Patients

In a prospective, single-center study, 54 consecutive patients with acute myocardial infarctions with clearly present wall motion abnormalities on preliminary echocardiography who were sufficiently stable were examined. The diagnosis of myocardial infarction was made by clinical presentation, electrocardiographic findings, and troponin and creatine kinase elevations. All patients underwent successful acute primary percutaneous intervention with recanalization of the infarct-related coronary artery. Echocardiography was performed during the first 72 hours and MRI on days 3 to 5 after infarction. All patients were in stable sinus rhythm. All patients gave informed consent for the study. Thirteen patients were excluded from further analysis: in six patients, echocardiographic image quality was too poor for further analysis, four patients had contraindications to MRI (severe renal insufficiency, pacemaker), and MRI was terminated in three patients because of claustrophobia. Of the remaining 41 patients, 34 had ST-segment elevation infarctions, and seven had non–ST-segment elevation infarctions. Further characteristics of the patients are given in Table 1 .

Follow-up to ascertain survival was obtained by telephone calls to practitioners caring for the patients or to the patients themselves.

Echocardiography

Transthoracic echocardiography was performed using a Vivid 7 system (GE Healthcare, Solingen, Germany) with patients in the left lateral decubitus position. A 4-MHz center frequency transducer (M4S) was used. The frame rate was between 70 and 100 frames/sec. Electrocardiographically triggered digital loops, each with three consecutive cardiac cycles and acquired during an end-expiratory breath-hold, were stored at the original frame rate in proprietary image storage and analysis software (EchoPAC; GE Healthcare). The three standard apical views and three short-axis views of the left ventricle (basal, midpapillary, and apical) were recorded in 2D and tissue color Doppler modes, the latter with frame rates > 120 frames/sec. Using the EchoPAC Dimension 06 software, the data were processed and analyzed offline. On the basis of an 18-segment model of the left ventricle (six basal, six middle, and six apical segments), we first assessed segmental left ventricular function visually by determining a WMS for each segment (1 = normokinetic, 2 = hypokinetic, 3 = akinetic, and 4 = dyskinetic).

Strain Imaging by Speckle-Tracking

Each of the 18 segments was analyzed for regional deformation (“2D strain”) using speckle-tracking analysis: longitudinal strain (LS) was measured in the three apical views. Radial strain (RS) and circumferential strain (CS) were measured in a basal, midpapillary, and apical parasternal view. The software automatically marked myocardial segments that were not evaluable, and the curves were checked by an experienced examiner for plausibility. All segments that were not evaluable were excluded from further analysis. Peak systolic strain was measured separately from each curve by the investigator, who was blinded to the MRI results.

Preejection Velocity

Preejection velocity (PEV) is a short-lived positive myocardial tissue velocity during the isovolumetric contraction phase before ejection. Aortic valve opening determined by continuous-wave Doppler was used to define the beginning of the ejection, and PEV was defined as any positive longitudinal tissue velocity above the noise level during the time interval from the beginning of the QRS complex on the electrocardiogram to the time point of aortic valve opening. Each of the 18 segments in the apical tissue Doppler cine-loops was investigated with regard to the presence of PEV.

MRI

MRI was performed using a 1.5-T Avanto system (Siemens Healthcare, Erlangen, Germany) as a reference standard for scar transmurality. For detection of late enhancement, a gadolinium contrast agent was used. MRI analysis was performed by a second, blinded investigator who used the same 18-segment model of the left ventricle as used in the echocardiographic analysis, with corresponding short-axis cross-sections. Segments were divided into three groups according to the fraction of wall thickness occupied on average in each segment by late enhancement: none (0%), nontransmural (1%–50%), or transmural (51%–100%).

Statistical Analysis

Peak systolic strain values were correlated with the transmural extent of myocardial scar by late enhancement on MRI, stratified into the described three subgroups. The presence of PEV was rated as none or nontransmural infarction, and the absence of PEV was rated as transmural scar. Concerning wall motion, a normokinetic wall was rated as a segment without infarction, a hypokinetic wall as nontransmural infarction, and an akinetic or a dyskinetic wall as transmural infarction. All data are expressed as means ± SD. The statistical analysis was performed using SPSS Statistics version 19 (IBM, Armonk, NY) and Excel 2010 (Microsoft Corporation, Redmond, WA). P values < .05 were considered significant. Bonferroni’s correction was used to correct for multiple comparisons. Receiver operating characteristic curves were constructed and areas under the curves compared to analyze how well strain data classified segments as transmurally or nontransmurally scarred on MRI, and optimal cutoffs were determined. To determine whether the results of the strain analyses differed by left ventricular wall, we calculated receiver operating characteristic curves for each wall (septal, anteroseptal, anterior, lateral, posterior, and inferior) and each level (basal, middle, and apical) separately. All comparisons were performed by segments, not patients. Furthermore, we calculated the category-free net reclassification improvement for the addition of CS to WMS to predict infarct transmurality.

Echocardiography

By 2D echocardiography, WMS could be determined in all 738 segments. Four hundred ten segments were normokinetic, 190 segments were hypokinetic, 116 segments were akinetic, and 22 segments were dyskinetic. Measurement of LS was possible in 699 segments, of RS in 613 segments, and of CS in 659 segments. PEV was assessable in 734 segments; it was present in 538 segments and absent in 196 segments.

MRI

By MRI, all 738 segments were evaluable for late enhancement: 400 had no late enhancement (normal), 125 showed delayed enhancement of 1% to 50% transmurality, and 213 segments showed 51% to 100% transmurality.

Comparison of Echocardiography and MRI

A representative example of corresponding echocardiographic and MRI data is presented in Figure 1 . The relation of visual wall motion analysis to the three categories of scar transmurality by MRI is shown in Figure 2 . The relations of longitudinal, radial, and circumferential peak systolic strain values to the three categories of scar transmurality by MRI are shown in Figure 3 . The relation of PEV to MRI-based scar transmurality is shown in Figure 4 .

(A) Representative example of >50% transmurally infarcted anteroseptal segment (scar; white arrow ) and noninfarcted (no scar) posterior segment in ( left ) an MRI short-axis view at the midpapillary level and ( right ) the corresponding echocardiographic view, with an overlay of the speckle-tracking software. The arrows point to the positions of the sample volumes (white arrow to yellow dot in infarcted area and hatched arrow to violet dot in noninfarcted area) from which radial and CS curves were derived. (B) Corresponding radial ( left ) and circumferential ( right ) strain curves from the infarcted ( yellow , white arrow ) and noninfarcted ( violet , hatched arrow ) areas. Strains from infarcted areas are lower. Note that RS is positive in systole and CS is negative. The dotted green vertical line denotes aortic valve opening (AVO). (C) Tissue Doppler (from color-coded tissue Doppler loops) from same patient showing absent PEV in the infarcted segment and preserved PEV in the noninfarcted segment.

Relation of visual wall motion analysis to the three categories of scar transmurality by MRI. Bars indicate the number of segments graded normokinetic, hypokinetic, akinetic, and dyskinetic in each category of scar transmurality. Box plots: box indicates median and 25th and 75th percentiles, whiskers enclose the 97.5th percentile of values, and outliers are marked with circles .

Relation of longitudinal, radial, and circumferential peak systolic strain values to the three categories of scar transmurality by MRI.

Presence or absence of positive PEV to the three categories of scar transmurality by MRI.

The ability of the different echocardiographic parameters to discriminate among 0% (no scar at all) versus 1% to 100% MRI transmurality (any scar), 1% to 50% (nontransmural scar) versus 51% to 100% MRI transmurality (transmural scar), and 0% (no scar at all) versus 51% to 100% MRI transmurality (transmural scar) was analyzed using receiver operating characteristic curves and characterized by their areas under the curves and best cutoffs of the respective parameters for discrimination.

Table 2 shows the discriminatory ability of the three types of myocardial strain for separating nontransmural from transmural scar, separated for left ventricular walls as well as ( Table 3 ) for the apical, middle, and basal segmental levels. Note that we use the inequality operators with regard to the absolute strain values, regardless of sign.

Table 4 shows the discriminatory ability of each echocardiographic parameter to separate no scar at all from any scar (1%–100% transmurality). Table 5 shows the discriminatory ability of each echocardiographic parameter to separate nontransmural scar (1%–50% transmurality) from transmural scar (51%–100% transmurality), and Table 6 displays the discriminatory ability of each echocardiographic parameter to separate no scar from transmural (51%–100% transmurality) scar. For all of these predictions, CS showed the highest area under the curve, although differences from other parameters were not always significant (see Tables 4–6 ).

Table 4

Results of receiver operating characteristic curves: AUCs and best cutoffs for the different echocardiographic parameters to differentiate noninfarcted (0% transmurality) and infarcted (1%–100% transmurality) myocardial segments

Variable	AUC	Cutoff	Sensitivity (%) (95% CI)	Specificity (%) (95% CI)
LS	0.81 ± 0.02	−13.5%	71 (66–76)	75 (71–79)
RS	0.77 ± 0.02	27.5%	71 (66–77)	66 (61–71)
CS	0.86 ± 0.01	−14.5%	81 (78–84)	81 (78–84)
WMS	0.82 ± 0.02	>1	77 (72–81)	81 (77–85)
PEV (−)	0.67 ± 0.02	Presence	45 (40–50)	90 (87–93)

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