Cardiac MR and viability

Case

Wednesday, April 27, 2011

80 yo F with PMH of HTN, HLD, DM, CVA with a history of continuous chest pain x 2 weeks. Patient was found to have a LBBB on unknown duration. Cardiac enzymes were negative. The patient was transferred to WHC for further management.













Dobutamine CMR• Contractile reserve can be assessed using low dose dobutamine stress test

• Allows for superior endocardial border definition facilitating more accurate wall motion and wall thickening

• Dobutamine CMR vs PET

• 35 patients with mild LV dysfunction

• Sensitivity of 88% and Specificity of 87% for detecting regions of viable myocardium

• Reduced predictive ability with more severe dysfunction is present at rest with specificity in the 80% range, but sensitivity limited to 50%

• If contractile function improves with dobutamine the there is likely viability

• Lack of improvement, however, does may not rule out viability as ischemia may develop at even low levels of dobutamine administration

Mahrholdt, et al. Heart 2007


Contrast Enhancement CMR

• Regions of myocardial infarct exhibit signal intensity (contrast enhancement) on T1-weighted images after administration gadolinium

• Gadolinium passively diffuses into the intracellular space due to rupture of myocyte membranes leading to increased contrast concentration in interstitial space between collagen fibers

• Contrast images are acquired mid-diastole

• The inversion time must be manually selected to null signal from normal myocardial regions

• This varies btw patients as a function of dose and and time after administration of contrast due to varying pharmacokinetics.



Contrast enhanced CMR using this technique has beenextensively validated in animal models of ischaemic injury anda variety of patient cohorts. Animal studies proved that ceCMRcan differentiate between viable and non-viable myocardiumregardless of wall motion abnormality at rest, the age of theinfarction, or the perfusion status with a near perfectcorrelation between enhancement on ceCMR and irreversibledamage at pathology (upper two rows in fig 2).5 Additionally,numerous patient studies have confirmed that ceCMR iseffective in identifying the presence, location and extent ofacute and chronic myocardial infarction.4 5

The comparison of ceCMR with other modalities for thediscrimination of viable and non-viable myocardium has beenfavourable. Ansari et al6 reported a strong correlation betweensegments defined as infarcted by ceCMR and defined as non-viable by thallium rest redistribution single photon emissioncomputed tomography (SPECT) (,50% of maximal thalliumuptake) in patients with prior myocardial infarction and leftventricular dysfunction, with an inverse relationship betweenthe area of contrast enhancement and diminished thalliumuptake. Klein et al7 found that the area of contrast enhancementmeasured by ceCMR correlated closely with myocardial infarctsdefined by PET in patients with ischaemic cardiomyopathy.Kuhl et al8 compared F-18 fluorodeoxyglucose (FDG) PET and

ceCMR in 26 patients. The study showed that segmentalglucose uptake by PET inversely correlated with the segmentalextent of contrast enhancement, and that using a cut off valueof 37% segmental enhancement optimally differentiated viablefrom non-viable segments defined by PET; using PET as thegold standard, this resulted in a sensitivity and specificity ofceCMR for detection of viable myocardium of 96% and 84%,respectively.

Because of its superior spatial resolution, CMR has theunique ability to assess small infarcts and to measure thetransmural extent of myocardial infarction. This advantage hasbeen used to detect micro-infarcts associated with successfulcoronary angioplasty, as well as the detection of subendocardialinfarcts which are missed by SPECT9 (fig 2) or do not exhibit awall motion abnormality.10

The ability to assess accurately the transmural extent ofinfarction has laid the foundation for subsequent investigationsin animals and humans demonstrating that the extent ofcontrast enhancement on a segmental or regional basis is usefulfor the prediction of improvement in contractile function afterrevascularisation in CAD patients.

Hillenbrand et al11 were the first to demonstrate in an animalmodel that the transmural extent of contrast enhancementpredicts myocardial salvage after acute myocardial infarction.

ce CMR

Histology

SPECT

Base ApexMidventricular

Figure 2 Contrast enhanced cardiovascular magnetic resonance (CeCMR), histology and single photon emission computed tomography (SPECT) imagesobtained in an animal with a medium sized infarct. There is a nearly perfect match between necrosis defined by histology and ceCMR. Whereas ceCMRallows the exact assessment of the transmural extent of infarction, SPECT defines segments as either viable or non-viable. Reproduced with permission fromWagner et al.9

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Use of contrast enhanced MRI to identifify reversible myocardial dysfunction

• Methods

• 50 patients prospectively enrolled

• Of these 41 patient had MRI before and after revascularization

• Inclusion criteria

• Scheduled to undergo revascularization

• Had regional wall motion abnormalities bu ventriculogram or echo

• Exclusion criteria

• Unstable angina

• NYHA Class IV heart failure

• Contraindication for MRI

• Results

• 80 percent of patient demonstrated hyperenhancement

• 50 percent with q waves on ekg showed hyperenhacement

• Before revascularization, 38 percent of pts had abnormal contractility and 33 percent had some areas of hyperenhancement

• Areas with dysfunctional, but non-hyperenhancing myocardium improved significantly after revascularization

CONTRAST-ENHANCED MAGNETIC RESONANCE IMAGING TO IDENTIFY REVERSIBLE MYOCARDIAL DYSFUNCTION

Volume 343 Number 20

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Figure 1.

Typical Cine Image and Contrast-Enhanced Image Obtained by MRI before Revascularization.Registration of the images was not required, because both types were acquired during the same MRI session. Twelve equal circum-ferential segments were analyzed in each short-axis view. For contrast-enhanced images, the transmural extent of hyperenhance-ment was determined for each segment with use of the following equation: percentage of area that was hyperenhanced=100¬areaA÷(area A+area B).

Cine Image Contrast-Enhanced Image

B

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Figure 2.

Typical Contrast-Enhanced Images Obtained by MRI in a Short-Axis View (Upper Panels) and a Long-Axis View (LowerPanels) in Three Patients.Hyperenhancement is present (arrows) in various coronary-perfusion territories — the left anterior descending coronary artery, theleft circumflex artery, and the right coronary artery — with a range of transmural involvement.

Left Anterior Descending!Coronary Artery Left Circumflex Artery Right Coronary Artery

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Copyright © 2000 Massachusetts Medical Society. All rights reserved.

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November 16, 2000

The New England Journal of Medicine

those determined by the third observer, and the con-cordance was 99 percent (defined as scores that werewithin 1 point of each other).

Relation between Viability and Improvement in Global Ventricular Function

For each patient, we estimated the percentage ofthe left ventricle that was dysfunctional but viable be-fore revascularization. We calculated this percentageby adding the number of segments that were dysfunc-tional but predominantly viable (defined as hyperen-hancement of no more than 25 percent of the tissuein each segment) and then dividing the total by thetotal number of segments in the left ventricle. An in-creasing extent of dysfunctional but viable myocar-dium before revascularization correlated with greaterimprovements in both the mean wall-motion score(P<0.001) and the ejection fraction after revascular-ization (P<0.001) (Fig. 5).

DISCUSSION

Contrast-enhanced MRI of the heart with gadolin-ium-based contrast agents has been performed since1984.

21

However, because this method produces onlymoderate differences in intensity between hyperen-hanced regions and regions without hyperenhance-ment, its use has primarily been limited to the studyof large, transmural acute infarcts.

12-14,16,22

Recent tech-nical refinements in contrast-enhanced MRI may im-prove the delineation of hyperenhanced regions 10-fold.

17

Using these new approaches, we found that theintensity of hyperenhanced regions was more than 500percent of that of regions without hyperenhancement,and the difference in image intensity between thesetwo regions was on average 14 SD.

An important advantage of contrast-enhanced MRIover other imaging methods that are used to assessmyocardial viability is that it shows the transmuralextent of viable myocardium. For example, the mid-

Figure 4.

Relation between the Transmural Extent of Hyperenhancement before Revascularization and the Likelihood ofIncreased Contractility after Revascularization.Data are shown for all 804 dysfunctional segments and separately for the 462 segments with at least severe hypokinesiaand the 160 segments with akinesia or dyskinesia before revascularization. For all three analyses, there was an inverserelation between the transmural extent of hyperenhancement and the likelihood of improvement in contractility.

0

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Copyright © 2000 Massachusetts Medical Society. All rights reserved.

Kim et al NEJM, 2000Wednesday, April 27, 2011

Viability post CABG• Methods

• 60 patients undergoing mutlivessel CABG were studies preoperatively, 6 days and 6 months post op

• Patients were also randomized to be off pump and on pump

• Exclusion: age > 75 yo, severe pre-existing LV dysfunction, CKD, typical MRI contraindications

• Results

• Preoporatively 21% of wall segments had abnormal regional function, whereas 14% showed evidence of hyperenhancement

• At 6 months, 57% of wall segments had improved contraction by at least one grade

• Strong correlation between the transmural extent of hyperenhancement and ther recovery of in regional function at 6 months

revascularization increased. Kim et al reported regionalfunction improvement at 3 months of 78% in segmentswithout HE, 59% in segments with 1% to 25% HE, butimprovement in only 2% in segments with !75% HE. Wefound that regional function improved in 82% of segmentswith no preexisting HE, 64% segments with 1% to 25% HE,and 37% of segments with 26% to 50% HE. The percentageof segments (with no, or "25% HE) with improved regionalfunction in our study is slightly higher than that observed byKim et al and is more likely to be closer to the true rate offunctional recovery, because our follow-up scan was at 6

rather than at 3 months after revascularization, as in thatstudy.We ascertained the predictive accuracy of preoperative

transmural HE for the recovery of late regional function in acohort “typical” (ie, with a mean age of 60 years with at leastmoderately preserved LV function and without major comor-bidity) of most patients referred for bypass surgery. If weused a cutoff value of "25% HE, we obtained a positivepredictive value of 73% and a negative predictive value of69% when all dysfunctional segments were considered.Studies that have evaluated the prediction of viability usingthallium scintigraphy and dobutamine echocardiography haveconsistently shown higher negative predictive values for theformer and higher positive predictive values for the latter.12,13Although no study has yet compared these 2 imaging tech-niques directly with DE-MRI, our findings place DE-MRI(when using "25% HE as a cutoff for viability) as havinghigher positive predictive value than thallium scintigraphy(but lower than dobutamine echocardiography) and highernegative predictive value than dobutamine echocardiography(but lower than thallium scintigraphy). When only segmentswith severe preoperative dysfunction (ie, severe hypokinesia,dyskinesia, or akinesia) were considered in our study, thepositive and negative predictive values were higher, at 81%and 72%, respectively. The ability of DE-MRI to evaluatethose segments that have severe dysfunction before surgery(and often the most difficult to evaluate with other imagingtechniques14) with high diagnostic accuracy is one of thestrengths of this technique. The addition of low-dose dobu-tamine stress MRI to the DE-MRI protocol may furtherincrease the diagnostic accuracy for viability detection, andfuture studies are awaited.Similar to the findings reported by Kim et al, we also

observed that there were a significant number of patients inour study who failed to demonstrate an improvement in lateregional function, despite having no or minimal HE in their

Figure 3. Three contrast-enhanced MRI scans in basal short-axis plane in same patient demonstrating extensive anterior andinferior HE before surgery (A), with no change either early (B) orlate (C) after surgery.

Figure 4. Relationship between transmural extent of HE beforesurgery and likelihood of increased regional function after sur-gery in all dysfunctional segments (left) and in all segments withsevere hypokinesia, akinesia, or dyskinesia.

Selvanayagam et al DE-MRI in Predicting Viability After CABG 1539

transmural extent of HE correlated closely with the likelihoodof improvement in regional function after surgery (Figure 4).When all segments that were dysfunctional preoperativelywere analyzed, the proportion with improved regional func-tion decreased as the transmural grade of HE increased(P!0.001). For example, regional function improved in 156of 190 segments (82%) with no preexisting HE but in only 16of 63 segments (25%) with 51% to 75% HE and 1 of 25segments (4%) with"76% HE. This relationship between thetransmural extent of HE and the improvement in regionalfunction was present irrespective of the degree of preopera-tive segmental dysfunction (Figure 4).

Relationship of New Perioperative HE to RegionalFunction at 6 MonthsTo investigate the impact of surgery-related irreversibleinjury on late regional myocardial function and viability, wesystematically analyzed segments with no or minimal HE(pre-CABG) in which the RWM worsened at 6 months. In the362 preoperatively dysfunctional segments with no HE oronly 1% to 25% HE, a total of 96 myocardial segments (27%)did not improve regional function at 6 months (Figure 4). Ofthese 96 segments, 35 (36%) demonstrated new perioperativeHE in the early postoperative MRI scan, indicating that theoccurrence of perioperative myocardial necrosis accounts fora portion of segments failing to improve late regional func-tion. Conversely, 61 segments (64%) failed to recover furtherdespite not showing any surgery-related HE. Furthermore, of2050 revascularized segments with normal contraction and noHE preoperatively, another 121 segments (6%) demonstratednew HE (in early postoperative MRI) and new RWM abnor-malities at 6 months. Of these segments, 86 (71%) demon-strated mild/moderate hypokinesis, 30 (25%) demonstratedsevere hypokinesis, and 5 (4%) demonstrated akinesis.

Interobserver/Intraobserver Variability for RWMScoring and HE GradeThe first 30 scans (1680 segments) were analyzed again bythe first observer after a 6-month period. The ! value for thiswas 0.7 (SE, 0.02; P!0.0001), indicating that the degree ofintraobserver agreement was good. The same segments were

also analyzed by a second blinded investigator with moderateto good agreement (!, 0.6; SE, 0.03; P!0.0001). For trans-mural grading of the 5 categories of HE in the same 30 scans,the ! value for assessment by a second investigator was 0.8(SE, 0.01; P!0.0001), and there was a positive correlation(Spearman r#0.8; P!0.001) between the scores determinedby the first and second observers.

Effects of OPCABG Versus ONCABG Surgery onGlobal LV Function at 6 MonthsAs previously reported,9 the mean preoperative cardiac indexwas similar in the 2 surgical groups (2.9$0.7, ONCABG;2.9$0.8, OPCABG; P#0.9), whereas the early postoperativeCI was significantly higher in the OPCABG group (2.7$0.6,ONCABG; 3.2$0.8, OPCABG; P#0.04).9 As shown in theTable, the cardiac index at 6 months was 3.3$0.5 mL · min%1

· m%2 in the OPCABG group and 3.3$0.6 mL · min%1 · m%2

in the ONCABG group (P"0.05). There was significantimprovement in the cardiac index in both surgical groups at 6months postoperatively compared with preoperative values(P#0.04). This improvement in cardiac function occurred asa result of a significant reduction in the end-systolic volumeindex at 6 months in both surgical groups (P#0.02 for bothgroups). There was no change in the end-diastolic volumeindex at 6 months, although there was a downward trend(toward smaller volumes) in both surgical groups.

DiscussionPrediction of Myocardial Viability by DE-MRIIn a cohort of patients undergoing exclusive surgical revas-cularization, our results confirm the primary hypothesis thatthe transmural grade of HE was significantly related to thelikelihood of improvement in regional function 6 monthsafter surgery, irrespective of the preoperative regional func-tion. In this respect, our results confirm the only previousstudy on this subject, by Kim et al.7 They found that when alldysfunctional segments were considered in a cohort of 41patients undergoing revascularization by either percutaneoustransluminal coronary angioplasty or CABG, the likelihoodof improvement in regional function after revascularizationdecreased progressively as the transmural extent of HE before

Figure 2. Change in HE mass over time.A, Mean ($SD) mass of hyperenhancedmyocardium at preoperative, early post-operative, and late postoperative scansin those patients with no (new) postoper-ative HE. Statistical comparison is madewith preoperative value. NS indicatesP"0.05. B, Change in mean ($SD) massof new hyperenhanced myocardiumbetween early postoperative and latepostoperative scans. *P!0.001.

1538 Circulation September 21, 2004

Selvanayagam et al Circulation, 2004Wednesday, April 27, 2011

Predicting Late Myocardial Recovery and Outcomes in Early hours of STEMI

• Methods

• 104 prospectively enrolled patients with successfully reperfused STEMI

• Exclusion criteria were recent MI (<6months), shock requiring IABP, respiratory failure, contraindications for MRI

• Subjects were followed prospectively at 33 months and MRI was repeated at 6 months

• Primary endpts were change in LVEF and LV dysfunction at 6 months.

• Secondary endpt was MACE

• Results

• LGE was the best predictor of late LV dysfunction

• LGE > 23% of volume accurately predicted late dysfunction (sensitivity 89%, specificity 74%)

• LGE > 23 % carried a hazard ration of 6.1 percent for adverse events (p<0.0001)

LGE percentage in the hyperacute phase of STEMI main-tained a significant association with 6-month LV dysfunc-tion, independent of LVEF during STEMI and CK-MBrise.

The occurrence of LV dysfunction at 6 months invariablyincreased with greater LGE. The ROC analysis determinedthat a cutoff of !23% LGE measured at the time ofSTEMI predicted 6-month LV dysfunction with a sensi-tivity of 89%, specificity of 74%, positive likelihood ratio of3.6, and negative likelihood ratio of 0.1. This cutoff wasselected to screen for patients at risk for developing LVdysfunction late after STEMI, correctly classifying 80% ofthe population. The 23% LGE cutoff seemed useful indichotomizing 2 groups with widely diverging recoveries in

LVEF from baseline to 6 months, across the entire range ofLVEF quartiles during STEMI (Fig. 2).

We verified whether LGE percentage during STEMIimproved the prediction of late LV dysfunction beyondcurrent risk factors. The ROC analysis indicated that LGEpercentage measured during STEMI significantly improvedthe diagnostic accuracy for 6-month LV dysfunction (AUC:0.92; 95% CI: 0.84 to 0.98) beyond pain-to-balloon time(AUC: 0.71; 95% CI: 0.60 to 0.82, p ! 0.001 comparedwith LGE percentage), CK-MB rise (AUC: 0.79; 95% CI:0.69 to 0.89, p ! 0.01), and LVEF during STEMI (AUC:0.84; 95% CI: 0.76 to 0.93, p ! 0.03) (Fig. 3). Thediagnostic accuracy of LGE percentage for predicting lateLV dysfunction did not differ, whether the infarct territory

Unadjusted Analysis of ORs From VariablesMeasured During STEMI for 6-Month LVEF <50%Table 3 Unadjusted Analysis of ORs From VariablesMeasured During STEMI for 6-Month LVEF <50%

OR 95% CI p Value

Age, yrs 1.00 0.96–1.04 1.00

Male 2.40 0.43–10.1 0.30

Hypertension 1.02 0.38–2.83 0.90

Dyslipidemia 0.44 0.17–1.11 0.10

Active/recent smoking 0.71 0.29–1.74 0.80

Diabetes 1.13 0.21–6.23 0.90

LDL-cholesterol on STEMI presentation, mmol/l 1.80 0.93–3.48 0.08

Blood glucose on STEMI presentation, mmol/l 1.04 0.89–1.21 0.70

ECG Q waves on STEMI presentation 6.80 2.16–21.5 0.001

ECG total ST-segment elevation on STEMI presentation, mm 1.06 0.97–1.16 0.20

LAD infarct territory 1.92 0.77–4.76 0.20

Pain-to-balloon time, min 1.10 1.03–1.17 0.005

Target vessel residual diameter stenosis* 1.01 0.99–1.03 0.40

Maximum CK-MB rise during STEMI, mmol/l 1.47 1.24–1.75 "0.00001

LVEDVi during STEMI, ml/m2 1.10 1.05–1.15 "0.00001

LVESVi during STEMI, ml/m2 1.16 1.08–1.23 "0.00001

LVEF during STEMI* 0.87 0.82–0.93 "0.00001

LV massi, g/m2 1.11 1.05–1.18 "0.00001

LGE volume during STEMI, % LV 17.00 8.47–34.1 "0.00001

Transmural LGE segments during STEMI* 1.93 1.42–2.62 "0.00001

Microvascular obstruction during STEMI* 11.00 3.68–32.9 "0.00001

Salvaged myocardium during STEMI* 0.95 0.87–0.99 0.02

n ! 101. p value for univariable logistic regression. *Values given as percentages.BSA ! body surface area; CI ! confidence interval; LDL ! low-density lipoprotein; OR ! odds ratio; other abbreviations as in Tables 1 and 2.

Multivariable Associations of VariablesMeasured During Acute STEMI With 6-Month LVEF <50%Table 4 Multivariable Associations of VariablesMeasured During Acute STEMI With 6-Month LVEF <50%

OR 95% CI p Value

Best overall multivariable model by stepwise forward selectionincluding all significant variables from Table 3

Presence of ECG Q waves at presentation 6.27 0.81–74.9 0.08

LGE during STEMI* 1.33 1.09–1.78 0.002

Pain-to-balloon time, min 1.15 1.01–1.32 0.09

Adjusted for LVEF during STEMI, LGE %, and CK-MB

LVEF during STEMI* 0.95 0.88–1.03 0.20

LGE during STEMI* 1.36 1.11–1.66 0.004

Maximum CK-MB rise after STEMI, mmol/l 1.00 0.99–1.01 0.40

*Values given as percentages.Abbreviations as in Tables 1 and 3.

2464 Larose et al. JACC Vol. 55, No. 22, 2010Predicting Late Recovery During Hyperacute STEMI June 1, 2010:2459–69

Figure 2 Relative Change in LVEF From STEMI to 6-Month Follow-Up, Assessed According to Quartiles of LVEF During STEMI

The LGE !23% during STEMI identifies a subgroup of patients with significantly worse functional recoverycompared with those with less LGE, across the entire range of LVEF quartiles during STEMI. Abbreviations as in Figure 1.

Figure 3 Receiver-Operator Characteristic Curves for LV Dysfunction at 6 Months

There is significant added value of LGE percentage during STEMI (per 1%, area under the receiver-operator characteristic curve [AUC]: 0.92) compared with traditionalmeasures including LVEF during STEMI (per 1%, AUC 0.84, p ! 0.03 vs. LGE), maximum creatine kinase-myocardial band (CKMB) (per 1 mmol/kg, AUC 0.79, p ! 0.01vs. LGE), and pain-to-balloon time (per 1 min, AUC 0.71, p ! 0.001 vs. LGE) for the prediction of LV dysfunction at 6 months. Abbreviations as in Figure 1.

2465JACC Vol. 55, No. 22, 2010 Larose et al.June 1, 2010:2459–69 Predicting Late Recovery During Hyperacute STEMI

was LAD or not (AUC: 0.95 for LAD infarct vs. 0.89 fornon-LAD infarct, p ! 0.3) and whether Q waves werepresent or not at STEMI presentation (AUC 0.93 forQ waves present vs. 0.88 for Q waves absent, p ! 0.3).

We additionally explored clinical outcomes: over 2.3 "0.4 year follow-up, MACE occurred in 23 (22%) subjects (1death, 2 MIs, 5 malignant arrhythmias requiring AICD, 4severe LV dysfunction #35%, 11 hospital stays for heartfailure). The previously defined cutoff of LGE !23%measured during hyperacute STEMI incurred a significantrisk of adverse events by univariable Cox proportionalhazards regression (hazard ratio: 10.1; 95% CI: 3.7 to 27.3,p # 0.0001) (Fig. 4). In addition, LGE percentage re-mained independently associated with MACE in multiva-riable Cox regression that included CK-MB rise and LVEFduring STEMI (hazard ratio: 1.72; 95% CI: 1.43 to 2.01,p ! 0.007).

Discussion

The major finding of this study is that LGE quantificationvery early during STEMI predicts late heart failure andadverse events beyond traditional risk factors such as infarctterritory, maximum CK-MB rise, pain-to-balloon time,presence of Q waves, and LVEF during STEMI. A secondmajor finding is that, during the hyperacute phase ofSTEMI, LGE volume incurred the strongest association toLV function change, beyond infarct transmurality, MVO,and SM. Significant variability in preload and afterloadconditions and difficulty in discriminating stunned fromnonviable myocardium at the time of STEMI have renderedmost early variables imperfect predictors of late systolicfunction and adverse events. However, strategies for theearliest possible risk assessment after STEMI have becomeessential not only to better target therapies but also tointroduce these therapies in the timeliest manner while

benefits might be greatest. We have demonstrated that,during STEMI, LGE percentage is the strongest predictorof late heart failure and adverse events, opening the door toimproved strategies for very early risk stratification.LVEF measurement after STEMI. Considerable efforthas gone toward earlier risk stratification and faster imple-mentation of prognosis-altering interventions in high-riskSTEMI (5,26). Treatment strategies based on residualLVEF after STEMI have shown important survival benefits(2–4,27). However, LVEF measured very early after MI isan imperfect predictor of later LVEF recovery: normalglobal EF at the time of STEMI might beget low EF inlater months—as observed in this study and others—likelyas a result of the gradual disappearance of the compensatoryincreased contractility of healthy segments and remodeling(6,26). In addition, low EF at the time of STEMI mightbeget normal EF after infarct healing, as systolic dysfunc-tion observed early after STEMI might be due to acombination of reversible myocardial stunning and irrevers-ible necrosis (28,29). The failure of recent treatment strat-egies such as AICD implantation based on assessment ofLVEF very early after STEMI, contrary to the successobserved when LVEF was measured $40 days after MI,might be due to the observed variability in LV remodelingduring early infarct healing (3,30).Predictors of residual systolic function after infarct healingand remodeling. Systolic function after STEMI varies asa function of the infarct territory (31), the sum of ST-segment elevation on ECG (32,33), microvascular dysfunc-tion (34,35), time to reperfusion (36), and time to peak CK(37). Although LVEF at the time of STEMI has beencorrelated to late systolic function in early studies (34), thishas since been called into question by more accurateradionuclide (38) and volumetric techniques (9). In fact, LVremodeling is a particularly heterogeneous process, difficult

Figure 4 Kaplan-Meier Event-Free Survival Estimates for LGE >23% Versus LGE <23% Very Early During STEMI

Number at risk reports the number of patients that entered the respective interval event-free, minus one-half of the numberof patients who presented an event in the respective interval. LGE ! late gadolinium enhancement; other abbreviations as in Figure 1.

2466 Larose et al. JACC Vol. 55, No. 22, 2010Predicting Late Recovery During Hyperacute STEMI June 1, 2010:2459–69

Larose et al JACC, 2010Wednesday, April 27, 2011

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Cardiac MR and viability

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