in parasternal long- and short-axis, apical 4- and 2-chamber views were obtained by 8-mm slice reformatted images. Contrast hyperenhancement was assessed visually by 2 experienced observers in consensus (1 radiologist and 1 cardiologist) unaware of the results of dobutamine echocardiography. The American Society of Echocardiography (ASE) 16-segment model was used for segmental evaluation (17). Hyperenhancement extent was considered subendocardial if <50% of the left ventricle thickness was involved (Figs. 1 and 2)Go and transmural if above (Fig. 3). No or subendocardial hyperenhancement was expected to reflect viability. Patients were considered having a transmural infarction whenever 2 or more adjacent segments exhibited transmural late hyperenhancement on 64-slice CT. All examinations achieved sufficient diagnostic quality for the assessment of the myocardial contrast changes.


Figure 1
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  		Figure 1 64-Slice CT Scan 51 Min After a Primary Angioplasty for an AMI of a 59-Year-Old Patient

Parasternal long-axis view (8-mm slice thickness) shows subendocardial hyperenhancement of the posterior wall (segments 4 and 10) (arrows). Low-dose dobutamine echocardiography confirmed myocardial viability of these segments. AMI = acute myocardial infarction; Ao = aorta; CT = computed tomography; LA = left atrium; LV = left ventricle.

 

Figure 2
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  		Figure 2 64-Slice Computed Tomography Scan 15 Min After Facilitated Angioplasty of a Right Coronary Artery

The apical 2 chambers (A) and parasternal short-axis (B) views show subendocardial hyperenhancement of the inferior wall of the left ventricle (LV) (arrows) and the papillary muscle (arrowheads). (C) Mitral regurgitation was diagnosed at echocardiography consistent with ischemic involvement of the papillary muscle. Myocardial viability was present at low-dose dobutamine echocardiography. LA = left atrium; RV = right ventricle.

 

Figure 3
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  		Figure 3 64-Slice CT Scan 21 Min After Left Anterior Descending Coronary Artery Reperfusion

(A) Parasternal short-axis view shows transmural hyperenhancement of segments 7, 8, 11, and 12 (arrows). (B) Apical 4-chamber view shows transmural hyperenhancement of segments 6, 12, 13, and 15 (arrows). This patient was confirmed having no viability at low-dose dobutamine echocardiography in all the involved segments. CT = computed tomography; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

 
Echocardiography.   Two to 4 weeks (20 ± 5 days) after AMI, patients were called back for low-dose dobutamine echocardiography by the same operator 2 days after withholding beta-blocker therapy. The evaluation was performed on a Philips Sonos 7500 (Andover, Massachusetts). Ninety-four percent (34 of 36) of the patients had completed angioplasty of the culprit coronary artery at this echocardiographic evaluation. The ASE 16 segments of the left ventricle (17) were respectively graded 1, 2, 3, and 4 if, respectively, normal, hypokinetic, akinetic, or dyskinetic. Planimetry of left ventricle diastolic and systolic volumes was measured by a Simpson biplane method, and the same volumes were divided by the body surface area (indexed volumes). Baseline ejection fraction was calculated. Low-dose dobutamine echocardiography was performed when an akinetic segment was identified at rest starting with a 5-µg/kg/min infusion and followed by 2.5-µg/kg/min increment stages. No more than 15 beats/min above the baseline heart rate was reached in order to avoid ischemia. In case of poor image quality, a microbubble contrast agent (Sulphur hexafluoride, Bracco) was injected to better visualize the different myocardial segments. Myocardial viability was expected to correspond to a normal or hypokinetic segment at rest or an akinesia improving with low-dose dobutamine. Patients were considered having a non-viable infarction whenever 2 or more adjacent akinetic segments did not show a contractile reserve at low-dose dobutamine echocardiography. A wall motion score index (WMSI) (mean score of all segments) was calculated at rest and after dobutamine infusion.

Statistics.   Statistical analysis was performed with StatView 5.0 software (SAS Institute Inc., Cary, North Carolina). Percentages are expressed with 95% confidence interval. Continuous variables were expressed as mean ± SD. Correlations were tested after transformation by z value of Fischer to evaluate the probability for rejecting the null hypothesis (r = 0). We reported correlation coefficient (r) and the assessed probability from z transformation (p). A p value <0.05 was regarded as statistically significant. Enhancement on 64-slice CT was compared with normal contractility or contractile reserve at low-dose dobutamine echocardiography accepted as reference method. This comparison was depicted as sensitivity, specificity, accuracy, positive and negative predictive values on patients, segments, and main culprit coronary arteries analysis.


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Our study population comprised 35 men and 1 woman (Table 1). Mean age was 57 ± 13 years. All patients were in sinus rhythm. Thirty-four patients had ST-segment elevation, 1 had ST-segment depression, and the last no ST-segment variation. Myocardial infarction was anterior (n = 16), inferior (n = 13), posterior (n = 3), and lateral (n = 4). Twenty-one patients had a primary angioplasty when entering the study. Five had a facilitated angioplasty after a thrombolytic therapy. The remaining had a coronary angiography after (n = 6) or not (n = 4) a thrombolytic therapy. The median delay between onset of myocardial infarction and first therapy was 3.25 h (range 1 to 120 h). Left anterior descending (n = 16), right (n = 13), circumflex (n = 6), and a diagonal branch (n = 1) were the culprit coronary arteries. Coronary angiography depicted 2 significant left main stenoses. The left anterior descending coronary artery was occluded (n = 10) or significantly stenosed (n = 14). These respective values were 3 and 19 for the circumflex and 4 and 16 for the right coronary artery. This yielded 11 trivascular, 9 bivascular, and 15 monovascular patients. The last patient had a normal coronary angiogram. The mean radiation dose for coronary angiography followed or not by angioplasty was 3.5 ± 2.5 mSv.


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  		Table 1 Baseline Characteristics of Our Study Population
 
64-slice CT.   Iomeprol volume injected during coronary angiography was 176 ± 78 ml. The time elapsed from the end of coronary angiography to 64-slice CT scanning was 24 ± 11 min (range 7 to 51 min). Heart rate during scanning was 75 ± 15 beats/min. Delayed hyperenhancement was transmural (63 segments) and subendocardial (46 segments). A total of 476 segments were normally enhanced. Three patients scanned 20 min after angiography also had subendocardial hypodensity.

Echocardiography.   All 576 echocardiographic segments could be analyzed. At baseline echocardiographic evaluation, 63 segments were akinetic, 38 hypokinetic, and 475 normokinetic. Low-dose dobutamine echocardiography yielded 53 akinetic, 18 hypokinetic, and 505 normokinetic segments. Baseline left ventricle diastolic and systolic volumes were 84.3 ± 30.3 ml and 38.2 ± 21.1 ml, respectively. This yielded left ventricle diastolic and systolic indexed volumes of 42.5 ± 16 ml/m2 and 19.5 ± 10.7 ml/m2, respectively. Baseline ejection fraction was 56.4 ± 11.2% (range 22% to 70%). Rest and low-dose dobutamine WMSI were 1.28 ± 0.33 and 1.21 ± 0.33, respectively. Rest WMSI was significantly correlated to left ventricle ejection fraction (r = –0.82, p < 0.0001).

Comparison of 64-slice CT enhancement and low-dose dobutamine echocardiography.   On a per-segment analysis, agreement was noted for 560 segments (97%): 465 with normal and 45 with subendocardial hyperenhancement were considered normal or having a contractile reserve at dobutamine echocardiography, and 50 segments with transmural hyperenhancement did not show a contractile reserve. Disagreement was noted for 16 (3%) segments: 2 with normal and 1 with subendocardial hyperenhancement were akinetic without a contractile reserve, and 13 with transmural hyperenhancement exhibited a contractile reserve at dobutamine echocardiography. Thus, 64-slice CT after coronary angiography for an AMI had 98% sensitivity, 94% specificity, 97% accuracy, and 99% positive and 79% negative predictive values for detecting viable myocardial segments at a very early stage of AMI.

On a per-patient analysis, agreement between our 2 evaluations was found for 34 (94%) patients: 11 had a transmural hyperenhancement and did not exhibit a contractile reserve, and 23 were considered viable at low-dose dobutamine echocardiography and not transmurally hyperenhanced on 64-slice CT. Disagreement was limited to 2 (6%) patients having transmural hyperenhancement but presenting a contractile reserve at dobutamine echocardiography. This led to sensitivity, specificity, accuracy, and positive and negative predictive values of 92%, 100%, 94%, and 100% and 85%, respectively, for 64-slice CT delayed hyperenhancement to predict viability.

On a culprit artery analysis, sensitivity, specificity, accuracy, positive and negative predictive values are presented in Table 2.


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  		Table 2 Comparison of 64-Slice CT Myocardial Lack of Hyperenhancement With Low-Dose Dobutamine Echocardiography
 
The number of transmural hyperenhanced segments was significantly correlated to rest (r = 0.91, p < 0.0001) and dobutamine (r = 0.95, p < 0.0001) WMSI, left ventricle diastolic (r = 0.39, p = 0.02) and systolic (r = 0.66, p < 0.0001) absolute and indexed volumes (r = 0.48, p = 0.003; r = 0.66, p < 0.0001), respectively, and to left ventricle ejection fraction (r = –0.80, p < 0.0001).


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Comparison with previous studies.   To the best of our knowledge, our study is the first evaluating the usefulness of late-enhancement 64-slice CT immediately after coronary angiography to assess AMI viability in such an early setting. Late enhancement CT performed in a 2-week delay after 28 reperfused AMIs was found to be as reliable as delayed enhancement MRI for evaluating infarct size (16). Acute myocardial infarction late hyperenhancement on MSCT is well correlated to histomorphometric infarct size staining (15) and accurately predicts its transmural extent. This agreement is better for acute than chronic myocardial infarctions (14). Paul et al. (18) also found a good correlation between late defects on multi-detector row CT scan 2 days after 34 AMIs with the infarct size assessed at 6 weeks by single-photon emission CT.

Comparison with MRI.   As for gadolinium in MRI, destruction of sarcolemmal membranes allows iodine entrance in damaged myocardial cells (14). Because 75% of myocardial volume is intracellular, iodine penetration in damaged myocardial cells increases its distribution volume. Low wash in and wash out also contribute to this late hyperenhancement. Iomerol and gadolinium, though having different molecular structures, share the same delayed kinetic in experimental AMIs (14). This slow iodine wash out from the damaged myocardium allowed infarct size assessment in our study as late as 51 min after the end of coronary angiography (Fig. 1). Previous MRI studies have highlighted the role of imaging time for accurately delineating the real infarct size (19). Modifying inversion time in MRI allowed correcting for different gadolinium doses and imaging delays (20). On the other hand, an experimental MSCT study showed that though signal intensity decreased over time, the real infarct size remained proportionately unchanged when compared with the left ventricle chamber and remote myocardium over 40-min delay (15).

Multislice CT offers a better spatial resolution than MRI and is less altered by the partial volume effect because of sections 10 to 20 times thinner. However, signal intensity and contrast-to-noise ratio is higher in MRI (14). Magnetic resonance imaging hyperenhancement overestimates the real infarct size especially when imaging is performed early after reperfusion probably because standard contrast media react with interstitial subendocardial edema (21). The possible iodine contrast interaction with peri-infarction edema is not yet evaluated.

Contractile reserve in the stunned segments.   The determination of the real infarct size in the setting of an AMI is blurred by the rest contractile state. The core of the infarct is surrounded by an area at risk containing stunned myocardial cells. In the mean time, experimental studies have demonstrated adjacent non-ischemic areas of impaired thickening extending with infarct transmurality (22). Contractile reserve evaluated after a myocardial infarction is an already validated method for predicting viability (23) and left ventricular remodeling (6). Though being safe even when performed in the first week after myocardial infarction (24,25), it is contraindicated in cases of persistent ventricular arrhythmia and could be hazardous even with low-dose dobutamine infusion when a non-culprit coronary stenosis has a very limiting flow. A MSCT evaluation after coronary angiography is safer, does not require additional iodine injection, and is, in this preliminary study, an immediate reliable and currently available evaluation of myocardial viable segments in the acute setting of myocardial infarction when CT scan is next to the catheterization laboratory. Using low kV settings, additional radiation dose (4 mSv) seems acceptable.

Disagreement between the 2 evaluations.   We expected CT scan to evaluate the same segments as echocardiography by closely comparing the same 4 views of the left ventricle, but we cannot exclude some variability in segmental localization of myocardial infarction. Therefore, we used the threshold of 2 segments to define non-viability on per-patient analysis to increase the robustness of the comparison. As previously shown by Gerber et al. (26), circumferential shortening differs between infarct core and border zone. Four of our 13 transmural hyperenhanced segments could be at the periphery of an infarct core and be tethered by adjacent normocontractile segments. On the other hand, recruitment of viable myocardial cells inside a layer of necrosis was also demonstrated experimentally (27), and a previous study (28) has described contactile reserve in 19% of segments exhibiting more than 50% hyperenhancement on MRI, which is in agreement with the 20% segments (13 of 63) in our study. This rate decreases when the transmural extent of delayed enhancement increases (28,29). Thus, we cannot exclude a better agreement between the 2 methods if the threshold was 75% of delayed hyperenhancement. We cannot also exclude iomeprol diffusion in edematous segments surrounding a myocardial infarction. Finally, myocardial infarct size could have partially shrunk at the first month as previously described on follow-up (30).

Our 3 false-positive segments on MSCT consisted of 2 normal and 1 subendocardial hyperenhancement found akinetic without contractile reserve at dobutamine echocardiography. The reason could be a possible increase in the delayed enhancement size as the 33% increase described by Rochitte et al. (31) on MRI during the first 2 days after AMI. We cannot exclude dobutamine echocardiography having missed a real contractile reserve (negative predictive value between 80% and 93%) (25,32,33). Higher dobutamine dose or follow-up could later confirm it.

Because of these rare discrepancies, no conclusion can be drawn regarding a potential role of the delay between coronary angiography and scanning or Iomeprol (Bracco) volume injected nor the patient status at entry.

Prediction of global left ventricle function.   Long-term improvement in the left ventricular ejection fraction and wall thickening score rely on the number of dysfunctional segments improving their contactility during follow-up (34). Similarly, the acute infarct size assessed by contrast-enhanced MRI is correlated with the 2-month follow-up ejection fraction and the left ventricle end-systolic volume (30). The correlation found in our study between the number of transmural late hyperenhanced segments and the left ventricle systolic volume and ejection fraction on the first month is in agreement with this concept.

Study limitations.   Standardization is difficult considering iodine volume and scanning delay variations. Due to the short delay between the procedures, such viability assessment can only be performed in routine when CT is next to the catheterization laboratory. Late enhancement 64-slice CT was compared with low-dose dobutamine echocardiography performed 2 to 4 weeks after AMI, which was previously found reliable for predicting viability. Follow-up study would have required a new echocardiographic evaluation, which was not in the scope of this preliminary study. Follow-up echocardiographic evaluation is also an imperfect reference method (35) because the expected contractile recovery (contractile reserve at low-dose dobutamine echocardiography) could only emerge in response to stress (36,37). Our 2 evaluations of myocardial viability were not simultaneous, but reperfusion of the culprit coronary artery was successful and uneventfully achieved for 94% of our patients during that elapsed delay. Our study enrolled only 2 patients (Patients #18 and #25) reperfused by coronary artery bypass graft after viability assessment by the 2 methods. However, MRI studies have shown that delayed enhancement did not rely on the reperfusion of the culprit coronary artery (38,39). Finally, no conclusion can be drawn from our 3 patients with subendocardial hypodensities because our scanning delay is probably not accurate for this evaluation of microvascular obstruction.

Clinical implications.   Therefore, 64-slice CT performed immediately after coronary angiography appears to offer a good accuracy and very good positive predictive value for viability assessment when compared with low-dose dobutamine echocardiography. Based on the results of this preliminary study, it could be sufficient to confirm the presence of viable segments in an AMI when hyperenhancement is absent or involves <50% of the myocardial wall thickness. However, we still recommend performing dobutamine echocardiography when hyperenhancement involves more than 50% of the myocardial wall to avoid missing 20% of transmural hyperenhanced segments exhibiting a contractile reserve. Such an immediate assessment of myocardial viability may play an important role in post-infarction therapeutic strategies in the future, especially after successful reperfusion with persistent significant stenosis of the culprit coronary artery.


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In this preliminary study, 64-slice CT without iodine reinjection immediately after coronary angiography for an AMI is a promising method of very early viability assessment. It offers all the following cumulated advantages: very early, quick, safe, easy, and diffusely available evaluation, which could be sufficient to define viability when hyperenhancement is absent or involves less than 50% of the myocardial thickness.


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  1. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death: I. myocardial infarct size versus duration of coronary artery occlusion in dogs. Circulation 1977;56:786-794.[Abstract/Free Full Text]
  2. Myers JH, Stirling MC, Choy M, Buda AJ, Gallagher KP. Direct measurement of inner and outer wall thickening dynamics with epicardial echocardiography Circulation 1986;74:164-172.[Abstract/Free Full Text]
  3. Burns RJ, Gibbons RJ, Yi Q, et al. CORE Study Investigators The relationships of left ventricular ejection fraction, end-systolic volume index and infarct size to six-month mortality after hospital discharge following myocardial infarction treated by thrombolysis J Am Coll Cardiol 2002;39:30-36.[Abstract/Free Full Text]
  4. Tillisch J, Brunken R, Marshall R, et al. Reversibility of cardiac wall-motion abnormalities predicted by positron tomography N Engl J Med 1986;314:884-888.[Abstract]
  5. Picano E, Sicari R, Landi P, et al. EDIC Study Group Prognostic value of myocardial viability in medically treated patients with global left ventricular dysfunction early after an acute uncomplicated myocardial infarction. A dobutamine stress echocardiographic study. Circulation 1998;98:1078-1084.[Abstract/Free Full Text]
  6. Bolognese L, Cerisano G, Buonamici P, et al. Influence of infarct-zone viability on left ventricular remodeling after acute myocardial infarction Circulation 1997;96:3353-3359.[Abstract/Free Full Text]
  7. Caldas MA, Tsutsui JM, Kowatsch I, et al. Value of myocardial contrast echocardiography for predicting left ventricular remodeling and segmental functional recovery after anterior wall acute myocardial infarction J Am Soc Echocardiogr 2004;17:923-932.[CrossRef][ISI][Medline]
  8. Wu KC, Zerhouni EA, Judd RM, 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]
  9. Gerber BL, Rochitte CE, Melin JA, et al. Microvascular obstruction and left ventricular remodeling early after acute myocardial infarction Circulation 2000;101:2734-2741.[Abstract/Free Full Text]
  10. Perrone-Filardi P, Pace L, Prastaro M, et al. Assessment of myocardial viability in patients with chronic coronary artery disease: rest-4-hour-24-hour 201Tl tomography versus dobutamine echocardiography Circulation 1996;94:2712-2719.[Abstract/Free Full Text]
  11. Vanoverschelde JL, D’Hondt AM, Marwick T, et al. Head-to-head comparison of exercise-redistribution-reinjection thallium single-photon emission computed tomography and low dose dobutamine echocardiography for prediction of reversibility of chronic left ventricular ischemic dysfunction J Am Coll Cardiol 1996;28:432-442.[Abstract]
  12. Hillenbrand HB, Kim RJ, Parker MA, Fieno DS, Judd RM. Early assessment of myocardial salvage by contrast-enhanced magnetic resonance imaging Circulation 2000;102:1678-1683.[Abstract/Free Full Text]
  13. Gerber BL, Garot J, Bluemke DA, Wu KC, Lima JAC. Accuracy of contrast-enhanced magnetic resonance imaging in predicting improvement of regional myocardial function in patients after acute myocardial infarction Circulation 2002;106:1083-1089.[Abstract/Free Full Text]
  14. Gerber BL, Belge B, Legros GJ, et al. Characterization of acute and chronic myocardial infarcts by multidetector computed tomography. Comparison with contrast-enhanced magnetic resonance. Circulation 2006;113:823-833.[Abstract/Free Full Text]
  15. Lardo AC, Cordeiro MAS, Silva C, et al. Contrast-enhanced multidetector computed tomography viability imaging after myocardial infarction. Characterisation of myocyte death, microvascular obstruction, and chronic scar. Circulation 2006;113:394-404.[Abstract/Free Full Text]
  16. Mahnken AH, Koos R, Katoh M, et al. Assessment of myocardial viability in reperfused acute myocardial infarction using 16-slice computed tomography in comparison to magnetic resonance imaging J Am Coll Cardiol 2005;45:2042-2047.[Abstract/Free Full Text]
  17. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echocardiography J Am Soc Echocardiogr 1989;2:358-367.[Medline]
  18. Paul JF, Wartski M, Caussin C, et al. Late defect on delayed contrast-enhanced multidetector row CT scans in the prediction of SPECT infarct size after reperfused acute myocardial infarction: initial experience Radiology 2005;236:485-489.[Abstract/Free Full Text]
  19. Oshinski JN, Yang Z, Jones JR, Mata JF, French BA. Imaging time after Gd-DTPA is critical in using delayed enhancement to determine infarct size accurately with magnetic resonance imaging Circulation 2001;104:2838-2842.[Abstract/Free Full Text]
  20. Wagner A, Mahrholdt H, Thomson L, et al. Effects of time, dose, and inversion time for acute myocardial infarct size measurements based on magnetic resonance imaging-delayed contrast enhancement J Am Coll Cardiol 2006;47:2027-2033.[Abstract/Free Full Text]
  21. Saeed M, Bremerich J, Wendland MF, Wyttenbach R, Weinmann HJ, Higgins CB. Reperfused myocardial infarction as seen with use of necrosis-specific versus standard extracellular MR contrast media in rats Radiology 1999;213:247-257.[Abstract/Free Full Text]
  22. Lima JAC, Becker LC, Melin JA, et al. Impaired thickening of nonischemic myocardium during acute regional ischemia in the dog Circulation 1985;71:1048-1059.[Abstract/Free Full Text]
  23. Pierard LA, DeLandsheere CM, Berthe C, Rigo P, Kulbertus HE. Identification of viable myocardium by echocardiography during dobutamine infusion in patients with myocardial infarction after thrombolytic therapy: comparison with positron emission tomography J Am Coll Cardiol 1990;15:1021-1031.[Abstract]
  24. Smart S, Wynsen J, Sagar K. Dobutamine-atropine stress echocardiography for reversible dysfunction during the first week after acute myocardial infarction: limitations and determinants of accuracy J Am Coll Cardiol 1997;30:1669-1678.[Abstract]
  25. Bolognese L, Antoniucci D, Rovai D, et al. Myocardial contrast echocardiography versus dobutamine echocardiography for predicting functional recovery after acute myocardial infarction treated with primary coronary angioplasty J Am Coll Cardiol 1996;28:1677-1683.[Abstract]
  26. Gerber BL, Rochitte CE, Bluemke DA, et al. Relation between Gd-DTPA contrast enhancement and regional inotropic response in the periphery and center of myocardial infarction Circulation 2001;104:998-1004.[Abstract/Free Full Text]
  27. Garot J, Bluemke DA, Osman NF, et al. Transmural contractile reserve after reperfused myocardial infarction in dogs J Am Coll Cardiol 2000;36:2339-2346.[Abstract/Free Full Text]
  28. Nelson C, McCrohon J, Khafagi F, Rose S, Leano R, Marwick TH. Impact of scar thickness on the assessment of viability using dobutamine echocardiography and thallium single-photon emission computed tomography. A comparison with contrast-enhanced magnetic resonance imaging. J Am Coll Cardiol 2004;43:1248-1256.[Abstract/Free Full Text]
  29. Wu KC, Lima JAC. Nonivasive imaging of myocardial viability. Current techniques and future developments. Circ Res 2003;93:1146-1158.[Abstract/Free Full Text]
  30. Ingkanisorn WP, Rhoads KL, Aletras AH, Kellman P, Arai AE. Gadolinium delayed enhancement cardiovascular magnetic resonance correlates with clinical measures of myocardial infarction J Am Coll Cardiol 2004;43:2253-2259.[Abstract/Free Full Text]
  31. Rochitte CE, Lima JAC, Bluemke DA, et al. Magnitude and time course of microvascular obstruction and tissue injury after acute myocardial infarction Circulation 1998;98:1006-1014.[Abstract/Free Full Text]
  32. Previtali M, Poli A, Lanzarini L, Fetiveau R, Mussini A, Ferrarrio M. Dobutamine stress echocardiography for assessment of myocardial viability and ischemia in acute myocardial infarction treated with thrombolysis Am J Cardiol 1993;72:124G-130G.[CrossRef][Medline]
  33. Watada H, Ito H, Oh H, et al. Dobutamine stress echocardiography predicts reversible dysfunction and quantitates the extent of irreversibly damaged myocardium after reperfusion of anterior myocardial infarction J Am Coll Cardiol 1994;24:624-630.[Abstract]
  34. Choi KM, Kim RJ, Gubernikoff G, Vargas JD, Parker M, Judd RM. Transmural extent of acute myocardial infarction predicts long-term improvement in contractile function Circulation 2001;104:1101-1107.[Abstract/Free Full Text]
  35. Kaul S. There may be more to myocardial viability than meets the eye! Circulation 1995;92:2790-2793.[Free Full Text]
  36. Lombardo A, Loperfido F, Trani C, et al. Contractile reserve of dysfunctional myocardium after revascularisation: a dobutamine stress echocardiography study J Am Coll Cardiol 1997;30:633-640.[Abstract]
  37. Afridi I, Qureshi U, Kopelen HA, Winters WL, Zoghbi WA. Serial changes in response of hibernating myocardium to inotropic stimulation after revascularisation: a dobutamine echocardiographic study J Am Coll Cardiol 1997;30:1233-1240.[Abstract]
  38. Fieno DS, Kim RJ, Chen EL, Lomasney JW, Klocke FJ, Judd RM. Contrast-enhanced magnetic resonance imaging of myocardium at risk. Distinction between reversible and irreversible injury throughout infarct healing. J Am Coll Cardiol 2000;36:1985-1991.[Abstract/Free Full Text]
  39. Kim RJ, Fieno DS, Parrish TB, et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function Circulation 1999;100:1992-2002.[Abstract/Free Full Text]



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