CLINICAL STUDY: MYOCARDIAL INFARCTION
Quantification of regional contractile function after infarction: strain analysis superior to wall thickening analysis in discriminating infarct from remote myocardium
Marco J. W. Götte, MD* d,
Albert C. van Rossum, MD, PhD* d,
Jos W. R. Twisk, PhD d,
Joost P. A. Kuijer, MSc d,
J. Tim Marcus, PhD d and
Cees A. Visser, MD, PhD* d
* Department of Cardiology, University Hospital ("Vrije Universiteit"), Amsterdam, The Netherlands
EMGO Institute, University Hospital ("Vrije Universiteit"), Amsterdam, The Netherlands
Department of Clinical Physics and Informatics, University Hospital ("Vrije Universiteit"), Amsterdam, The Netherlands
d Institute for Cardiovascular Research, Amsterdam, The Netherlands
Manuscript received February 16, 2000;
revised manuscript received August 1, 2000,
accepted November 3, 2000.
Reprint requests and correspondence: Dr. M. J. W. Götte, Department of Cardiology, University Hospital VU, De Boelelaan 1117, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands
mjw.gotte{at}azvu.nl
 |
Abstract
|
|---|
OBJECTIVES
Using two-dimensional wall thickening (WT) (expressed as percentage) and strain analysis, regional contractile myocardial function was quantified and compared in 13 control subjects and 13 patients with a first myocardial infarction (MI). The findings in the patient group were related to global ventricular function and infarct size.
BACKGROUND
In patients with coronary artery disease, regions with dysfunctional myocardium cannot be differentiated easily from regions with normal function by planar WT analysis. Physiologic factors, in combination with limitations of conventional imaging techniques, affect the calculation of WT. Quantitative assessment of contractile function by magnetic resonance (MR) tissue tagging and strain analysis may be less affected by these factors.
METHODS
Two-dimensional regional WT and strain were calculated in three short-axis MR cine and tagged images, respectively. Left ventricular volumes and ejection fraction (EF) were obtained from a series of contiguous short-axis cine images.
RESULTS
In patients with infarct-related ventricles, WT and strain analysis both revealed reduced myocardial function, as compared with control subjects (p < 0.005 and p < 0.001, respectively). However, WT analysis yielded no significant regional differences in function between infarct-related and remote myocardium (p = 0.064), whereas strain analysis did (p < 0.005). For detecting dysfunctional myocardium of electrocardiographically and angiographically defined infarct areas, WT analysis had a sensitivity of 69% and a specificity of 92%, whereas strain analysis demonstrated a sensitivity of 92% and a specificity of 99%. The EF correlated with WT (r = 0.76, p < 0.005) and strain (r = 0.89, p < 0.001).
CONCLUSIONS
Two-dimensional strain analysis is more accurate than planar WT analysis in discriminating dysfunctional from functional myocardium, and it provides a strong correlation between regional myocardial and global ventricular function.
|
Abbreviations and Acronyms
|  c | = circumferential shortening | | r | = radial stretch | | EDVI | = end-diastolic volume index | | EF | = ejection fraction | | ESVI | = end-systolic volume index | | LAD | = left anterior descending coronary artery | | MI | = myocardial infarction | | MR | = magnetic resonance | | WT | = wall thickening |
|
One of the most important hallmarks of ischemic heart disease is regional myocardial dysfunction (1–3). The extent and degree of contractile dysfunction after myocardial infarction (MI) are both important factors in determining the long-term prognosis after MI (4–6). An accurate variable of regional myocardial function is systolic wall thickening (WT) (expressed as a percentage) (7,8). Wall thickening is directly related to myocardial function, and abnormalities in WT are correlated with the extent of infarct size (3,7,9).
Magnetic resonance (MR) imaging has emerged as an important imaging modality for accurate assessment of regional myocardial function by quantitative WT analysis (8–11). Quantification of WT depends on accurate myocardial border delineation, which is facilitated by the high image quality provided by MR imaging. Detection of the excursion of endocardial and epicardial surfaces is affected by through-plane motion and the curvature of the heart wall (12), which can be compensated by three-dimensional WT analysis (13). However, the lack of traceable reference points within the myocardium prevents a quantitative description of intramural function. Zerhouni et al. (14) introduced MR tissue tagging, a method for noninvasive selective labeling of myocardial tissue. This was followed by the introduction of grid-tagging, which provides a large number of traceable tags within the myocardium (15,16). Using this grid-tagging technique in conjunction with two-dimensional strain analysis, quantitative analysis of regional intramural function can be performed independent of accurate border delineation (17–19). In the present study, regional myocardial function was expressed by two different variables: 1) planar WT, and 2) two-dimensional strain. Our aim was to assess the most accurate variable for quantification of regional function after MI. The following comparative investigations were performed, for both WT and strain as the dependent variables. First, regional function in the infarct-related region was tested in patients versus control subjects. Second, within the patient group, regional function was tested in the infarct region versus the remote noninfarct-related region. Third, also within the patient group, regional function was tested against global left ventricular function.
|
Methods
|
|---|
Subjects.
The Committee on Research Involving Human Subjects of the University Hospital, "Vrije Universiteit," in Amsterdam, approved the study protocol, and all subjects gave written, informed consent. Thirteen patients (12 men, age 57 ± 11 years) with a first MI were included. Thirteen age-matched male volunteers (age 53 ± 7 years) with no clinical evidence or history of cardiac disease served as control subjects. The diagnosis of MI was based on a typical history of chest pain, electrocardiographic changes compatible with infarction and an increase in plasma creatinine phosphokinase levels of more than twice the upper limit of normal, with an associated increase in the creatinine phosphokinase-MB fraction. Based on angiographic and electrocardiographic findings, it was confirmed that the left anterior descending (LAD) coronary artery was the infarct-related coronary artery in all patients. The patients were studied 103 ± 17 days after MI.
MR imaging.
Cardiac-triggered MR imaging was performed at 1.5-tesla (Vision, Siemens Medical Systems, Erlangen, Germany), using a phased-array body coil. Patients were imaged in the supine position.
Cine images
Localizing scout images were followed by a horizontal long-axis, four-chamber cine series. Using the end-diastolic frame of the horizontal long-axis view for positioning, 7 to 11 single breath-hold, short-axis series were acquired to encompass the whole left ventricle to calculate ventricular volumes, ejection fraction (EF) and mass. A gradient-echo pulse sequence with segmented k-space was applied. Acquiring 7-ky lines per heartbeat, the data acquisition window within the cardiac cycle was 80 ms. Echo sharing yielded a temporal resolution of 40 ms. Imaging variables were: 1) flip angle 25°; 2) repetition time 10 ms; 3) echo time 4.8 ms; 4) acquisition matrix 126 x 256; and 5) field of view 220 x 250 mm. The slice thickness was 6 mm, and the interslice gap 4 mm, yielding a slice distance of 10 mm.
Tagged images
The imaging protocol for acquiring tagged images has been described previously (20,21). The end-systolic phase of the horizontal long-axis cine series, defined as that with the smallest ventricular cavity volume, was used for planning tagged images in three parallel, short-axis planes at the basal, midventricular and apical levels. Tagging with a 7-mm tag-tag distance was achieved by spatial modulation of magnetization (16). The multiple expiration breath-hold technique was used to suppress the effect of respiratory motion on the tagged images, without compromising the temporal resolution (22). Acquiring 3-ky lines per heartbeat, the temporal resolution within the cardiac cycle was 30 ms. The flip angle used was 15°, repetition time was 10 ms and echo time was 3.8 ms. The matrix size was 144 x 256, the field of view was 250 x 250 mm and the corresponding resolution was 1.74 x 0.98 mm. The slice thickness was 6 mm. The entire imaging session, including both cine and tagged gradient-echo images, lasted 35 min.
Image analysis.
Cine images: WT and global function
The short-axis cine images were processed using the MASS software package (Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands) loaded on a Sun Sparc station (Sun Microsystems, Mountain View, California). The analysis procedures for calculation of systolic WT, left ventricular volumes, EF and mass have been described previously (23,24). Briefly, the end-diastolic phase was defined as the phase obtained directly after detection of the R-wave. The end-systolic phase was defined as the image frame with the smallest left ventricular cavity. Epicardial and endocardial contours were manually traced. The papillary muscles, trabeculae and epicardial fat were excluded from the analysis.
Wall thickening
After tracing, the centerline method was employed at the end-diastolic and end-systolic contours to calculate WT at both time frames (Fig. 1) (8). Only data obtained from cine images corresponding with the level of the three tagged images were used for WT analysis. To ensure proper matching of the cine and tagged short-axis slices, the right ventricle insertion sites, papillary muscle location and base-to-apex location were used as landmarks.
View larger version (96K):
[in this window]
[in a new window]
|
Figure 1 Calculation of two-dimensional WT and strain on short-axis cine MR images (A) and tagged images (B), respectively. The end-diastolic images are shown on the left and the end-systolic images on the right. For calculation of WT, the centerline method was used. The white arrow (a) is one of the 100 chords, representing the end-diastolic WT. The other white arrow (a') represents the end-systolic WT at that point. According the formula (a' – a) x 100/a, the percent change in WT between end-diastole and end-systole can be calculated. On the tagged images, the white diamonds indicate the intersection points of the tagging grid. By using groups of three intersection points, multiple triangular elements of the myocardium can be created (C). The variables r and c both represent a line segment in the undeformed state, in the radial and circumferential directions, respectively. The variables r' and c' represent the same line segment in the deformed state. (For the two-dimensional strain computation of a triangle, see Appendix.) MR = magnetic resonance; WT = wall thickness.
|
|
Global function
The end-diastolic and end-systolic volume indexes (EDVI and ESVI, respectively) were calculated by summation of the product (area x slice distance) for all slices and indexed for body surface area. From these volumes, stroke volume index and EF were calculated.
Tagged images: strain analysis
The tagged short-axis images were processed on a Silicon Graphics workstation using a dedicated software package (SPAMMVU, University of Pennsylvania, Philadelphia, Pennsylvania) (17). The tagging grid was automatically marked and followed during contraction (25). The tag intersection points were used to define triangular elements of the myocardium across the heart wall (Fig. 1). Homogeneous strain analysis was used to compute the deformation of each triangle (16,17). The strain components—radial stretch (r) and circumferential shortening (c)—were computed with respect to the radial and circumferential directions, respectively (see Appendix). Positive radial strains (r) represent the local contribution to WT. Negative values for r imply local wall thinning. Negative circumferential strains (c) quantify local circumferential shortening. Positive circumferential strains represent circumferential lengthening. The reproducibility of results using these strain variables has been reported (26).
Segmental analysis
For regional analysis of myocardial function, 12 circumferential segments of 30° each were defined at each of the three tagged and corresponding short-axis cine images. Assignment of a centerline or triangular element to a segment was determined by the position of the centerline or triangle’s centroid at end-diastole. The values of WT derived from the centerlines and the values of the strain variables derived from the triangular elements were averaged within these segments, yielding 12 regional values of the myocardial function variables per each short-axis level—36 in total. Segments with values for WT, r and c that exceeded the mean value ± 2 SD of the control group were defined as abnormal, indicating dysfunctional myocardium.
Definition of infarct-related, adjacent and remote areas
To compare the regional contractile function of patients with that of corresponding healthy volunteers, the anteroseptal and anterior segments at the basal level, the septal and anterior segments at the midventricular level and the septal, anterior and anterolateral segments at the apical level were considered specific for the perfusion territory of the LAD, and thus for the infarct-related area. The two segments adjacent to each side of the defined infarct area were considered the adjacent area. The segments in between the two adjacent areas and opposite of the infarct area were considered to be the remote area (Fig. 2). The distribution of the perfusion territory of the LAD and the corresponding distribution of the circumferential segments specific for the infarct area were based on previous reports (21,27).
View larger version (21K):
[in this window]
[in a new window]
|
Figure 2 Schematic definition of circumferential segments at the basal level (top), mid-ventricular level (middle) and apical level (bottom). The perfusion territory of the LAD was considered to be at the basal level in segments 10 to 3, at the mid level in segments 9 to 3 and at the apical level in segments 9 to 4. The infarct-related area is indicated by the dashed segments, the adjacent area by the solid segments and the remote area by the open segments. LAD = left anterior descending coronary artery.
|
|
Statistical analysis.
Statistical analysis was performed using the SPSS software package, version 7.5. The function in infarct-related, adjacent and remote myocardium in the infarct group was compared with that in comparable regions in the control group by using the nonparametric Mann-Whitney U test. In the infarct group, the differences in function between the infarct and remote areas were analyzed by using the Wilcoxon test for paired samples. Receiver-operating characteristic curves were created to evaluate the sensitivity and specificity of WT and strain analysis, respectively, for the detection of abnormal contractile function in the perfusion territory of the infarct-related coronary artery. Linear regression analysis was performed to correlate regional function quantified by WT and strain analysis (averaged for the 36 segments) to global ventricular function and enzymatic infarct size, respectively. A p value <0.05 was considered to be significant. Data are presented as the mean value ± SD.
|
Results
|
|---|
All patients received reperfusion therapy: seven patients had thrombolysis and six had primary percutaneous transluminal coronary angioplasty. The averaged peak creatine kinase, MB level was 238 ± 119 U/liter. Angiography was performed in all but one patient, confirming that the LAD was the infarct-related vessel. Nine patients received angiotensin-converting enzyme inhibitors and beta-blockers at the time of image acquisition. The clinical characteristics are shown in Table 1.
View this table:
[in this window]
[in a new window]
|
Table 1 Clinical Characteristics of Patients With Left Anterior Descending Coronary Artery-Related Infarcts (n = 13)
|
|
Global function.
The global function variables are summarized in Table 2. The ventricular volumes were significantly increased in the infarct group as compared with the control group (EDVI: p < 0.01; ESVI: p < 0.001), whereas the EF in the infarct group was reduced (p = 0.001). The stroke volume index did not differ between the two groups.
Regional function.
WT analysis
As shown in Table 3, regional WT in the infarct group, as compared with the control group, was reduced in all areas of the left ventricle, including the infarct-related area (p < 0.005), the adjacent area (p < 0.05) and the remote area (p = 0.005). In the infarct group, WT in the infarct area was not significantly different from WT in the remote area (p = 0.064) (Fig. 3). In Figure 4A, WT in 12 circumferential segments at the midventricular level is shown in patients and control subjects. Despite the fact that all patients had sustained an anterior MI, in none of the 12 segments, WT in the infarct group exceeded the mean values ± 2 SD of the control group. Receiver-operating characteristic curve analysis for WT analysis indicates the optimal cutoff value for the detection of dysfunctional myocardium in the perfusion territory of the infarct-related coronary artery—the LAD. A cutoff value of 35% was found to correspond with the highest sensitivity (69%) and specificity (92%).
View this table:
[in this window]
[in a new window]
|
Table 3 Regional Myocardial Function in the Perfusion Territory of the Left Anterior Descending Coronary Artery (LAD-Infarct Area) and the Area Adjacent to and Remote From the LAD Perfusion Territory, as Assessed by Wall Thickening and Strain Analysis
|
|
View larger version (11K):
[in this window]
[in a new window]
|
Figure 3 Contractile function in patients with MI in the infarct-related and remote myocardium, as quantified by WTh analysis and strain analysis. Strain analysis revealed significant differences in contractile function between infarct-related and remote myocardium, whereas WTh did not. r = radial stretch; MI = myocardial infarction; WTh = wall thickening.
|
|
WT analysis in relation to global function
The EF correlated with the mean ventricular contractile function, expressed as WT averaged for all 36 segments (r = 0.76, p = 0.002) (Fig. 5A). No correlation between EF and the number of segments with abnormal WT (r = 0.17, p = NS), indicating the extent of the area with dysfunctional myocardium, was found.
Strain analysis
Strain analysis demonstrated significant differences in regional function between the infarct group and the control group in all areas of the left ventricle (infarct-related and adjacent areas: p < 0.001 for r and c; remote area: p < 0.001 for r and p < 0.01 for c) (Table 3). The infarct group demonstrated significant differences in regional function between the infarct and remote areas (r: 9 ± 7% vs. 20 ± 7%, p = 0.001; c: –10 ± 7% vs. –16 ± 4%, p < 0.005) (Fig. 3). In Figure 4, B and C, r and c at the midventricular level are shown. In the infarct group, four segments were found with values for r that exceeded the mean values ± 2 SD of the control group. In the same four segments, values for c also exceeded the mean values ± 2 SD of the control group. These septal and anterior segments were highly concordant with the perfusion territory of the infarct-related LAD (Fig. 2). By using receiver-operating characteristic curves, the optimal cutoff value for the detection of dysfunctional myocardium in the perfusion territory of the LAD by strain analysis was found to be 20% for r, with a corresponding sensitivity of 92% and a specificity of 99%. For c, the best cutoff value was found to be –20%, with a sensitivity of 92% and a specificity of 92%.
Strain analysis in relation to global function
The correlation between EF and mean contractile function, as quantified by strain analysis, was higher than that found for WT (r = 0.84 for r, p < 0.001) and (r = –0.89 for c, p < 0.001), as shown in Figure 5, B and C, respectively. In contrast to WT analysis, a close relationship between global ventricular function and the number of segments with abnormal strain values was observed. For r, the correlation coefficient (r) was 0.83 (p < 0.001), and for c, r = 0.91 and p < 0.001.
|
Discussion
|
|---|
Accurate assessment of regional contractile function is important for determining long-term prognosis and patient management after MI. It has been demonstrated that WT is a useful measure of regional function and is more precise than wall motion analysis (3,7). However, the differentiation of regions with abnormal contractile function from regions with normal function by planar WT in patients with coronary artery disease is difficult because of the wide range of thickening in normal and abnormal regions (13,28). In the present study, regional myocardial function was expressed by two different variables—planar WT and two-dimensional strain. Our aim was to assess the most accurate variable for quantification of regional function after MI.
Observations in the present study.
Contractile function in normal volunteers
In healthy subjects, the mean WT (59%) was comparable with those values from previous reports. Pflugfelder et al. (10) reported an overall WT in young healthy subjects of 48 ± 28%. Sechtem et al. (11) found WT ranging from 18% to 100% in normal subjects. The maximal WT was found to be in the lateral free wall (67%), and the minimal WT was found in the septum (56%). This heterogeneity in function has been recognized previously (10,11,29,30) and can be explained by different physiologic factors, including the myocardial fiber architecture (31), wall stress and heterogeneity of myocardial perfusion (32). For r, the same distribution was found as for WT, with greater values in the lateral regions (34%) and lower values in the septal regions (28%). The variance in c was smaller than that found for r. This finding has been addressed before by Young et al. (19) and Waldman et al. (33) and can be explained by the fiber architecture of the myocardial wall, which is heterogeneous in the transmural direction and more uniform in the circumferential orientation, and by strain that varies most in the radial direction.
Regional contractile function in infarct-related ventricles
In infarct-related ventricles, WT and strain analysis both demonstrated reduced myocardial function in all segments, including the noninfarct-related lateral segments. This may be considered an adaptive mechanism. Different loading conditions and the tethering effect of the infarct-related myocardium may reduce function in the remote myocardium. Reduced function in the noninfarct-related myocardium will lead to redistribution of regional wall stress and smaller compliance mismatch between functioning and nonfunctioning myocardium (34). Reduction of wall stress in the infarct-related ventricle is important, because wall stress determines oxygen consumption and is a stimulus for ventricular remodeling (35,36). Our results are in line with the experimental findings in canine hearts of Azhari et al. (37). Using three-dimensional WT and strain analysis, they also found better results for strain analysis for mapping ischemic myocardial regions. However, the difference between these two methods was less, compared with our study, probably because of the higher accuracy of three-dimensional WT analysis. The correlation between global ventricular and regional myocardial function quantified by WT (r = 0.76, p = 0.002) was higher than that previously reported. Germain et al. (29) found no correlation between EF and the WT score (r = –0.01), whereas Sheehan et al. (38) reported a correlation between EF and the hypokinesia score (r = –0.47). The correlation between EF and myocardial function was even higher when myocardial function was quantified by two-dimensional strain analysis (r = 0.84, p < 0.001). The findings in this study suggest that strain analysis may be of greater help than WT analysis to understand the complicated interaction between regional dysfunction and long-term deterioration of global function after MI.
Study limitations.
Because of the limited number of patients, the results should be interpreted with care. Nevertheless, even with these small numbers, the strain data seem convincingly superior to WT in detecting and discriminating dysfunctional myocardium. The effect of through-plane motion and the curvature of the ventricular wall are important factors influencing planar WT analysis. It has been demonstrated by Beyar et al. (13) that three-dimensional WT analysis is more accurate than planar analysis. The former method reduces artifacts induced by image planes oriented obliquely through the ventricular wall, allowing less variability in normal thickening and thus better discrimination of an ischemic from a nonischemic zone. In this study, WT analysis is based on manual tracing, whereas strain analysis is performed automatically. This may have increased the variability in the thickening measurements as compared with the automatically performed strain measurements. The more detailed visualization of trabeculae provided by the improved image quality of the newer MR systems is another factor contributing to the problem of accurate border delineation. One effect is that the individual trabeculae are often excluded from the wall in diastole; during systole, these trabeculae join and are included within the wall. This confluence of trabeculae mimics WT (24). With tagging, myocardial material points are marked and a mere confluence of trabeculae cannot mimic radial strain. All these factors contribute to the large standard deviation of the measurements and, therefore, reduce the accuracy of planar WT analysis. Radial strain is the local contribution of myocardial deformation to WT. Using strain analysis, a gradual increase in radial stretch from the epicardium to the endocardium can be observed (39). Therefore, the contribution of regional myocardial deformation to WT is dependent on localization. In this study, using a tag-to-tag distance of 7 mm, the number of material points within the heart wall is limited. Therefore, the transmural distribution of myocardial strain cannot be calculated. Consequently, the mid-wall function is more heavily weighted, as compared with the epicardial and endocardial function. Refinement of the tagging grid, with a smaller tag-to-tag distance, may help to address this limitation. In the present study, only two-dimensional homogeneous strains were measured. A more comprehensive measurement method and analysis would account for three-dimensional strains. In addition, by using finite element methods, both two-dimensional and three-dimensional analyses could be generalized to be continuous and nonhomogeneous when using all data simultaneously and interpolating them (33).
|
Conclusions
|
|---|
Two-dimensional strain analysis is more accurate than WT analysis in discriminating dysfunctional from functional myocardium and, therefore, it improves the detection of regional differences in function. Two-dimensional strain analysis provides a strong correlation between regional myocardial function and global ventricular function.
|
Appendix
|
|---|
For the two-dimensional strain computation of a triangle, we first transformed the two vectors describing the short sides X1 and X2 of the triangle into the radial-circumferential coordinate system. The deformation gradient tensor F was then computed by solving [X1' X2'] = F · [X1 X2], where X1' and X2' denote the vectors of the triangle in the deformed state. Polar decomposition, F = R · U, is a mathematical operation that separates the rigid body rotation, R, from stretch, U; the radial and circumferential strains were computed from the diagonal elements of the stretch tensor, U, by r = Urr – 1 and c = Ucc – 1.
|
Footnotes
|
|---|
This study was supported by grant 95.097 from the Netherlands Heart Foundation.
|
References
|
|---|
1. Baxley WA, Reeves TJ. Abnormal regional myocardial performance in coronary artery disease. Prog Cardiovasc Dis. 1971;13:405–421[CrossRef][Medline]
2. Heikkilä J, Tabakin BS, Hugenholtz PG. Quantification of function in normal and infarcted regions of the left ventricle. Cardiovasc Res. 1972;6:516–531[Abstract/Free Full Text]
3. Lieberman AN, Weiss JL, Jugdutt BI, et al. Two-dimensional echocardiography and infarct size: relationship of regional wall motion and thickening to the extent of myocardial infarction in the dog. Circulation. 1981;63:739–746[Free Full Text]
4. Holman BL, Goldhaber SZ, Kirsch CM, et al. Measurement of infarct size using single photon emission computed tomography and technetium-99m–pyrophosphate: a description of the method and comparison with patient prognosis. Am J Cardiol. 1982;50:503–511[CrossRef][Medline]
5. Sanz G, Castaòer A, Betriu A, et al. Determinants of prognosis in survivors of myocardial infarction: a prospective clinical angiographic study. N Engl J Med. 1982;306:1065–1070[Medline]
6. Weiss JL, Marino PN, Shapiro EP. Myocardial infarct expansion: recognition, significance and pathology. Am J Cardiol. 1991;68:35D–40D[CrossRef][Medline]
7. Sasayama S, Franklin D, Ross J Jr, Kemper SW, McKnown D. Dynamic changes in left ventricular wall thickness and their use in analyzing cardiac function in the conscious dog: a study based on a modified ultrasonic technique. Am J Cardiol. 1976;38:870–879[CrossRef][Medline]
8. Holman ER, Vliegen HW, van der Geest RJ, et al. Quantitative analysis of regional left ventricular function after myocardial infarction in the pig assessed with cine magnetic resonance imaging. Magn Reson Med. 1995;34:161–169[Medline]
9. Holman ER, Buller VGM, de Roos A, et al. Detection and quantification of dysfunctional myocardium by magnetic resonance imaging: a new three-dimensional method for quantitative wall-thickening analysis. Circulation. 1997;95:924–931[Abstract/Free Full Text]
10. Pflugfelder PW, Sechtem UP, White RD, Higgins ChB. Quantification of regional myocardial function by rapid cine MR imaging. Am J Roentgenol. 1988;150:523–529[Abstract/Free Full Text]
11. Sechtem UP, Sommerhoff BA, Markiewicz W, White RD, Cheitlin MD, Higgins ChB. Regional left ventricular wall thickening by magnetic resonance imaging: evaluation in normal persons and patients with global and regional dysfunction. Am J Cardiol. 1987;59:145–151[CrossRef][Medline]
12. Pandian NG, Kerber RE. Two-dimensional echocardiography in experimental coronary stenosis. I. Sensitivity and specificity in detecting transient myocardial dyskinesis: comparison with sonomicrometers. Circulation. 1982;66:597–602[Abstract/Free Full Text]
13. Beyar R, Shapiro EP, Graves WL, et al. Quantification and validation of left ventricular wall thickening by a three-dimensional volume element magnetic resonance imaging approach. Circulation. 1990;81:297–307[Abstract/Free Full Text]
14. Zerhouni EA, Parish DM, Rogers WJ, Yang A, Shapiro EP. Human heart: tagging with MR imaging: a method for noninvasive assessment of myocardial motion. Radiology. 1988;169:59–63[Abstract/Free Full Text]
15. Axel L, Dougherty L. MR imaging of motion with spatial modulation of magnetization. Radiology. 1989;171:841–845[Abstract/Free Full Text]
16. Axel L, Dougherty L. Heart wall motion: improved method of spatial modulation of magnetization for MR imaging. Radiology. 1989;172:349–350[Abstract/Free Full Text]
17. Axel L, Gonçalves RC, Bloomgarden D. Regional heart wall motion: two-dimensional analysis and functional imaging with MR imaging. Radiology. 1992;183:745–750[Abstract/Free Full Text]
18. Young AA, Axel L, Dougherty L, Bogen DK, Parenteau CS. Validation of tagging with MR imaging to estimate material deformation. Radiology. 1993;188:101–108[Abstract/Free Full Text]
19. Young AA, Imai H, Chang Ch, Axel L. Two-dimensional left ventricular deformation during systole using magnetic resonance imaging with spatial modulation of magnetization. Circulation. 1994;89:740–752[Abstract/Free Full Text]
20. Marcus JT, Götte MJW, van Rossum AC, et al. Myocardial function in infarcted and remote regions early after infarction in man: assessment by MR tagging and strain analysis. Magn Reson Med. 1997;38:803–810[Medline]
21. Götte MJW, van Rossum AC, Marcus JT, Kuijer JPA, Axel L, Visser CA. Recognition of infarct localization by specific changes in intramural myocardial mechanics. Am Heart J. 1999;138:1038–1045[CrossRef][Medline]
22. Fisher SE, McKinnon GC, Scheidegger MB, Prins W, Meier D, Boesiger P. True myocardial motion tracking. Magn Reson Med. 1994;31:401–413[Medline]
23. van der Geest RJ, de Roos A, van der Wall EE, Reiber JHC. Quantitative analysis of cardiovascular MR images. Int J Card Imaging. 1997;13:247–258[CrossRef][Medline]
24. Marcus JT, Kuijer JPA, Götte MJW, Heethaar RM, van Rossum AC. Left ventricular mass measured by MRI: effect of endocardial trabeculae on the observed wall thickness. (abstr)J Cardiovasc Magn Reson. 1999;4:371
25. Kass M, Witkin A, Terzopoulos D. Snakes: active contour models. Int J Comp Vision. 1988;1:321–331[CrossRef]
26. Kuijer JPA, Marcus JT, Götte MJW, van Rossum AC, Heethaar RM. Variance components of two-dimensional strain parameters in left ventricular heart wall obtained by MR tagging. (abstr)Proc Int Soc Magn Reson Med. 1999;7:1992
27. van Rugge FP, van der Wall EE, Spanjersberg SJ, et al. Magnetic resonance imaging during dobutamine stress for detection and localization of coronary artery disease: quantitative wall motion analysis using a modification of the centerline method. Circulation. 1994;90:127–138[Abstract/Free Full Text]
28. Buchalter MB, Sims C, Dixon AK, et al. Measurement of regional function using labelled magnetic resonance imaging. Br J Radiol. 1991;64:953–958[Abstract/Free Full Text]
29. Germain P, Roul G, Constantinesco A, et al. Comparison between abnormalities in segmental endocardial motion and abnormalities in segmental wall thickening after anterior myocardial infarction: a cine magnetic resonance study. Eur Heart J. 1996;17:1350–1361[Abstract/Free Full Text]
30. Naito H, Arisawa J, Harada K, Yamagami H, Kozuka T, Tamura S. Normal nonuniformity of left ventricular contraction: assessment by cine magnetic resonance imaging with presaturation myocardial tagging. Acta Radiol. 1996;37:767–774[Medline]
31. Greenbaum RA, Ho SY, Gibson DG, Becker AE, Anderson RH. Left ventricular fibre architecture in man. Br Heart J. 1981;45:248–263[Abstract/Free Full Text]
32. Gallagher KP, Kumada T, Koziol JA, McKown MD, Kemper WS, Ross J Jr. Significance of regional wall thickening abnormalities relative to transmural myocardial perfusion in anesthetized dogs. Circulation. 1980;62:1266–1274[Abstract/Free Full Text]
33. Waldman LK, Fung YC, Covell JW. Transmural myocardial deformation in the canine left ventricle: normal in vivo three-dimensional finite strains. Circ Res. 1985;57:152–163[Abstract/Free Full Text]
34. Mitchell GF, Lamas GA, Vaughan DE, Pfeffer MA. Left ventricular remodeling in the year after first anterior myocardial infarction: a quantitative analysis of contractile segment lengths and ventricular shape. J Am Coll Cardiol. 1992;19:1136–1144[Abstract]
35. McKay RG, Pfeffer MA, Pasternak RC, et al. Left ventricular remodeling after myocardial infarction: a corollary to infarct expansion. Circulation. 1986;74:693–702[Abstract/Free Full Text]
36. Pouleur H, Rousseau MF, van Eyll C, Charlier AA. Assessment of regional left ventricular relaxation in patients with coronary artery disease: importance of geometric factors and changes in wall thickness. Circulation. 1984;69:696–702[Abstract/Free Full Text]
37. Azhari H, Weiss JL, Rogers WJ, Siu CO, Shapiro EP. A noninvasive comparative study of myocardial strains in ischemic canine hearts using tagged MRI in 3-D. Am J Physiol. 1995;268:H1918–H1926
38. Sheehan FH, Szente A, Mathey DG, Dodge HT. Assessment of left ventricular ejection fraction in acute myocardial infarction: the relationship between global ejection fraction and regional wall motion. Eur Heart J. 1985;6(Suppl E):117–125[Abstract/Free Full Text]
39. Bogaert J, Maes A, van de Werf F, et al. Functional recovery of subepicardial myocardial tissue in transmural infarction after successful reperfusion. Circulation. 1999;99:36–43[Abstract/Free Full Text]
This article has been cited by other articles:
|
|
|
|
 
B. Grenne, C. Eek, B. Sjoli, T. Dahlslett, M. Uchto, P. K. Hol, H. Skulstad, O. A. Smiseth, T. Edvardsen, and H. Brunvand
Acute coronary occlusion in non-ST-elevation acute coronary syndrome: outcome and early identification by strain echocardiography
Heart,
October 1, 2010;
96(19):
1550 - 1556.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. P. Cupps, A. K. Taggar, L. M. Reynolds, J. S. Lawton, and M. K. Pasque
Regional myocardial contractile function: multiparametric strain mapping
Interact CardioVasc Thorac Surg,
June 1, 2010;
10(6):
953 - 957.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Karatasakis, E. Leontiadis, I. Peristeri, A. Manginas, E. Goussetis, S. Graphakos, E. Papadakis, and D. V. Cokkinos
Intracoronary infusion of selected autologous bone marrow stem cells improves longitudinal myocardial strain and strain rate in patients with old anterior myocardial infarction without recent revascularization
Eur Heart J Cardiovasc Imaging,
June 1, 2010;
11(5):
440 - 445.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Cramariuc, E. Gerdts, E. S. Davidsen, L. Segadal, and K. Matre
Myocardial deformation in aortic valve stenosis: relation to left ventricular geometry
Heart,
January 15, 2010;
96(2):
106 - 112.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
I. Yoshioka, Y. Saiki, A. Ichinose, K. Takase, S. Takahashi, T. Ohashi, M. Sato, and K. Tabayashi
Tagged cine magnetic resonance imaging with a finite element model can predict the severity of retrosternal adhesions prior to redo cardiac surgery
J. Thorac. Cardiovasc. Surg.,
April 1, 2009;
137(4):
957 - 962.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Neizel, D. Lossnitzer, G. Korosoglou, T. Schaufele, H. Peykarjou, H. Steen, C. Ocklenburg, E. Giannitsis, H. A. Katus, and N. F. Osman
Strain-Encoded MRI for Evaluation of Left Ventricular Function and Transmurality in Acute Myocardial Infarction
Circ Cardiovasc Imaging,
March 1, 2009;
2(2):
116 - 122.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
O. Gjesdal, T. Helle-Valle, E. Hopp, K. Lunde, T. Vartdal, S. Aakhus, H.-J. Smith, H. Ihlen, and T. Edvardsen
Noninvasive Separation of Large, Medium, and Small Myocardial Infarcts in Survivors of Reperfused ST-Elevation Myocardial Infarction: A Comprehensive Tissue Doppler and Speckle-Tracking Echocardiography Study
Circ Cardiovasc Imaging,
November 1, 2008;
1(3):
189 - 196.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Carlsson, N. F. Osman, P. C. Ursell, A. J. Martin, and M. Saeed
Quantitative MR measurements of regional and global left ventricular function and strain after intramyocardial transfer of VM202 into infarcted swine myocardium
Am J Physiol Heart Circ Physiol,
August 1, 2008;
295(2):
H522 - H532.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. F.L. Schinkel, D. Poldermans, A. Elhendy, and J. J. Bax
Assessment of Myocardial Viability in Patients with Heart Failure
J. Nucl. Med.,
July 1, 2007;
48(7):
1135 - 1146.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. J.W. Gotte, T. Germans, I. K. Russel, J. J.M. Zwanenburg, J. T. Marcus, A. C. van Rossum, and D. J. van Veldhuisen
Myocardial Strain and Torsion Quantified by Cardiovascular Magnetic Resonance Tissue Tagging: Studies in Normal and Impaired Left Ventricular Function
J. Am. Coll. Cardiol.,
November 21, 2006;
48(10):
2002 - 2011.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. J. Pomerantz, J. R. Wollmuth, M. D. Krock, B. P. Cupps, P. Moustakidis, N. T. Kouchoukos, V. G. Davila-Roman, and M. K. Pasque
Myocardial Systolic Strain is Decreased After Aortic Valve Replacement in Patients With Aortic Insufficiency
Ann. Thorac. Surg.,
December 1, 2005;
80(6):
2186 - 2192.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Sipola, K. Lauerma, P. Jaaskelainen, M. Laakso, K. Peuhkurinen, H. Manninen, H. J. Aronen, and J. Kuusisto
Cine MR Imaging of Myocardial Contractile Impairment in Patients with Hypertrophic Cardiomyopathy Attributable to Asp175Asn Mutation in the {alpha}-Tropomyosin Gene
Radiology,
September 1, 2005;
236(3):
815 - 824.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. R. Messroghli, G. J. Bainbridge, K. Alfakih, T. R. Jones, S. Plein, J. P. Ridgway, and M. U. Sivananthan
Assessment of Regional Left Ventricular Function: Accuracy and Reproducibility of Positioning Standard Short-Axis Sections in Cardiac MR Imaging
Radiology,
April 1, 2005;
235(1):
229 - 236.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. J. Pennell, U. P. Sechtem, C. B. Higgins, W. J. Manning, G. M. Pohost, F. E. Rademakers, A. C. van Rossum, L. J. Shaw, and E. K. Yucel
Clinical indications for cardiovascular magnetic resonance (CMR): Consensus Panel report
Eur. Heart J.,
November 1, 2004;
25(21):
1940 - 1965.
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. F. Azevedo, L. C. Amado, D. L. Kraitchman, B. L. Gerber, N. F. Osman, C. E. Rochitte, T. Edvardsen, and J. A.C. Lima
Persistent diastolic dysfunction despite complete systolic functional recovery after reperfused acute myocardial infarction demonstrated by tagged magnetic resonance imaging
Eur. Heart J.,
August 2, 2004;
25(16):
1419 - 1427.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. S. Maniar, B. P. Cupps, D. D. Potter, P. Moustakidis, C. J. Camillo, C. M. Chu, M. K. Pasque, and T. M. Sundt III
Ventricular function after coronary artery bypass grafting: Evaluation by magnetic resonance imaging and myocardial strain analysis
J. Thorac. Cardiovasc. Surg.,
July 1, 2004;
128(1):
76 - 82.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. Kim, W. D. Gilson, C. M. Kramer, and F. H. Epstein
Myocardial Tissue Tracking with Two-dimensional Cine Displacement-encoded MR Imaging: Development and Initial Evaluation
Radiology,
March 1, 2004;
230(3):
862 - 871.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Castillo, J. A. C. Lima, and D. A. Bluemke
Regional Myocardial Function: Advances in MR Imaging and Analysis
RadioGraphics,
October 1, 2003;
23(90001):
S127 - 140.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. L. Kraitchman, S. Sampath, E. Castillo, J. A. Derbyshire, R. C. Boston, D. A. Bluemke, B. L. Gerber, J. L. Prince, and N. F. Osman
Quantitative Ischemia Detection During Cardiac Magnetic Resonance Stress Testing by Use of FastHARP
Circulation,
April 22, 2003;
107(15):
2025 - 2030.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Z. Y. Fang, S. Yuda, V. Anderson, L. Short, C. Case, and T. H. Marwick
Echocardiographic detection of early diabetic myocardial disease
J. Am. Coll. Cardiol.,
February 19, 2003;
41(4):
611 - 617.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C. Pislaru, P. C. Anagnostopoulos, J. B. Seward, J. F. Greenleaf, and M. Belohlavek
Higher myocardial strain rates duringisovolumic relaxation phase than duringejection characterize acutely ischemic myocardium
J. Am. Coll. Cardiol.,
October 16, 2002;
40(8):
1487 - 1494.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Hoffmann, E. Altiok, B. Nowak, N. Heussen, H. Kuhl, H.-J.u. Kaiser, U. Bull, and P. Hanrath
Strain rate measurement by doppler echocardiography allows improvedassessment of myocardial viability inpatients with depressed left ventricular function
J. Am. Coll. Cardiol.,
February 6, 2002;
39(3):
443 - 449.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. P. Abraham and R. A. Nishimura
Myocardial strain: can we finally measure contractility?
J. Am. Coll. Cardiol.,
March 1, 2001;
37(3):
731 - 734.
[Full Text]
[PDF]
|
|
|
|
Top
Abstract
Methods
