FOCUS ISSUE: CARDIAC IMAGING: CLINICAL RESEARCH
Differentiation of Subendocardial and Transmural Infarction Using Two-Dimensional Strain Rate Imaging to Assess Short-Axis and Long-Axis Myocardial Function
Jonathan Chan, MB, BS, MRCP (UK),
Lizelle Hanekom, MB, BS,
Chiew Wong, MB, BS, FRACP,
Rodel Leano, BSc,
Goo-Yeong Cho, MD, PhD and
Thomas H. Marwick, MB, BS, PhD, FACC*
University of Queensland, Brisbane, Australia
Manuscript received January 18, 2006;
revised manuscript received July 14, 2006,
accepted July 17, 2006.
* Reprint requests and correspondence: Dr. Thomas Marwick, University of Queensland, Department of Medicine, Princess Alexandra Hospital, Ipswich Road, Brisbane, Qld 4102, Australia. (Email: tmarwick{at}soms.uq.edu.au).
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Abstract
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OBJECTIVES: This study sought to differentiate the transmural extent of infarction (TME) by assessment of the short-axis and long-axis function of the left ventricle (LV) using 2-dimensional (2D) strain.
BACKGROUND: The differentiation of subendocardial infarction from transmural infarction has significant prognostic and clinical implications.
METHODS: Contrast-enhanced magnetic resonance imaging (CE-MRI) and dobutamine stress echocardiography (DBE) were performed in 80 patients (age 63 ± 10 years) with chronic ischemic LV dysfunction. Myocardial function was assessed in the short axis at the midventricular level using peak strain rate (SR) and strain (S) in circumferential and radial dimensions, and was assessed in the long axis using longitudinal SR and S. Wall motion analysis was performed during DBE to assess for contractile reserve.
RESULTS: Transmural infarct segments had lower circumferential S (–10.7 ± 6.3) and SR (–1.0 ± 0.4) than subendocardial infarcts (S: –15.4 ± 7.0, p < 0.0001; SR: –1.4 ± 0.8, p = 0.02) and normal myocardium (S: p < 0.0001; SR: p < 0.0001). Transmural and subendocardial infarct segments had similar radial S and SR. Subendocardial infarct segments showed significant reduction of longitudinal S (–13.2 ± 5.6) and SR (–0.91 ± 0.45) compared with normal myocardium (S: –17.8 ± 5.4, p < 0.0001; SR: –1.1 ± 0.41, p < 0.0001), but there were no significant differences between subendocardial and transmural infarct segments (p = 0.09). Wall motion analysis by DBE could not identify subendocardial infarction on CE-MRI (TME 1% to 50%: DBE scar 38%, DBE viable 38%, DBE ischemic 24%, p = NS).
CONCLUSIONS: The combined assessment of long-axis and short-axis function using 2D strain may be used to identify TME.
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Abbreviations and Acronyms
| | 2D = 2-dimensional | | AUC = area under the curve | | CE-MRI = contrast-enhanced magnetic resonance imaging | | DBE = dobutamine stress echocardiography | | LV = left ventricle/ventricular | | ROC = receiver-operating characteristic | | S = peak systolic 2-dimensional strain | | SR = peak systolic 2-dimensional strain rate | | TME = transmural extent of infarction |
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The identification of the transmural extent of myocardial infarction (TME) is clinically important because it has both management and prognostic implications. Transmural infarcts are associated with a poorer prognosis and more adverse cardiac events (1). Kim et al. (2) have shown that subendocardial or nontransmural infarcts (TME <50%) are associated with functional recovery after revascularization.
Magnetic resonance imaging can be considered the gold standard for identification of TME because of its high spatial resolution and ability to directly visualize the extent of scar as delayed contrast enhancement (3–5). Dobutamine stress echocardiography (DBE) has been used to assess for contractile reserve as an index of viability, but subendocardial infarction may be a source of ambiguity because this may augment function in response to dobutamine without improving resting function after revascularization. Previous studies using tissue Doppler and strain rate imaging have shown that there is a transmural gradient of function across the short axis of infarcted tissue (6,7). Similarly, transmural gradients have been documented in longitudinal views of infarcted myocardium using strain rate imaging (8).
The complex anatomical orientation of myocardial fibers, through their contribution to myocardial short-axis and long-axis function (9–11), may give a clue to the transmural extent of infarction. Although tissue Doppler imaging is limited by tethering (12) and Doppler-based strain-rate imaging is limited by angle dependency (13), the newer technique of 2-dimensional (2D) strain seems to reliably measure radial, longitudinal, and circumferential motion, and for the first time offers an echocardiographic technique for quantifying contraction in each of these dimensions. We investigated whether differences in fiber orientation and therefore direction of motion could be used to identify TME.
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Methods
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Study population.
We studied 80 unselected patients (ages 63 ± 10 years, 81% men) with chronic ischemic heart disease and a documented previous myocardial infarction. Patients with structural heart disease, significant valvular abnormalities, previous revascularizations, and any contraindications to magnetic resonance imaging (MRI) were excluded. All patients underwent transthoracic echocardiography and contrast-enhanced magnetic resonance imaging (CE-MRI) within a median interval of 10 days. Interobserver variation was assessed by random selection of 20 patients and measurement of peak longitudinal, circumferential, and radial strains by two independent observers using identical images from the same loop of the cardiac cycle. The same 10 patients were used for intraobserver variability, in which a single blinded observer repeated the measurements after an interval of 10 days. We obtained informed consent from all patients.
Echocardiography and 2D strain.
Echocardiographic images were obtained with a 3.5-MHz transducer in the left lateral decubitus position using a commercially available system (Vivid 7, GE Vingmed, Horten, Norway). Two-dimensional grayscale images were acquired in the apical 4-chamber, apical 2-chamber, apical long-axis, and midventricular short-axis views using a narrow sector angle (30° to 60°) and frame rates from 50 to 70 frames/s. Digital storage of cardiac cycles triggered to the QRS complex were saved on a magneto-optical disk for off-line analysis (EchoPac 6.1, GE Medical Systems, Horten, Norway). The left ventricle was analyzed using a 16-segment model (14). The endocardial borders were traced at the end-systolic frame from the 3 apical views and midventricular short-axis views, and an automated tracking algorithm outlined the myocardium in successive frames throughout the cardiac cycle. After the tracking quality was verified for each segment (with subsequent manual adjustment of the region of interest if necessary), myocardial motion was analyzed by speckle-tracking within the region of interest bound by endocardial and epicardial borders. Myocardial longitudinal, circumferential, and radial strain and strain-rate profiles were obtained and both peak systolic strain and strain-rate values were measured at rest and during low-dose dobutamine (Fig. 1).
DBE.
A standard dobutamine stress protocol was adopted, starting at an infusion rate of 5 µg/kg/min and increasing at 3-min intervals up to 40 µg/kg/min (15). Intermittent hand-grip and/or atropine (up to 2 mg intravenously) was used if a maximum heart rate of 85% beats/min was not attained with dobutamine alone. Harmonic echocardiographic images were performed in 5 views and saved in digital format at baseline, low dose (5 and 10 µg/kg/min), and peak (40 µg/kg/min). Images were interpreted off-line by the consensus of 2 observers using the same 16-segment model. Segments were considered viable if they were dysfunctional at rest and had augmented contractile function at low dose (up to 10 µg/kg/min). Segments were considered to be infarcted if they were dysfunctional at rest and showed no contractile reserve at low or peak doses. Measurements of 2D strain and strain-rate values were repeated on images acquired during low-dose dobutamine infusion.
MRI.
Delayed contrast-enhanced MRI was performed using a 1.5-T scanner (Siemens Sonata, Siemens, Erlangen, Germany) to acquire 8 to 11 short-axis images during breath hold after intravenous administration of 0.1 mmol/kg gadoversetamide (Optimark, Mallinkrodt, St. Louis, Missouri). Delayed contrast-enhanced images were obtained after 15 min using an inversion recovery TurboFLASH sequence. Voxel size was adjusted to 2.1 x 1.3 x 6 mm for all views. A 16-myocardial-segment model was used, and care was taken to ensure correct alignment of the apex, mitral annulus, aortic valve, and septum, to achieve the same segmentation as with echocardiography (14). Quantification of TME after contrast was performed using an offline analysis program (Efilm, Merge, Milwaukee, Wisconsin). The combination of wall motion and TME was grouped into four categories (control = TME 0% and normal wall motion; dysfunctional = TME 0% and abnormal wall motion; subendocardial = TME 1% to 50%; transmural >50%). This cutoff value of >50% was previously shown to a have a negative predictive value for viability of up to 92% (2). Wall motion analysis and TME were independently assessed by a reader who was blinded to patient data and other echocardiographic measurements.
Statistical analysis.
All data are expressed as mean values ± SD. Differences in circumferential peak systolic 2D strain (S) and peak systolic 2D strain rate (SR), radial S and SR, and longitudinal S and SR among different groups of TME were analyzed by analysis of variance with Bonferroni post-hoc analysis using statistical software (SPSS version 11.0, SPSS Inc., Chicago, Illinois). Receiver-operating characteristic (ROC) curves were used to evaluate the ability to distinguish transmural from nontransmural infarction in segments with wall motion abnormalities and to determine optimal cutoff values for sensitivity and specificity. Intraobserver and interobserver reliabilities were reported using the Pearson correlation. A p value of <0.05 was considered statistically significant.
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Results
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Patient characteristics.
The baseline clinical and cardiac characteristics of the 80 patients (mean age 63 ± 10, 81% men) with chronic ischemic heart disease and history of myocardial infarction are listed in Table 1. In general, this was a group of patients with dilated ischemic cardiomyopathy with mild to moderate systolic dysfunction (ejection fraction 41 ± 9%) and no previous revascularizations. The median time interval from index myocardial infarction to initial cardiac imaging was 89 days. Fifty-five patients had clinical indications to undergo coronary angiography, of whom 16 had single-vessel disease (stenosis >70%), 10 had 2-vessel disease, and 29 had 3-vessel disease.
Feasibility of CE-MRI and echocardiographic parameters.
In a total of 1,280 segments from 80 patients, CE-MRI could be analyzed in all. Normal wall motion was identified in 650 segments, 205 were dysfunctional with no scar on MRI, 212 segments had subendocardial infarcts with TME 1% to 50%, and 213 had transmural infarcts (TME >50%). Long-axis function could be assessed with 2D strain rate imaging in 1,097 segments (86%). In the evaluation of short-axis left ventricular (LV) function, only midventricular short-axis views were acquired by echocardiography, and 412 of a total of 480 segments (86%) were analyzable by 2D strain. The main causes for exclusion were suboptimal image quality with speckle tracking.
Resting function.
The nature of circumferential, radial, and longitudinal function, according to the presence of scar and categories of transmurality, is summarized in Tables 2 and 3, and according to TME in Figures 2 to 4.
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Table 2. Short-Axis Left Ventricular Function With Circumferential S and SR and Radial S and SR in Control, Dysfunctional, and Subendocardial Infarct and Transmural Infarct Segments
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Table 3. Long-Axis Function With Longitudinal S and SR in Control, Dysfunctional, Subendocardial Infarct, and Transmural Infarct Segments
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Rotational function
Circumferential strain parameters (S and SR) were relatively preserved in subendocardial infarcts compared with dysfunctional segments without scar and compared with normal control segments. Transmural infarct segments had significant reduction in circumferential S and SR compared with subendocardial infarct segments (Table 2). The relationship between circumferential SR with different grades of TME showed the mean circumferential S and SR to be particularly reduced with TME >75% (Fig. 2).
To establish and validate a cutoff of circumferential S and SR, we divided the patients into a definition group (n = 50) and a validation group (n = 30). The ability to distinguish transmural from nontransmural infarction in segments with wall motion abnormalities was evaluated by developing an ROC curve; the area under the curve (AUC) for circumferential strain was 0.71 (95% confidence interval 0.62 to 0.80), with an optimal cutoff of –13.1%. When this cutoff was applied to the validation group of 30 patients, in transmural infarct segments with TME >50% (n = 22), 77% of segments were correctly identified, and when applied to nontransmural infarcts (TME 0% to 50%, n = 58), 60% of segments were correctly identified.
Radial function
Radial strain is relatively preserved in subendocardial infarction, with no statistically significant differences compared with controls, but transmural infarcts had reduced radial strain compared with control segments, especially when TME >75% (p = 0.005) (Fig. 3). However, there was no significant difference in radial S or SR between subendocardial and transmural infarction (Table 2).
Long-axis function
Longitudinal S and SR are both significantly reduced in all infarcted segments compared with dysfunctional segments and control segments, irrespective of extent of scarring (Table 3). There was no significant difference in longitudinal S and SR between subendocardial and transmural infarction (Fig. 4).
Dobutamine stress responses.
Of 212 segments identified as having subendocardial infarction on CE-MRI, wall motion analysis by DBE identified augmentation in 38%. This contrasted with 213 transmural infarct segments (TME >50%), in which DBE identified augmentation in 24% (p < 0.001).
In the evaluation of short-axis function during low-dose dobutamine stimulation, circumferential S (AUC = 0.71) was significantly reduced in transmural compared with subendocardial infarcts (p < 0.002), and transmural infarcts also had lower SR (p = 0.03, AUC = 0.65) (Table 2). Long-axis function is further reduced in transmural infarct segments with significant differences in longitudinal S (AUC = 0.65) and SR (AUC = 0.67) between subendocardial and transmural infarction (Table 3).
Reproducibility.
There was good intraobserver and interobserver agreement for longitudinal SR (r = 0.91; r = 0.86) as well as longitudinal S (r = 0.92; r = 0.82). Similar good intraobserver and interobserver correlations were shown with circumferential SR (r = 0.85; r = 0.67) and circumferential S (r = 0.84; r = 0.76). However radial SR and S showed greater variability and less reproducibility (intraobserver radial SR: r = 0.34, radial S: r = 0.65; interobserver radial SR: r = 0.44, radial S: r = 0.75).
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Discussion
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The results of this study are that subendocardial infarction is associated with a significant reduction in longitudinal S and SR, whereas radial and circumferential function are relatively preserved. In contrast, transmural infarction is associated with a reduction of both long-axis and short-axis function. The majority of transmural scars (65%) showed lack of contractile reserve with DBE, but wall motion analysis did not correctly identify subendocardial infarction.
Longitudinal ventricular function.
The differential effects of subendocardial infarction on longitudinal and circumferential/radial function in this study may be a consequence of the helical wrapping of cardiac fibers into 3 different anatomical layers (9–11). The innermost subendocardial layer of fibers have an oblique clockwise orientation in the longitudinal direction, with the most significant contribution to long-axis function. The middle layer is wrapped circumferentially, and the outer subepicardial layer is arranged in an oblique anticlockwise direction and contributes to thickening and short-axis function via cross-fiber shortening (11,16–18). Our results of longitudinal S and SR measurements further reinforce our observation that long-axis function is lost early in subendocardial infarction. These findings are consistent with previous studies using strain rate imaging and MRI tagging, which has shown that long-axis function resides predominantly in the subendocardium (8,19). A recent study by Zhang et al. (20) defined a long-axis strain rate imaging cutoff value of >–0.59 s–1 to differentiate transmural from subendocardial infarction with sensitivity of 91% and specificity of 100%, but this work classified transmurality as a TME of 100%. We classified transmural from subendocardial infarction using a clinically significant TME cutoff of 50% because Kim et al. (2) have shown that fewer than 18% of segments are likely to show functional recovery after revascularization if TME exceeds 50%. During low-dose dobutamine stimulation, there was a significant differentiation in long-axis strain values between subendocardial and transmural infarcts that were not previously observed in resting strain parameters. These findings are consistent with detection of viability, whereby long-axis fibers are recruited during dobutamine stimulation in viable subendocardial infarcts, but such recruitment is not possible in nonviable transmural infarcts.
Radial ventricular function.
With respect to LV short-axis function, our data show that circumferential S and SR are well preserved in subendocardial infarcts because the circumferential fibers are predominantly in the mid layer of myocardium (9). Circumferential function has previously been shown to arise from the midwall (21) and is preserved in subendocardial infarctions (6,22). From our ROC curve analysis, a cutoff circumferential S value of <–13.6 has a sensitivity of 73% and specificity of 72% for differentiating transmural infarction. Although radial thickening by 2D strain indexes could not significantly differentiate infarct transmurality, radial 2D strain is still relatively preserved in subendocardial infarction. This is consistent with previous observations that the inner half of the ventricular wall has 71% contribution to wall thickening (23). Others have shown a contribution of 58%, 25%, and 17% from inner, middle, and outer walls, respectively (24). In a previous study, we have shown that >50% of infarcted segments with TME 25% to 75% still retained resting systolic thickening (25). Our observed significant reduction in radial strain only after TME >75% supports the theory of cross-fiber shortening, whereby passive radial thickening of segments with nontransmural infarction is generated by viable epicardial fibers (11,16,17). In our study, the novel technique of 2D strain was used in preference to conventional tissue Doppler-based strain rate imaging because it is relatively angle independent (13), allowing interrogation of apical segments, and probably less subject to cardiac translational motion and tethering (26), as well as having a higher signal-to-noise ratio and favorable spatial resolution.
Study limitations.
Only midventricular short-axis views were acquired for assessment of LV short-axis function. The absence of apical and basal short-axis views precluded us from measurements of rotational torsion, which would have permitted assessment of the LV mechanics of twisting and descent.
The limits in spatial resolution of echocardiographic methods has only enabled differentiation of TME into subendocardial and transmural infarct and not TME as a continuous variable. Our inability to establish a clear relationship between radial strain parameters and TME likely reflects the greater variability of radial compared with longitudinal 2D strain, albeit with a lesser variation than tissue velocity-based strain (27).
Finally, about 8% of our segments were not analyzable by 2D strain, secondary to limitations of image quality and poor acoustic windows, which affect tracking quality.
Clinical implications.
Identification of subendocardial infarction is clinically important because it is associated with better prognosis and greater likelihood of benefit from revascularization. Magnetic resonance imaging is the gold standard for identifying TME, but it has a number of limitations, including cost and accessibility. Wall motion analysis with DBE can be used to assess for contractile reserve, but we have shown that its ability to differentiate TME is limited. The use of 2D strain for the combined assessment of short-axis and long-axis cardiac function may allow differentiation of transmurality of chronic infarction and overcomes the limitations of conventional tissue Doppler and strain rate imaging. In subendocardial infarction, 2D circumferential strain parameters are preserved but 2D longitudinal strain parameters are reduced. In transmural infarcts, both short-axis and long-axis 2D strain parameters are significantly reduced.
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Footnotes
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Supported in part by a project grant (210217) from the National Health and Medical Research Council, Canberra, Australia.
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C.-M. Yu, J. E. Sanderson, T. H. Marwick, and J. K. Oh
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Top
Abstract
Methods
p < 0.0001 versus control; 
p = 0.02 versus TME 1% to 25%; 
p < 0.001 versus TME 1% to 25%; ||p = 0.01 versus TME 26% to 50%. For panel B: *p = NS versus control or TME 0%; 
