|Year : 2019 | Volume
| Issue : 2 | Page : 45-52
Recovery of left ventricular twist and left ventricular untwist rate in patients with ST-segment elevation acute myocardial infarction
Department of Noninvasive Functional Diagnostics and Imaging, University National Heart Hospital, Sofia, Bulgaria
|Date of Web Publication||29-Aug-2019|
Department of Noninvasive Diagnostic Imaging, National Heart Hospital, Sofia 1309
Source of Support: None, Conflict of Interest: None
Background: Left ventricular (LV) functional recovery and morphological remodeling after acute myocardial infarction (AMI) followed by reperfusion remain incompletely understood. The aim of the study was to describe the recovery of LV twist (LVT) and LV untwist rate (LVUR) upon revascularization after AMI using two-dimensional (2D) speckle tracking. Methods: We evaluated 88 subjects: 22 normal volunteers (mean age 31 ± 5 years), and 66 patients with AMI (mean age 65 ± 12 years), of which 40 had an inferior AMI and 26 an anterior one. All AMI patients had ST-segment elevation. Echocardiography was performed in all subjects. Patients were scanned within 36 h (baseline) after revascularization (percutaneous coronary intervention) and after 4 months (4 mFU). Apical and basal short-axis images were acquired (frame rate 67 ± 5 frames/s) and analyzed offline to extract the rotation (rate) curves. From these, maximal systolic LVT and peak LVUR were derived. Finally, the infarct size (IS) was estimated based on magnetic resonance imaging delayed enhancement and expressed as a percentage of the total LV volume. Results: At 36 h, LVT and LVUR were significantly reduced in both AMI groups when compared to normals. At 4 mFU, both AMI groups showed recovery in ejection fraction (EF) and reduction in IS (7.24 ± 10.07 vs. 20.13 ± 13.9, P < 0.0001 for inferior AMI and 13.13 ± 10.3 vs. 24.40 ± 15, P < 0.0001 for anterior AMI). LVT and LVUR increased significantly but remained below normal levels. Correlation of LVT and LVUR with IS was significant, but weak (r = 0.34 and r = 0.34, respectively). In addition, a fair correlation of LVT with EF (r = 0.64) and a weak correlation of LVUR with end-diastolic volume (r = 0.43) were found. Conclusion: LVT and LVUR are reduced in AMI patients early after reperfusion and recover incompletely upon follow-up. Interestingly, recovery of LVT characteristics as measured with this 2D speckle tracking-based method showed to be independent of infarct location or extent. LVT and LVUR might be good parameters to monitor the recovery of global LV function after treatment.
Keywords: Acute myocardial infarction, echocardiography, left ventricle function, twist, untwist rate
|How to cite this article:|
Hristova K. Recovery of left ventricular twist and left ventricular untwist rate in patients with ST-segment elevation acute myocardial infarction. J Indian Acad Echocardiogr Cardiovasc Imaging 2019;3:45-52
|How to cite this URL:|
Hristova K. Recovery of left ventricular twist and left ventricular untwist rate in patients with ST-segment elevation acute myocardial infarction. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2019 [cited 2019 Sep 15];3:45-52. Available from: http://www.jiaecho.org/text.asp?2019/3/2/45/265751
| Introduction|| |
Left ventricular (LV) functional recovery and morphological remodeling after acute myocardial infarction (AMI) followed by reperfusion remain incompletely understood.
The assessment of the changes of LV function in patients with AMI and undergoing percutaneous coronary intervention (PCI) has been previously described as very important for prognosis and therapy. Infarct size (IS) has been considered an established marker of LV remodeling.
The twisting motion of the left ventricle about its long axis results from the contraction of the obliquely oriented epicardial and endocardial fibers. Twist during systole and untwist during diastole play an important role in assessing the systolic and diastolic LV function. LV twist (LVT) generates positive torsional deformation forces developing in the subepicardium, added to the negative torsional deformation forces in the subendocardium. As is well known, counterclockwise LVT viewed from the apex toward the base develops during ejection, thus representing the systolic shortening of the myofibers across the LV wall. Near the end of systole, the rapid clockwise recoil of twist or untwisting begins to develop, which occurs during the isovolumetric relaxation and early diastolic filling.,
In the assessment of LV contractile function after AMI, LVT and LV untwist rate (LVUR) may provide information about extent and nature of LV remodeling and dysfunction. Recently, speckle-tracking echocardiography has become a simple echocardiographic method for assessment of LVT and LVUR. This technique has been validated against sonomicrometry and magnetic resonance imaging (MRI), which are currently considered the gold standard for assessment of rotational parameters.,,
In the last few years, a few studies evaluated LVT and LVUR in patients with myocardial infarction (MI).,,,,, However, prospectively to investigate the influence of transmural necrosis, infarct size (IS) and effect of regional myocardial injuries on rotational mechanics have never been systematically evaluated.
In the present study, we described the recovery of LVT and LVUR on revascularization after AMI in two groups of patients (with anterior and inferior AMI) in acute phase, up to 4 months' follow-up, using two-dimensional (2D) speckle tracking.
| Methods|| |
We assessed LVT and LVUR in 88 individuals: 22 healthy volunteers (mean age 31 years ± 5) with no history of cardiovascular or other congenital diseases and 66 patients with ST-elevation AMI (mean age 65 years ± 12).
Of these, 40 patients had inferior AMI (mean age) and 26 patients (mean age) had anterior AMI with ST-elevation on the electrocardiogram (ECG), matching the location of the infarction. Diagnosis of AMI was based on the presence of symptoms consistent with myocardial ischemia, ST-segment elevation in ≥2 contiguous ECG leads, and positive biomarkers for myocardial ischemia. All patients with AMI underwent urgent coronary angiography, followed by primary PCI.
Echocardiography was performed in the supine position, using a commercial ultrasound machines Vivid 7 and a 2.5 MHz M3S probe (GE Vingmed Ultrasound Horten, Norway) in all individuals.
Patients were scanned within 36 h (baseline) after revascularization (PCI) and after 4 months (4 mFU).
LV volumes and LV ejection fraction (EF) were calculated from apical 2- and 4-chamber view, using Simpson's method.
Apical and basal short-axis images were acquired at high frame rates (frame rate 67 ± 5 frames/s). Care was taken to ensure that the basal short-axis level contained the mitral valve, and the apical level was acquired distal to the papillary muscles. At each plane, three consecutive cardiac cycles were acquired during breath-hold and digitally stored for offline analysis. Pulse wave Doppler examination of the mitral inflow and LV outflow were used for the determination of timing of cardiac events.
Measurement of rotation, twist and untwist rate
Rotation, LVT, and LVUR measurements were performed offline using 2D strain dedicated software package EchoPac (version 108.1.4, GE Vingmed, Horten, Norway).
Basal and apical short-axis images were used to extract the rotation (rate) curves. The endocardial border was manually traced at an end-systolic frame of each short axis. A region of interest then was chosen to fit the entire myocardium. The software allows each short-axis images to be automatically divided into six standard segments: anteroseptal, anterior, lateral, posterior, inferior, and septal. The speckle-tracking software calculated the LV rotation from the apical and basal short-axis images as the average angular displacement of the six standard segments, referring to LV, frame by frame. Counterclockwise rotation was marked as a positive value and clockwise rotation as negative value when viewed from the LV apex. The software automatically calculated LVT, defined as the net differences of apical and basal rotation in degrees. The opposite rotation after LVT was defined as LV untwist, and the time derived of LV untwist was defined as LVUR and calculated in degrees per second.
Identification of infarct size
In patients with an AMI, myocardial salvage is the hallmark of successful coronary intervention and results in long-term reestablishment myocardial contractile function.
The identification of infarction was based on an assessment of an area of delayed hyperenhancement from MRI images. All patients with AMI after PCI were examined with MRI for assessment of total myocardial scar volume and after 4 months were followed up.
The IS was expressed as percentage of the total myocardial volume (scar volume/myocardial volume ×100). We used 17 segments model of the LV, and the transmural extent of hyperenhancement was graded as a percentage of scar tissue in each segment: 0%, 1%–25%, 26%–50%, and 51%–75% (nontransmural) and 76%–100% (transmural). The number of LV segments with transmural necrosis was performed in percentage.
On the basis of the location of infarction, patients were categorized as having anterior AMI and inferior AMI.
Values are expressed as mean ± standard deviation or as percentages. Between-group comparisons were made using ANOVA one-way analysis of variances with Tukey's post hoc analysis for multiplay comparisons, using standard statistical software (Statistica 7.0, StatSoft. Inc., 2007, Dell Software, Texas, USA).
P < 0.05 in the two-tailed test was considered statistically significant.
Multivariable regression analysis was performed to determine the independent association of LVT and LVUR.
| Results|| |
The clinical and echocardiographic characteristics of all study participants are shown in [Table 1].
|Table 1: Clinical and echocardiographic characteristics of the study population|
Click here to view
Effect of revascularization of rotational and morphological parameters
[Table 2] presents the LV rotational parameters in the control group and two patient groups.
Compared with the normals, the patients in both groups with AMI in first 36 h had significantly lower values for LVT (12.28 ± 3.26 vs. 5.73 ± 2.43, anterior AMI/5.52 ± 2.41, inferior AMI, P < 0.0001) and for LVUR (−70.82 ± 24.03 vs. −38.99 ± 15.93, anterior AMI/−38.73 ± 15.61, inferior AMI, P < 0.0001).
In the first 36 h, mean IS for anterior AMI group was 24.40% ± 15% and for inferior was AMI 20.13% ± 13.9% of LV mass (P = 0.32). In the same time, the infarct transmurality extent of delayed enhancement was 28% for the anterior AMI group versus 22% for the inferior AMI group.
There were no differences for LVT and LVUR between patients with anterior and inferior AMI. Similar abnormalities were noted in the IS and infarct transmurality between the two AMI groups.
After 4 months' follow-up, the LVT and LVUR increased significantly in both groups, compared with the basal levels [Table 2]. Compared with controls, we did not find significant differences for LVT and LVUR, but the values remained below the values in the controls. There are no significant differences for LVT and LVUR between the anterior AMI and inferior AMI groups too [Figure 1].
|Figure 1: Comparison between left ventricular twist, left ventricular untwist rate at baseline and follow-up|
Click here to view
Four months after PCI, we found significant decrease of IS in both groups – for anterior AMI (13.13% ± 10.3%, P < 0.0001) and for inferior AMI (7.24% ± 10.07%, P < 0.0001). A transmurality, calculated as percentage of the number of LV segments, also was significantly decreased – up to 18% by anterior AMI group, P < 0.0001 and up to 11% by inferior AMI group, P < 0.0001 [Table 1].
When we compared both MI groups, there were no differences for IS (P = 0.29) and infarct transmurality (P = 0.16) after 4 months.
Correlation between left ventricular twist, left ventricular untwist rate, morphological, and functional parameters
In univariate regression analysis in patients with AMI, LVT and LVUR had significant correlation with EF, IS, LV mass, end-diastolic volume (EDV), stroke volume (SV), at baseline and after 4 months' follow-up.
Multivariate regression analysis in patients with AMI was performed to determine the independent predictors of LVT and LVUR. Among these variables, we found a strong correlation for LVT and EF (r = 0.62, P < 0.0001) [Figure 2], moderate correlation between LVUR and EDV (r = 0.43, P < 0.0001) [Figure 3] and between IS and LVT (r = 0.31, P < 0.05) and LVUR (r = 0.36, P < 0.05) as for baseline and after 4 months' follow-up [Figure 4].
|Figure 2: Correlation between left ventricular twist and ejection fraction (%)|
Click here to view
|Figure 3: Correlation between left ventricular untwist rate and end-diastolic volume (ml)|
Click here to view
|Figure 4: Correlation between infarct size and left ventricular twist and left ventricular untwist rate|
Click here to view
| Discussion|| |
The objective of this study was to evaluate the LVT and untwist rate in two different groups with patients having AMI and their recovery after revascularization and the relation between LV rotational mechanics with LV function. The main findings can be summarized as follows:
- LVT is strongly related to LV systolic function and LVUR is weakly related to diastolic function
- Impairment of LV function was associated with decreasing LVT, LVUR, IS and infarct volume, but the infarct location was not reflective of the global LV function.
Recently, more sensitive methods for the assessment of LV rotation in clinical practice have been applied. The accuracy of 2D speckle tracking for the measurement of LVT and LVUR has been validated in several previous studies.,
Systolic left ventricular twist and ischemia
LVT and torsion are not interchangeable because torsion represents twist normalized by the longitudinal axis of the LV. While the magnitude of the LVT is determined by contractile force. It has been suggested that measurement of LVT could be implemented as a clinical index of contractility and potentially become a sensitive marker of myocardial dysfunction.
Myocardial ischemia and infarction produced necrosis of the tissue and reflected in the geometric remodeling, accompanied with changes in contractile function of the LV. There are limited data concerning the impact of AMI on LVT, but the experimental and clinical part of those studies showed that systolic function is compromised and LVT is reduced.,,,,, Some of the studies are focused on site of the infarct – especially for left anterior descending territory region for anterior AMI , or right coronary artery for inferior AMI., Further confirmation of ischemia-driven reduction in systolic torsion was shown during coronary angioplasty balloon occlusion. Garot et al. studied patients within 24 h of MI and found similar results. Finally, Bansal et al. studied ischemic patients during the stress; they found reduced LV torsion in patients group with previous AMI; but, there were no differences for the global systolic torsion between the patients with anteroapical and inferoposterior infarct. In our study, we confirmed that LVT is reduced in patients with AMI. The strong significant correlation with EF [Figure 2] reflects that damages of any part of myofibers correlated with reducing of LV function and reducing of LVT. The systolic twist recovered after 4 months and was close to the healthy controls, but the values remained below normal possibly due to some segments being abnormal because of chronic MI. In the present study, there are no differences between anterior and inferior group AMI, and the results are in line with the results claimed from Park et al. This supports our finding's suggestions that LVT is a global property of the left ventricle.
Diastolic left ventricular untwist rate and ischemia
Notomi hypothesized that untwist during diastole is the consequence of elastic restoring forces accumulated during systole resulting from the complex interaction of torsional deformation. Nevertheless, this is a passive or active process, and where this elastic energy is stored remains a source of controversy. Importantly, this diastolic untwisting motion occurs predominantly during the isovolumetric relaxation and early diastolic filling of the left ventricle., Based on different studies,,, the assessment of LVUR can be used as a noninvasive index for LV relaxation. Most of the studies proved the effect of LVUR for assessment of the different stages of the diastolic dysfunction.,,,,,
There are limited studies, which focused on the LVUR and patient with AMI,,, but they all demonstrated that untwist rate is significantly lower and compared with grade of diastolic dysfunction. In patients with AMI, impairment in LVUR may be related to increased ventricular stiffness and consequent diastolic dysfunction due to recent acute ischemia and infarction.
The results that we found are consistent with the previous studies; LVUR significantly decreased in patients' group, compared with the normals, as there we did not find differences between the infarct site.
Four months after revascularization, an expected significant increase of the LVUR was found, but the values are below normals. The reason of this may be explained by the presence of extensive, diffuse LV fibrosis in patients with AMI,, or with impaired LV filling, even that EF is the normal range.
In the present study, a good relation between the LVUR and diastolic function was observed and we found moderate relation between the LVEDV and LVUR and a weak, but significant relation with changes in the SV [Figure 3].
LVUR is strongly related with diastolic function, and any changes in the volume loading decreased early diastolic untwisting.,,,,
Effect of infarct size, infarct location, and transmurality
The acute loss of myocardium results in remodeling involving the infarcted zone and remote noninfarcted myocardium, which may continue for weeks or months.,,,, Postinfarction ventricular remodeling is determined by the size, location, and transmurality of the infarct, the extent of the myocardial stunning, and the patency of the infarct-related artery. Coronary anatomy assumes differences between the anterior and inferior AMI, which could be contributed to different size of infarction as and different location along the human's heart.
Anterior wall MI is accompanied with larger region of wall motion abnormalities and ischemia.
In recent years, there are limited data concerned with the impact of MI and LVT and LVUR. Nagel et al. using tagged MRI data found severely compromised LV systolic function in patients with anterior AMI. Takeuchi et al. found that LV systolic torsion was significantly reduced in patients with anterior AMI and LV dysfunction, but torsion was normal in group with anterior AMI with preserved LV systolic function. In small study with patients with acute AMI Park et al. reported that there were no differences for LV torsion for anterior and inferior AMI groups. Nevertheless, the relative impact of infarct location and size on LVT and LVUR have not been reported. Some studies confirm that the size of the infarction can be the primary pathologic culprit, responsible for adverse LV remodeling. Smaller infarction resulted in lesser LV remodeling; larger infarction resulted in greater ventricular remodeling and LV dilatation, acute LV failure, arrhythmias, and sudden cardiac death. However, when studying the patients prospectively in both groups, we found that patients with anterior AMI have larger amount of hyperenhancement myocardium and larger percentage of segments with transmural infarction. Our results are in agreement with other studies that the patients with anterior AMI have a larger IS that inferior AMI group. The size of the infarct affected the amount of remaining contracting myocardium and thus may underlie the observed alteration of torsion and recoil that may result in increased gradients of oxygen demand and ventricular dysfunction. Injured myocardium in both patients group after 4 months' follow up was smaller than the initial, which reflected on the scar volume and LV remodeling, resulting in improvement of EF, EDV, ESV and SV. In our study, we did not find significant differences for the IS in both MI groups as in the baseline, as in after 4 months' follow up, and we did not find the differences for the LVT and LVUR between the anterior AMI group and inferior AMI group, as well. This finding likely reflects the role of LVT and LVUR as a global property of the left ventricle where the extent of damage to any part of the helical myofibers distribution affects the LV function.
This could be explained with adaptive response in the first 72 h after AMI, during the early remodeling,, when the infarct expansion causes deformation of the border zone and remote myocardium with early ventricular dilatation and increased wall stress being the major determinants of remodeled ventricle. This could explain the extreme decrease of the LVT and LVUR in both groups and no differences between different AMI location at baseline level.
The subepicardial fibers are the predominant source of LVT because they have a mechanical advantage over the subendocardial fibers (contributing to untwist).,,,, In the early stage of ischemia (30–50 s), the contribution of the endocardial untwisting force is reduced, and since the epicardial force is unchanged twist is increased. However, with progressing ischemia, the shortening of epicardial fibers decreases  and this notion is supported by our finding.
In phase of late remodeling (beyond 72 h), the process involves myocyte hypertrophy and alteration in ventricular architecture to distribute the increased wall stress, form a collagen scar to stabilize the distending forces and prevent future deformation. Several studies , demonstrated that the early revascularization reduced IS and was associated with improvement of later regional and global ventricular function. As was described, IS, location, and collateral flow determine the likelihood of late remodeling. In phase of late remodeling (in our study, 4 mFU), the LVT and LVUR have increased but remain below from values in control group. The improvement of the LV function reflects on the twist and untwisting and the reduction of the IS increased LVT and LVUR.
However, when studying the patients prospectively in both groups, we found that patients with anterior AMI have larger amount of hyperenhancement myocardium and larger percentage of segments with transmural infarction. Our results are consistent with other studies stating that the patients with anterior AMI have a larger IS than inferior AMI group.
Regional transmurality of hyperenhancement has been shown to affect the probability of regional functional recovery after acute infarction. More detailed analysis of the injured myocardium after 4 months in our study showed reduced abnormal myocardium represented as percentage of nontransmural and transmural segments to scar volume, which reflected in LV remodeling and improvement in LVT and LVUR.
EF is good predictor of LV dysfunction and cardiovascular events but cannot reveal all of LV remodeling.,, Therefore, more precise predictor may be possible when IS and presence on transmurality can be considered. In our study, EF was negatively correlated with IS%, so even small infarct had a negative impact on global LV function [Figure 5].
There are certain limitations inherent to the technique of 2D speckle-tracking itself, such as high-quality recordings, high-tracking quality, and correct recognition of anatomic structures to identify the basal and short axis levels. Our results were obtained using the highest frame rate, that allows accurate tracking; retracing and repositioning the regions of interest was done as needed.
The control group was younger than patients group, but as Takeuchi and others reported LVT increased with advanced age and LVUR decreased.,,, Furthermore, when considering age-related changes for LVT/LVUR, we did not find significant differences between normal and patients group after 4 months of follow-up.
| Conclusion|| |
LVT and LVUR have been investigated with different measurement methods during the past two decades, using cardiac magnetic resonance as the gold standard. The results obtained over the years are helpful for developing a standardized method to quantify LVT and have facilitated the interpretation and value of LVT before it can be used as a clinical tool.
The measurement of LVT and untwist rate in patient with AMI and early after reperfusion is feasible in a few studies, but they do not provide prospectively information.
LVT and LVUR are reduced in AMI patients early after reperfusion and recover incompletely on follow-up. LVT and LVUR might be used as a marker for IS and postmyocardial remodeling. The recovery of LVT characteristics as measured with this 2D speckle-tracking-based method showed to be independent of infarct location or extent.
LVT and LVUR might be good parameters to monitor the recovery of global LV function after treatment. This fast, widely available technique may contribute to a more rapid introduction of LVT/LVUR as a clinical tool for the detection of myocardial dysfunction.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Tarantini G, Razzolini R, Cacciavillani L, Bilato C, Sarais C, Corbetti F, et al.
Influence of transmurality, infarct size, and severe microvascular obstruction on left ventricular remodeling and function after primary coronary angioplasty. Am J Cardiol 2006;98:1033-40.
Takeuchi M, Otsuji Y, Lang RM. Evaluation of left ventricular function using left ventricular twist and torsion parameters. Curr Cardiol Rep 2009;11:225-30.
Sengupta PP, Tajik AJ, Chandrasekaran K, Khandheria BK. Twist mechanics of the left ventricle: Principles and application. JACC Cardiovasc Imaging 2008;1:366-76.
Sengupta PP, Khandheria BK, Narula J. Twist and untwist mechanics of the left ventricle. Heart Fail Clin 2008;4:315-24.
Tibayan F, Rodriguez F, Langer F, Zasio M, Bailey L, Liang D, et al
. Alteration in left ventricular torsion and diastolic recoil after myocardial infarction with and without chronic ischemic mitral regurgitation. Circulation 2004;110;109-14.
Helle-Valle T, Crosby J, Edvardsen T, Lyseggen E, Amundsen BH, Smith HJ, et al.
New noninvasive method for assessment of left ventricular rotation: Speckle tracking echocardiography. Circulation 2005;112:3149-56.
Notomi Y, Lysyansky P, Setser RM, Shiota T, Popović ZB, Martin-Miklovic MG, et al.
Measurement of ventricular torsion by two-dimensional ultrasound speckle tracking imaging. J Am Coll Cardiol 2005;45:2034-41.
Garot J, Pascal O, Diébold B, Derumeaux G, Gerber BL, Dubois-Randé JL, et al.
Alterations of systolic left ventricular twist after acute myocardial infarction. Am J Physiol Heart Circ Physiol 2002;282:H357-62.
Bansal M, Leano RL, Marwick TH. Clinical assessment of left ventricular systolic torsion: Effects of myocardial infarction and ischemia. J Am Soc Echocardiogr 2008;21:887-94.
Takeuchi M, Nishikage T, Nakai H, Kokumai M, Otani S, Lang RM, et al.
The assessment of left ventricular twist in anterior wall myocardial infarction using two-dimensional speckle tracking imaging. J Am Soc Echocardiogr 2007;20:36-44.
Bertini M, Nucifora G, Marsan NA, Delgado V, van Bommel RJ, Boriani G, et al.
Left ventricular rotational mechanics in acute myocardial infarction and in chronic (ischemic and nonischemic) heart failure patients. Am J Cardiol 2009;103:1506-12.
Han W, Xie MX, Wang XF, Lü Q, Wang J, Zhang L, et al.
Assessment of left ventricular torsion in patients with anterior wall myocardial infarction before and after revascularization using speckle tracking imaging. Chin Med J (Engl) 2008;121:1543-8.
Nagel E, Stuber M, Lakatos M, Scheidegger MB, Boesiger P, Hess OM, et al.
Cardiac rotation and relaxation after anterolateral myocardial infarction. Coron Artery Dis 2000;11:261-7.
Notomi Y, Setser RM, Shiota T, Martin-Miklovic MG, Weaver JA, Popović ZB, et al.
Assessment of left ventricular torsional deformation by Doppler tissue imaging: Validation study with tagged magnetic resonance imaging. Circulation 2005;111:1141-7.
Buchalter MB, Rademakers FE, Weiss JL, Rogers WJ, Weisfeldt ML, Shapiro EP, et al.
Rotational deformation of the canine left ventricle measured by magnetic resonance tagging: Effects of catecholamines, ischaemia, and pacing. Cardiovasc Res 1994;28:629-35.
Kroeker CA, Tyberg JV, Beyar R. Effects of ischemia on left ventricular apex rotation. An experimental study in anesthetized dogs. Circulation 1995;92:3539-48.
Park S, Kim YH, Hong SJ, Lim DS, Shim WJ. Different impact of anterior and inferior myocardial infarction on left ventricular torsion. Eur J Echocardiogr 2008;937:116-7.
Cimino S, Agati L, Lucisano L, Mancone M, Petronilli V, Cicogna F, et al
. Value of two-dimensional longitudinal strains analysis to assess the impact of thrombus aspiration during primary percutaneous coronary intervention on left ventricular function: A speckle trackingimaging substudy of the EXPIRA trial. Echocardiography 2014;31:842-7.
Knudtson ML, Galbraith PD, Hildebrand KL, Tyberg JV, Beyar R. Dynamics of left ventricular apex rotation during angioplasty: A sensitive index of ischemic dysfunction. Circulation 1997;96:801-8.
Opdahl A, Helle-Valle T, Remme EW, Vartdal T, Pettersen E, Lunde K, et al.
Apical rotation by speckle tracking echocardiography: A simplified bedside index of left ventricular twist. J Am Soc Echocardiogr 2008;21:1121-8.
Park SJ, Miyazaki C, Bruce CJ, Ommen S, Miller FA, Oh JK. Left ventricular torsion by two-dimensional speckle tracking echocardiography in patients with diastolic dysfunction and normal ejection fraction. J Am Soc Echocardiogr 2008;21:1129-37.
Ashikaga H, Criscione JC, Omens JH, Covell JW, Ingels NB Jr. Transmural left ventricular mechanics underlying torsional recoil during relaxation. Am J Physiol Heart Circ Physiol 2004;286:H640-7.
Notomi Y, Popovic ZB, Yamada H, Wallick DW, Martin MG, Oryszak SJ, et al.
Ventricular untwisting: A temporal link between left ventricular relaxation and suction. Am J Physiol Heart Circ Physiol 2008;294:H505-13.
Wang J, Khoury DS, Yue Y, Torre-Amione G, Nagueh SF. Left ventricular untwisting rate by speckle tracking echocardiography. Circulation 2007;116:2580-6.
Dong SJ, Hees PS, Siu CO, Weiss JL, Shapiro EP. MRI assessment of LV relaxation by untwisting rate: A new isovolumic phase measure of tau. Am J Physiol Heart Circ Physiol 2001;281:H2002-9.
Takeuchi M, Borden WB, Nakai H, Nishikage T, Kokumai M, Nagakura T, et al.
Reduced and delayed untwisting of the left ventricle in patients with hypertension and left ventricular hypertrophy: A study using two-dimensional speckle tracking imaging. Eur Heart J 2007;28:2756-62.
Saito M, Okayama H, Nishimura K, Ogimoto A, Ohtsuka T, Inoue K, et al.
Determinants of left ventricular untwisting behaviour in patients with dilated cardiomyopathy: Analysis by two-dimensional speckle tracking. Heart 2009;95:290-6.
Esch BT, Warburton DE. Left ventricular torsion and recoil: Implications for exercise performance and cardiovascular disease. J Appl Physiol (1985) 2009;106:362-9.
Foster E, Lease KE. New untwist on diastole: What goes around comes back. Circulation 2006;113:2477-9.
Weber KT. Extracellular matrix remodeling in heart failure: A role for de novo
angiotensin II generation. Circulation 1997;96:4065-82.
Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: Pathophysiology and therapy. Circulation 2000;101:2981-8.
Moon MR, Ingels NB Jr, Daughters GT 2nd, Stinson EB, Hansen DE, Miller DC. Alterations in left ventricular twist mechanics with inotropic stimulation and volume loading in human subjects. Circulation. 1994;89:142-50.
Hahn JY, Song YB, Gwon HC, Choe YH, Kim JH, Sung J, et al.
Relation of left ventricular infarct transmurality and infarct size after primary percutaneous coronary angioplasty to time from symptom onset to balloon inflation. Am J Cardiol 2008;102:1163-9.
Yokota H, Heidary S, Katikireddy CK, Nguyen P, Pauly JM, McConnell MV, et al.
Quantitative characterization of myocardial infarction by cardiovascular magnetic resonance predicts future cardiovascular events in patients with ischemic cardiomyopathy. J Cardiovasc Magn Reson 2008;10:17.
Bogaert J, Bosmans H, Maes A, Suetens P, Marchal G, Rademakers FE. Remote myocardial dysfunction after acute anterior myocardial infarction: Impact of left ventricular shape on regional function: A magnetic resonance myocardial tagging study. J Am Coll Cardiol 2000;35:1525-34.
Engblom H, Hedström E, Heiberg E, Wagner GS, Pahlm O, Arheden H, et al
. Rapid initial reduction of hyperenhanced myocardium after reperfused first myocardial infarction suggests recovery of the peri-infarction zone: One-year follow-up by MRI. Circ Cardiovasc Imaging 2009;2:47-55.
Takeuchi M, Nakai H, Kokumai M, Nishikage T, Otani S, Lang RM. Age-related changes in left ventricular twist assessed by two-dimensional speckle-tracking imaging. J Am Soc Echocardiogr 2006;19:1077-84.
Nakai H, Takeuchi M, Nishikage T, Kokumai M, Otani S, Lang RM. Effect of aging on twist-displacement loop by 2-dimensional speckle tracking imaging. J Am Soc Echocardiogr 2006;19:880-5.
Kim HK, Sohn DW, Lee SE, Choi SY, Park JS, Kim YJ, et al.
Assessment of left ventricular rotation and torsion with two-dimensional speckle tracking echocardiography. J Am Soc Echocardiogr 2007;20:45-53.
McKay RG, Pfeffer MA, Pasternak RC, Markis JE, Come PC, Nakao S, et al.
Left ventricular remodeling after myocardial infarction: A corollary to infarct expansion. Circulation 1986;74:693-702.
Marino P, Zanolla L, Zardini P; Gruppo Italian Per lo Studio Della Streptochinasi Nell'Infarto Miocardico. Effect of streptokinase on left venricular remodelling and function after myocardial infarction: the GISSI trial. JACC 1989;14:1149-58.
Ndrepepa G, Mehilli J, Martinoff S, Schwaiger M, Schömig A, Kastrati A. Evolution of left ventricular ejection fraction and its relationship to infarct size after acute myocardial infarction. J Am Coll Cardiol 2007;50:149-56.
De Bruyne B, Heyndrickx GR. Changes in infarct size and left ventricular ejection fraction: New prognostic factors after acute myocardial infarction? J Am Coll Cardiol 2007;50:157-8.
Ross J. Is there a true increase in myocardial stiffness with acute ischemia? Am J Cardiol 1989;63:87-91.
Prinzen FW, Arts T, van der Vusse GJ, Reneman RS. Fiber shortening in the inner layers of the left ventricular wall as assessed from epicardial deformation during normoxia and ischemia. J Biomech 1984;17:801-11.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2]