Abstract
Background
Myocardial viability assessment adds value to the therapeutic decision-making of patients with ischemic heart disease. In this feasibility study, we investigated whether established echocardiographic measurements of post-systolic shortening (PSS), strain, strain rate and wall motion score (WMS) can discover viable myocardial segments. Our hypothesis is that non-viable myocardial segments are both akinetic and without PSS.
Methods
The study population consisted of 26 examinations strictly selected by visible dysfunction. We assessed WMS, strain by speckle tracking and strain rate by tissue Doppler. The segments (16*26 = 416) were categorized into either normokinetic/hypokinetic or akinetic/dyskinetic and whether there was PSS. The reference method was the presence of scar with segmental percentage volume scar fraction >50%, detected by late gadolinium-enhanced cardiovascular magnetic resonance. Agreement with echocardiography was evaluated by Kappa coefficient.
Results
WMS had Kappa coefficient 0.43 (sensitivity 99%, specificity 35%). Kappa coefficient of strain was 0.28 (sensitivity 98%, specificity 23%). By combining PSS in akinetic segments with WMS and strain, the Kappa coefficient was 0.06 and 0.08 respectively.
Conclusion
Segmental viability was best shown by the presence of systolic function. Post-systolic shortening adds no value to the assessment of segmental myocardial viability.
Introduction
Myocardial viability has for decades been a cornerstone in the therapeutic decision-making of patients with ischemic heart disease [Citation1]. For clinical purposes, viability refers to the ability of a segment to regain its contractile function. The gold standard imaging measurement for detecting myocardial viability is not established [Citation2]. Positron Emission Tomography (PET) shows metabolic integrity while magnetic resonance (MR) displays scar that may restrict contraction, but both methods are time-consuming and expensive. Echocardiography is available, cheap, fast and with few contraindications. Several echocardiographic measurements, both at rest and during stress, are candidates for viability diagnostics. Most of them are established as global measurements [Citation3–5], but in the present study, we focus on the measurements at a segmental level, as viable segments are more relevant in relation to revascularization.
The presence of resting contraction denotes viability. This can be assessed semi-quantitatively by wall thickening as wall motion score (WMS). Strain and strain rate are quantitative measurements of longitudinal shortening [Citation6–8] and can be measured by tissue Doppler imaging (TDI) [Citation6] or by speckle tracking echocardiography (STE) [Citation9,Citation10]. One aim of this study was to assess whether strain and strain rate could improve accuracy in assessing systolic contraction. Another candidate for detecting viable segments is the presence of post-systolic shortening (PSS), which is the shortening of a segment after aortic valve closure (AVC). PSS was already described in 1935 by Tennant and Wiggers [Citation11], but was then considered an artefact (). PSS is either passive recoil of a stretched segment, active shortening due to delayed relaxation, interacting with the relaxation of adjacent segments, or a combination [Citation12–14]. The mechanism is dependent on the level of ischemia. PSS can occur in acute ischemia [Citation15–17], but can also persist [Citation12]. PSS is difficult to visualize in B-mode echocardiography but can be measured by strain rate/strain. The relationship of PSS to myocardial viability has been investigated, where some studies suggest there is a relationship [Citation5,Citation18–21], whilst others could not find the same concordance, especially not at rest [Citation22,Citation23].
Figure 1. Modified from Tennant and Wiggers, 1935 [Citation11]. Shows the movement of the ventricles after occlusion of the coronary artery. Numbers indicate the number of heartbeats after occlusion, showing the development of post-systolic shortening (PSS) from 30–125 beats (slope D-K) after occlusion. From beat 51–125 (slope G-K) there is no systolic shortening, but only stretch and recoil. Shaded area: PSS.
![Figure 1. Modified from Tennant and Wiggers, 1935 [Citation11]. Shows the movement of the ventricles after occlusion of the coronary artery. Numbers indicate the number of heartbeats after occlusion, showing the development of post-systolic shortening (PSS) from 30–125 beats (slope D-K) after occlusion. From beat 51–125 (slope G-K) there is no systolic shortening, but only stretch and recoil. Shaded area: PSS.](/cms/asset/8c7f2be0-0174-4252-a15c-259bcc1418d2/icdv_a_2181390_f0001_b.jpg)
A reasonable hypothesis is that the presence of PSS in chronic infarcts with akinesia:
Demonstrates contractile tension in segments that are akinetic during ordinary systole, and
Disappears with too extensive scarring of the segment, precluding the possibility of both systolic and post-systolic shortening.
Thus, our hypothesis is that the presence of PSS in the setting of akinesia denotes viability, while akinesia without PSS suggests non-viability. The present feasibility study which only included examinations with obviously visible dysfunction aimed to compare strain, strain rate, post-systolic shortening (PSS) and WMS alone or in combination in diagnosing viable myocardial segments. The reference method was late-gadolinium-enhanced cardiovascular magnetic resonance (LGE-CMR) [Citation24,Citation25].
Methods
Study design
In this study, we retrospectively analyzed echocardiographic examinations from a former study. In the time period of recruitment, 82 patients with first-time myocardial infarction and peak troponin T > 500 ng/L were eligible for participation. Out of these, 56 ST-segment-elevation myocardial infarction (STEMI) and 15 non-ST-segment myocardial infarction (NSTEMI) patients were included in the original study [Citation26]. Exclusion criteria were prior myocardial infarction (MI), bundle branch block with QRS duration >130 ms, valvular disease, previous heart surgery, age >75 years, extensive co-morbidity, chronic atrial fibrillation, and contraindications to LGE-CMR. Coronary angiography identified the culprit lesion in all patients. A control group of 35 healthy controls were also a part of the original echocardiographic material. They did not undergo LGE-CMR, but were assessed in this study as all analyses were done blinded for the LGE-CMR-result and patient characteristics. Thus we semi-quantitatively assessed 106 examinations (71 patients + 35 healthy controls) with Wall Motion Score (WMS) in a 16-segment model [Citation27]. We only included examinations with visible dysfunction (i.e. WMS ≥ 2 in ≥ 2 segments), to purely investigate the added value of deformation measurements and test our hypothesis that akinesia and no PSS denote non-viability. Additionally, we wanted to reduce the interference of noise and physiologic PSS in healthy segments. WMS was assessed by two operators together (MH, AS), remaining echocardiographic assessment was done by one single operator (MH). Details about the echocardiographic acquisitions and magnetic resonance imaging are described thoroughly in the referred article [Citation26]. The study was approved by the Regional Committee for Medical Research Ethics and conducted according to the second Helsinki Declaration.
Echocardiographic acquisitions and measurements
Echocardiographic acquisitions were performed with GE Vivid 7 (69%) and GE Vivid E9 (31%) (GE Vingmed, Horten, Norway). We used EchoPac 202x (GE Vingmed), for analysis. Segments with WMS 1 (normokinetic) or 2 (hypokinetic) were categorized as kinetic; viable, and 3 (akinetic) and 4 (dyskinetic) as akinetic; non-viable. We measured segmental longitudinal peak segmental strain values using mid-wall strain by speckle tracking in the Automated Function Imaging (AFI) software built-in EchoPac. Segments with strain > −5% were categorized as akinetic; non-viable. We assessed tissue Doppler curves to find peak values of strain rate and categorized them as either akinetic; non-viable or kinetic; viable. Strain rate values > −0.25 s−1 were categorized as akinetic: non-viable [Citation26].
We used the post-systolic index (PSI) from the AFI in EchoPac to determine the presence of PSS. PSI is defined as ‘((peak strain over whole beat – end-systolic strain)/peak strain over whole beat x 100%)’ (). PSS was defined as present when PSI > 20% in line with earlier studies [Citation28,Citation29]. According to our hypothesis, we created new variables by combining PSS in the following manner ():
Figure 2. Screenshot from EchoPac 202x AFI software. Strain curves from apical 4-chamber (4CH), apical 2-chamber (2CH) and apical long axis (APLAX). The peak strain over the whole beat is marked with a white square on the curves. The bulls-eye plot shows the post-systolic index (PSI) in different segments. In basal and mid posterior segments, the PSI is 40 and 35 accordingly, this corresponds to the yellow and cyan curve in the APLAX-view.
Figure 3. Illustration of our hypothesis.
Akinetic segments by WMS, strain and strain rate with no PSS were categorized as non-viable.
Kinetic segments, and akinetic segments with PSS were categorized as viable.
We also combined WMS and strain; segments considered viable either by WMS or strain, were categorized as viable.
Late-gadolinium-enhanced cardiovascular magnetic resonance
The LGE-CMR acquisitions were performed by 1,5 T Siemens Avanto (Siemens Medical, Erlangen, Germany). For details about the imaging protocol see the original article [Citation26]. The total myocardial area and the area of infarcted myocardium were semiautomatically drawn by two investigators. An area with signal intensity 2SD above normal myocardium was considered infarcted. The infarct size was calculated as infarct volume in the percentage of total myocardial volume. The reference method for non-viable segments was defined as the presence of a scar with a percentage volume fraction > 50% detected by LGE-CMR [Citation26,Citation30,Citation31] ().
Figure 4. Scar visualization by late gadolinium enhancement CMR. White hyper-enhanced areas in the septal and anterior wall corresponding to the left anterior descending coronary artery. The expansion of the ischemic injury is starting from the subendocardium and progresses almost to the epicardium, indicating transmural infarction (segmental infarct volume fraction >50%).
Statistical analyses
The specificity, sensitivity, negative -and positive predictive values for detecting viable segments between the different echo measurements and LGE-CMR were calculated. Agreement was assessed by Kappa coefficient. Non-parametric comparison of LGE-CMR volume fraction in PSS vs no-PSS group was done by Wilcoxon rank-sum test and the Median test. Statistical analyses were performed by STATA/MP 17.
Results
Study population and segment characteristics
Seventy-three echocardiographic examinations with hypokinesia (WMS = 2) in 1 segment or less were excluded. Furthermore, 5 examinations did not have LGE-CMR, 1 examination did not have TDI acquisitions, and 1 examination had too extensive framerate variation to do strain-analysis by speckle tracking, these examinations were excluded. This left 26 echocardiographic examinations with 16 segments each, a total of 416 segments for further analysis (). The majority of the included patients had STEMI (84%), and the median infarct volume fraction was 15%. The patients were examined with echocardiography and LGE-CMR between day 15 and day 51 (median 28) after the MI. Patient characteristics are listed in . LGE-CMR characterized 361 (87%) of all segments as viable. Corresponding numbers for WMS were 378 (94%), strain rate 375 (94%), strain 327 (95%), combining strain and WMS 329 (98%), combining strain rate and PSS 329 (98%) and combining strain and PSS 339 (99%) (). Of the 17 segments akinetic by strain, 15 (88%) of these had PSS. Seventeen segments were categorized as akinetic by WMS, 13 (76%) of these segments had PSS. Only 10 (56%) of the akinetic segments by strain rate had PSS (). The assessment had the highest feasibility for WMS with 402 (97%) out of 416 segments evaluated ().
Figure 5. Study selection. WMS: Wall Motion score; TDI: Tissue Doppler Imaging; LGE-CMR: Late-Gadolinium Enhanced Cardiovascular Magnetic Resonance; AFI: Automated Function Imaging.
Table 1. Baseline patient characteristics, angiographic findings, and diagnosis.
Table 2. Cross tables (2x2) of each of the echocardiographic measurements. Number and percentages of segments with concordance to late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).
Table 3. Cross tables (2 × 2) of a number of akinetic segments with concordance to post-systolic shortening.
Viability measurements
All Kappa coefficients for the echocardiographic measurements were low or moderate. WMS had the highest Kappa coefficient of 0.43, a sensitivity of detecting viable segments of 99% and a specificity of 35%. Strain and strain rate had Kappa coefficients of 0.28 and 0.29 respectively. PSS had a negative Kappa coefficient and combining PSS with strain and strain rate gave even poorer concordance to LGE-CMR (). But still, there is a significant difference between the infarcted volume fraction by LGE-CMR in the 37 segments with PSS compared to the 305 segments without PSS (median 57% (IQR 16–68%) vs median 0% (IQR 0–15%), p < 0.001).
Table 4. Statistics for viability by the echocardiographic measurements versus late gadolinium enhancement cardiac magnetic resonance (LGE-CMR).
Discussion
In our study, the presence of systolic contraction had the best segmental correspondence with LGE-CMR in detecting viable segments. The main viability indicator, whatever method, still seems to be the presence of systolic contraction. The presence of PSS in neither akinetic nor all segments did not add information in characterizing viable segments.
Systolic contraction
WMS has been suggested as a prognostic indicator after MI [Citation32,Citation33] and WMSI is a measure of infarct size [Citation34]. WMS is feasible and is less dependent on image quality than deformation measurements. However, the demonstration of viability by systolic contraction is trivial and WMS is a semi-quantitative and highly subjective measurement. In line with this, strain and strain rate did not add significant accuracy, with no significant improvement, neither in correspondence with LGE-CMR, nor in sensitivity nor specificity. The high sensitivity, low specificity and Kappa-values are probably related to the relatively low number of non-viable segments compared to viable segments.
Post-systolic shortening
Post-systolic shortening (PSS) is studied as a marker of acute ischemia, and it has been shown that PSS persists after the reperfusion of the myocardium [Citation35,Citation36]. In chronic ischemia, the evidence seems more diverging, as in the present study [Citation12,Citation22,Citation23]. The main hypothesis was that in the absence of systolic contraction, PSS might be a marker of viability. Thus, the added value of PSS should be seen by combining PSS and systolic shortening either by strain or strain rate.
Mechanisms of PSS
Different mechanisms for PSS have been suggested. One theory is that PSS is a mix between passive recoil and active contraction [Citation13,Citation14], another suggestion is that PSS may be recoil after elongation due to traction from neighbor myocardial cells and thus mainly a passive phenomenon, but also a marker of preserved elasticity [Citation37]. From a physiological aspect, it is not possible to describe the phenomena solely as either active or passive, as the mechanism differs with the level and duration of ischemia. In 1984, Brutsaert [Citation38] described three factors that controlled the relaxation: (1) load (2) inactivation and (3) uniformity. In the present study, we studied chronic infarctions, and all three factors are affected. Early in the ischemic cascade the load and the inactivation are altered due to reduced reuptake of Ca2+ in SERCA-pump due to hypoxia, later the load is reduced due to prolonged reduced systolic function and relative myocardial loading. As ischemia is regional, the physiological uniformity also is disturbed, leading to a reduced ability to relax. This may explain why PSS is more prominent in acute infarctions than in chronic infarctions as in this material. According to our hypothesis, we wanted to evaluate PSS as an additional resting viability marker. Some studies have shown that resting echocardiography with this addition is sufficient for viability testing [Citation21], while others conclude that stress testing by dobutamine is needed [Citation22,Citation37]. In our study, however, PSS did not increase sensitivity for viability.
Earlier studies have shown diverging results in the ability of PSS to assess viable segments. In concordance with our results, Weideman et al. [Citation39] did an experimental trial on pigs and found that it was the systolic measurements and not the PSS that were useful to distinguish between viable and non-viable segments. The missing relationship between PSS and viability is also shown in some clinical studies [Citation22,Citation23,Citation40]. Others have shown that PSS is a predictor of myocardial recovery [Citation18,Citation19]. Lately, PSS also has been suggested as a marker for future heart failure [Citation41] and in patients with stable angina as a predictor of significant coronary artery disease and future cardiovascular events [Citation28]. The diverging results are probably due to the complexity of PSS. Studies on PSS have been conducted with different reference methods, different patient populations, different ways of quantification and even the mechanism behind PSS is not fully uncovered.
The measurement of PSS
In this study, we used PSI as the measurement of PSS [Citation42]. Other measurements are possible, such as velocity [Citation40] and the occurrence of peak strain after aortic valve closure (AVC) [Citation23]. The optimal quantification of PSS is thus still undecided.
Cut-off values
In the present study, we chose a cut-off value of PSS by PSI >20% as in earlier studies [Citation28,Citation29]. Cut-off values between 5%-35% on global PSI have been suggested [Citation42,Citation43]. PSS may also occur in healthy individuals. In a study by Voigt et al., 31% of healthy individuals had PSS [Citation29] and in a study by Brainin et al., they found a median PSI value of 2.0% among 620 healthy individuals with variation between age and sex [Citation42]. We used a cut-off of 20% and only patients with visible dysfunction were included, thus physiologic PSS should not affect our results. We used MR and categorized viable segments as segments with volume fraction >50% scar. A change in this cut-off would affect the accuracy [Citation44].
Limitations
The acquisitions were mostly from the scanner Vivid 7(69%). Newer scanners are now available and have both better image quality and frame rates. Good image quality and high frame rate are essential in accurate deformation analysis, especially when it comes to PSS. More studies, especially with modern scanners with good image quality and high frame rate are needed to fully understand both mechanisms, assessment, and implications of PSS. The LGE-CMR is quantitatively analyzed by an older software (Segment v1.7). New and improved algorithms for the quantification of scar is now available [Citation45]. Additionally, the CMR only included the late enhancement protocol, other myocardial injuries (e.g. stunning, edema) could potentially impact myocardial wall function, although the systolic function mostly recovers a few days after myocardial infarction [Citation36,Citation46–49]. We have categorized the segments using cut-off values. The cut-off values are not well established and there is no global consensus, furthermore, the values were applied to each segment and not globally which obviously can affect the results. The segments are compared to a reference method (LGE-CMR), therefore we can calculate sensitivity, specificity and predictive values. Still, the segments within each patient are statistically dependent, and other statistical tests could be considered. Aiming to reduce the interference of noise, poor image quality and physiologic PSS in healthy segments, we only included examinations with obviously visible dysfunction. Consequently, the final study population was small, and few segments had PSS. The exclusion of examinations with no or little visible dysfunction may potentially favor WMS.
Conclusion
Segmental viability was moderately detected by the presence of systolic function quantified by the echocardiographic measurements of wall motion score, peak strain or strain rate. Post-systolic shortening added no value to the assessment of segmental myocardial viability.
Disclosure statement
The authors have no relevant financial or non-financial competing interests to declare.
Data availability statement
Data not available due to ethical restrictions.
Additional information
Funding
References
- Allman KC. Noninvasive assessment myocardial viability: current status and future directions. J Nucl Cardiol. 2013; 20(4):618–637.
- Neumann F-J, Sousa-Uva M, Ahlsson A, et al. 2018 ESC/EACTS guidelines on myocardial revascularization. Eur Heart J. 2019;40(2):87–165.
- Altiok E, Tiemann S, Becker M, et al. Myocardial deformation imaging by two-dimensional speckle-tracking echocardiography for prediction of global and segmental functional changes after acute myocardial infarction: a comparison with late gadolinium enhancement cardiac magnetic resonance. J Am Soc Echocardiogr. 2014; 27(3):249–257.
- Gjesdal O, Helle-Valle T, Hopp E, et al. 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. 2008; Nov1(3):189–196.
- Mollema SA, Delgado V, Bertini M, et al. Viability assessment with global left ventricular longitudinal strain predicts recovery of left ventricular function after acute myocardial infarction. Circ Cardiovasc Imaging. 2010;3(1):15–23.
- Heimdal A, Stoylen A, Torp H, et al. Real-time strain rate imaging of the left ventricle by ultrasound. J Am Soc Echocardiogr. 1998; 11(11):1013–1019.
- Stoylen A, Heimdal A, Bjornstad K, et al. Strain rate imaging by ultrasound in the diagnosis of regional dysfunction of the left ventricle. Echocardiography. 1999;16(4):321–329.
- Stoylen A, Heimdal A, Bjornstad K, et al. Strain rate imaging by ultrasonography in the diagnosis of coronary artery disease. J Am Soc Echocardiogr. 2000;13(12):1053–1064.
- Bohs LN, Trahey GE. A novel method for angle independent ultrasonic imaging of blood flow and tissue motion. IEEE Trans Biomed Eng. 1991;38(3):280–286.
- Modesto KM, Cauduro S, Dispenzieri A, et al. Two-dimensional acoustic pattern derived strain parameters closely correlate with one-dimensional tissue doppler derived strain measurements. Eur J Echocardiogr. 2006;7(4):315–321.
- Tennant R, Wiggers CJ. The effect OF coronary occlusion ON myocardial contraction. Washington: American Journal of Physiology; 1935.
- Ingul CB, Stoylen A, Slordahl SA. Recovery of stunned myocardium in acute myocardial infarction quantified by strain rate imaging: a clinical study. J Am Soc Echocardiogr. 2005; 18(5):401–410.
- Lyseggen E, Skulstad H, Helle-Valle T, et al. Myocardial strain analysis in acute coronary occlusion: a tool to assess myocardial viability and reperfusion. Circulation. 2005; 20112(25):3901–3910.
- Skulstad H, Edvardsen T, Urheim S, et al. Postsystolic shortening in ischemic myocardium: active contraction or passive recoil? Circulation. 2002;106(6):718–724. 6
- Celutkiene J, Sutherland GR, Laucevicius A, et al. Is post-systolic motion the optimal ultrasound parameter to detect induced ischaemia during dobutamine stress echocardiography? Eur Heart J. 2004;25(11):932–942.
- Kukulski T, Jamal F, Herbots L, et al. Identification of acutely ischemic myocardium using ultrasonic strain measurements. A clinical study in patients undergoing coronary angioplasty. J Am Coll Cardiol. 2003;41(5):810–819.
- Voigt JU, Exner B, Schmiedehausen K, et al. Strain-rate imaging during dobutamine stress echocardiography provides objective evidence of inducible ischemia. Circulation. 2003; 29107(16):2120–2126.
- Eek C, Grenne B, Brunvand H, et al. Postsystolic shortening is a strong predictor of recovery of systolic function in patients with non-ST-elevation myocardial infarction. Eur J Echocardiogr. 2011;12(7):483–489.
- Hosokawa H, Sheehan FH, Suzuki T. Measurement of postsystolic shortening to assess viability and predict recovery of left ventricular function after acute myocardial infarction. J Am Coll Cardiol. 2000;35(7):1842–1849.
- Song JK, Song JM, Kang DH, et al. Postsystolic thickening detected by doppler myocardial imaging: a marker of viability or ischemia in patients with myocardial infarction. Clin Cardiol. 2004; 27(1):29–32.
- Yang HS, Kang SJ, Song JK, et al. Diagnosis of viable myocardium using velocity data of doppler myocardial imaging: comparison with positron emission tomography. J Am Soc Echocardiogr. 2004;17(9):933–940.
- Hanekom L, Jenkins C, Jeffries L, et al. Incremental value of strain rate analysis as an adjunct to wall-motion scoring for assessment of myocardial viability by dobutamine echocardiography: a follow-up study after revascularization. Circulation. 2005;112(25):3892–3900.
- Lim P, Pasquet A, Gerber B, et al. Is postsystolic shortening a marker of viability in chronic left ventricular ischemic dysfunction? Comparison with late enhancement contrast magnetic resonance imaging. J Am Soc Echocardiogr. 2008; 21(5):452–457.
- Hundley WG, Bluemke DA, Finn JP, et al. ACCF/ACR/AHA/NASCI/SCMR 2010 expert consensus document on cardiovascular magnetic resonance: a report of the American college of cardiology foundation task force on expert consensus documents [conference paper]. Circulation. 2010;121(22):2462–2508.
- Leiner T, Bogaert J, Friedrich MG, SCMR Position Paper, et al. On clinical indications for cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2020;22(1):76. 2020 2020/11/09
- Thorstensen A, Amundsen BH, Dalen H, et al. Strain rate imaging combined with wall motion analysis gives incremental value in direct quantification of myocardial infarct size. Eur Heart J Cardiovasc Imaging. 2012;13(11):914–921.
- Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American society of echocardiography and the European association of cardiovascular imaging. J Am Soc Echocardiogr. 2015;28(1):1–39 e14. Jan
- Brainin P, Hoffmann S, Fritz-Hansen T, et al. Usefulness of postsystolic shortening to diagnose coronary artery disease and predict future cardiovascular events in stable angina pectoris. J Am Soc Echocardiogr. 2018;31(8):870–879 e3. Aug
- Voigt JU, Lindenmeier G, Exner B, et al. Incidence and characteristics of segmental postsystolic longitudinal shortening in normal, acutely ischemic, and scarred myocardium. J Am Soc Echocardiogr. 2003;16(5):415–423.
- Kim RJ, Wu E, Rafael A, et al. The use of contrast-enhanced magnetic resonance imaging to identify reversible myocardial dysfunction. N Engl J Med. 2000;343(20):1445–1453.
- Thiele H, Kappl MJ, Linke A, et al. Influence of time-to-treatment, TIMI-flow grades, and ST-segment resolution on infarct size and infarct transmurality as assessed by delayed enhancement magnetic resonance imaging. Eur Heart J. 2007;28(12):1433–1439. Jun
- Møller JE, Hillis GS, Oh JK, et al. Wall motion score index and ejection fraction for risk stratification after acute myocardial infarction. Am Heart J. 2006;151(2):419–425.
- Bansal M, Jeffriess L, Leano R, et al. Assessment of myocardial viability at dobutamine echocardiography by deformation analysis using tissue velocity and speckle-tracking. JACC Cardiovasc Imaging. 2010;3(2):121–131.
- Eek C, Grenne B, Brunvand H, et al. Strain echocardiography and wall motion score index predicts final infarct size in patients with non-ST-segment-elevation myocardial infarction. Circ Cardiovasc Imaging. 2010;3(2):187–194.
- Asanuma T, Nakatani S. Myocardial ischaemia and post-systolic shortening. Heart. 2015; 101(7):509–516.
- Ingul CB, Malm S, Refsdal E, et al. Recovery of function after acute myocardial infarction evaluated by tissue Doppler strain and strain rate. J Am Soc Echocardiogr. 2010;23(4):432–438. Apr
- Claus P, Weidemann F, Dommke C, et al. Mechanisms of postsystolic thickening in ischemic myocardium: mathematical modelling and comparison with experimental ischemic substrates. Ultrasound Med Biol. 2007;33(12):1963–1970.
- Brutsaert DL, Rademakers FE, Sys SU. Triple control of relaxation: implications in cardiac disease. Circulation. 1984;69(1):190–196.
- Weidemann F, Dommke C, Bijnens B, et al. Defining the transmurality of a chronic myocardial infarction by ultrasonic strain-rate imaging: implications for identifying intramural viability: an experimental study. Circulation. 2003; 107(6):883–888.
- Terkelsen CJ, Poulsen SH, Norgaard BL, et al. Does postsystolic motion or shortening predict recovery of myocardial function after primary percutanous coronary intervention? J Am Soc Echocardiogr. 2007; May20(5):505–511.
- Brainin P, Haahr-Pedersen S, Sengelov M, et al. Presence of post-systolic shortening is an independent predictor of heart failure in patients following ST-segment elevation myocardial infarction. Int J Cardiovasc Imaging. 2018; 34(5):751–760.
- Brainin P, Biering-Sørensen SR, Møgelvang R, et al. Post-systolic shortening: normal values and association with validated echocardiographic and invasive measures of cardiac function. Int J Cardiovasc Imaging. 2019; 35(2):327–337.
- Voigt JU, Nixdorff U, Bogdan R, et al. Comparison of deformation imaging and velocity imaging for detecting regional inducible ischaemia during dobutamine stress echocardiography. Eur Heart J. 2004;25(17):1517–1525.
- Shah BN, Khattar RS, Senior R. The hibernating myocardium: current concepts, diagnostic dilemmas, and clinical challenges in the post-STICH era. Eur Heart J. 2013; 34(18):1323–1336.
- Engblom H, Tufvesson J, Jablonowski R, et al. A new automatic algorithm for quantification of myocardial infarction imaged by late gadolinium enhancement cardiovascular magnetic resonance: experimental validation and comparison to expert delineations in multi-center, multi-vendor patient data. J Cardiovasc Magn Reson. 2016; 18(1):27.
- Bolli R. Basic and clinical aspects of myocardial stunning. Prog Cardiovasc Dis. 1998;40(6):477–516.
- Weidemann F, Wacker C, Rauch A, et al. Sequential changes of myocardial function during acute myocardial infarction, in the early and chronic phase after coronary intervention described by ultrasonic strain rate imaging. J Am Soc Echocardiogr. 2006; 19(7):839–847.
- Ripa RS, Nilsson JC, Wang Y, et al. Short- and long-term changes in myocardial function, morphology, edema, and infarct mass after ST-segment elevation myocardial infarction evaluated by serial magnetic resonance imaging. Am Heart J. 2007;154(5):929–936.
- Carlsson M, Ubachs JFA, Hedström E, et al. Myocardium at risk After acute infarction in humans on cardiac magnetic resonance: quantitative assessment during follow-up and validation with single-photon emission computed tomography. JACC Cardiovasc Imaging. 2009; 2(5):569–576.