Author + information
- Received June 22, 2015
- Revision received September 30, 2015
- Accepted October 8, 2015
- Published online December 1, 2015.
- ∗Menzies Institute for Medical Research, University of Tasmania, Hobart, Australia
- †Department of Cardiovascular Sciences, KU Leuven, Leuven, Belgium
- ↵∗Reprint requests and correspondence:
Dr. Thomas H. Marwick, Menzies Institute for Medical Research, 17 Liverpool Street, Hobart, Tasmania 7000, Australia.
The outcomes associated with heart failure after myocardial infarction are still poor. Both global and regional left ventricular (LV) remodeling are associated with the progression of the post-infarct patient to heart failure, but although global remodeling can be accurately measured, regional LV remodeling has been more difficult to investigate. Preliminary evidence suggests that post-MI assessment of LV mechanics using stress and strain may predict global (and possibly regional) LV remodeling. A method of predicting both global and regional LV remodeling might facilitate earlier, targeted, and more extensive clinical intervention in those most likely to benefit from novel interventions such as cell therapy.
- ischemic heart disease
- left ventricular curvature
- left ventricular mechanics
- left ventricular remodeling
- left ventricular strain
- left ventricular wall stress
Myocardial Infarction and Heart Failure
After myocardial infarction (MI), patients continue to experience increased long-term mortality related to heart failure (HF). The prelude to this is progressive left ventricular remodeling (LVr), a process of infarct expansion, eccentric hypertrophy, and left ventricular (LV) volume expansion over a period of months to years, which may be regional or global and may occur early (within the first 3 days post-MI) or late. As the prognosis of HF is poor, attenuating the process of LVr is a priority, and angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, β-blockers, and mineralocorticoid receptor antagonists have proven effective. Unfortunately, despite the widespread use of these agents in the post-MI population, a significant proportion of post-MI patients still develop HF.
Although global LV dilation is a well-recognized form of LVr, less emphasis has been placed on regional LVr, despite its role as a sensitive marker of HF risk (1). Disturbances of LV geometry in ischemic heart disease are associated with outcome, independent of global LVr (1), and regional LVr may contribute to this prognostic effect (2). The ability to predict or track regional LVr post-MI (Figure 1) may facilitate the detection and follow-up of the highest-risk patients and guide selection for the eventual development of specific interventions including cell therapy.
Pathophysiology of LVr
A number of factors have been associated with global LVr post-MI, including older age, high body mass index, anterior infarction (which is probably a surrogate of infarct size) and high brain natriuretic peptide. The biological mechanisms responsible for the development of LVr post-MI include cellular, humoral, and LV mechanics-based pathways.
The cellular contributors to LVr involve the inflammatory response associated with MI, as well as changes in adrenergic activation and the aberrant stimulation of the renin-angiotensin-aldosterone system (3). Pro-inflammatory molecules are released from ischemic myocardium, which are chemo-attractive to proinflammatory cells such as macrophages and neutrophils. These cells are involved in apoptosis, phagocytosis, production of reactive oxygen species, and collagen deposition. Myocyte death and collagen deposition in the perivascular space are cardinal features of LVr (3).
Prolonged periods of increased sympathetic activity post-MI have been associated with an increase in cell death, release of pro-inflammatory cytokines, and impaired contractility. Similarly, ACE and angiotensin (AT) are produced from both the infarcted and remote myocardium by inflammatory and endothelial cells, with the greatest concentration of AT and ACE in the infarct zone. The consequent release of AT2 and aldosterone mediate hypertrophy, apoptosis, and fibrosis, all of which are contributors to LVr. Systemic activation of the renin-angiotensin-aldosterone system leads to volume overload and exacerbates LVr by increasing wall stretch (3,4).
Alterations in the mechanisms of gross and regional LV contraction after infarction are now recognized as important contributors to progressive LVr (5). Two important components of LV mechanics are LV strain and LV wall stress, which share common directional considerations (Figure 2).
LV wall stress is defined as the magnitude and direction of force within the LV wall per unit cross-sectional area (Figure 3). LV wall tension describes the cumulative force within the myocardium that resists LV cavity dilation and develops LV pressure: it is, hence, closely related to LV afterload (6). Myocardial tension arises from contractile fibers generating this force, together with a contribution from interstitial tissues. Although tension in healthy myocardium likely encompasses both active and passive components, tension in infarcted myocardium is completely passive. LV wall stress is proportionate to LV wall tension and inversely proportionate to LV wall thickness. Compensated LV dilation after MI stretches the remaining cardiac myofibers and may maintain wall tension independent of changes in contractility. As tension within the myocardium is predominately generated within the contractile fibers, it is likely that the direction of stress changes from endocardium through to epicardium—although the clinical relevance of this remains unclear. Regardless, disturbances of LV wall stress likely forms part of a feedback cycle responsible for progressive LVr and the eventual manifestation of overt HF post-MI (7). In the immediate post-infarct period, the relationship between LV wall tension and volume may change, due to an inability of the infarcted myocardial region to resist changes in pressure, probably due to myocyte slippage. This may explain initial infarct dilation, and is supported by evidence of impaired LV compliance post-MI (8). The resulting increase in systolic LV wall stress has been used to explain the early thickening of remote LV segments post-MI (9).
LV pressure represents the force of blood on the myocardium, and therefore influences LV wall tension. Pressure overload implies a higher systolic wall tension and stress, and is a stimulus to the development of concentric LV hypertrophy. However, consideration of LV wall stress should not be confined to systole, and may also be assessed in diastole (10). Increased LV volume may imply an increased diastolic LV wall tension and stress, resulting in eccentric hypertrophy post-MI. The qualitative differences between systolic and diastolic stress and tension remain unclear, and their influence on different patterns of LVr are an important research topic.
LVr increases wall stress through the alterations seen in LV geometry post-MI: namely, an increased regional radius of curvature and decreased wall thickness (Central Illustration). Increased LV wall stress may serve as an independent stimulus for further LVr and contractile dysfunction through afterload mismatch and episodic subendocardial ischemia (11). However, in compensated LVr, stress is likely unchanged and may not be a good prognostic marker. However, although it is likely that LV wall stress is an important risk marker for LVr, it is difficult to measure. A potential solution is to follow LV strain, which is intrinsically related to LV wall stress.
LV strain is a dimensionless quantity that describes myocardial deformation (Online Appendix 1). Natural strain () is an index of systolic function (12), calculated as the change in length of the myocardial segment over a small time interval, and can be normalized to instantaneous LV geometry. Lagrangian strain is calculated at an arbitrary time point. Effectively, this version of LV strain is normalized to LV geometry. Natural and Lagrangian strain are not always equivalent, especially during rapid LV deformation. LV strain is related to LV pressure, LV geometry, and ultrastructure and therefore is a reflection of LV wall stress (13). Cardiac ultrastructure is complex, and includes contractile fibers of variable orientation in different layers of the LV wall (14). This means that the LV can develop stress and hence strain in many different directions (13–15). There have thus been multiple derivations of LV strain described that attempt to describe strain in each respective direction. Longitudinal strain (2-dimensional [2D]) describes deformation in a direction from apex to base, radial strain (2D) describes changes in myocardial thickness throughout the cardiac cycle, and circumferential strain (2D) describes myocardial deformation in a direction that is tangential to the wall at a particular point of interest. Torsional strain is the difference in circumferential strain between apex and base. Area strain is the result of the summation of LV principal strains, unrelated to a single LV kinetic axis.
The degree of LV distension resulting from LV stress depends on the elastic modulus of the LV, which is altered post-MI (16) and thereby reduces LV strain, whereas hypertrophy may reduce LV strain on individual cardiomyocytes. Thus, the different clinical courses seen in patients with similar scar loads may be explained through differences in LV geometry and subsequent changes to LV wall stress and strain. LV strain has been shown to cause myocyte growth in vitro through the addition of sarcomeres (17). Furthermore, LV strain has been theorized to directly cause AT2 release, in addition to causing transcription of genes involved in myocyte hypertrophy (18); hence, volume overload-induced wall stretch may contribute to the hypertrophy classically described in LVr post-MI.
It appears that progressive LVr may be the result of imbalance between the required increase in left ventricular end-diastolic volume (LVEDV) to maintain stroke volume in the presence of poor contractility and the resulting mechanical changes, specifically increased internal wall force. In this context, progressive LV stiffening may be viewed as a compensatory measure that reduces the effect of increased wall stress causing regional stretching and progressive dilation.
Assessment of LV Mechanics and Geometry Using Cardiac Imaging
LV strain is now a quantity that can be measured clinically to a high degree of accuracy using both echocardiography (speckle tracking echocardiography, tissue Doppler imaging), and cardiac magnetic resonance (CMR) (15). Briefly, tissue Doppler imaging was the first technique used to assess LV strain, as the integral of strain rate itself measured from the differential tissue velocity curves. As with all Doppler methods, this approach is angle dependent and requires alignment of the Doppler beam to the direction of motion. Speckle tracking echocardiography, which is based on tracking the patterns of myocardial specular reflectors throughout the cardiac cycle, is angle independent. The restriction of tracking to the imaging plane leads to the loss of some signal as the reflectors travel out of plane. Three-dimensional (3D) speckle tracking echocardiography overcomes this issue, but the frame-rate of this method is relatively low. CMR-based measures of LV strain may be obtained through the use of myocardial tagging, whereby the region of interest (usually a grid) displays a different density to the surrounding tissue by exposure to a magnetic pulse before the imaging sequence begins. The relationship between myocardial regions (“tags”) allows the determination of regional deformation (19). These tags decay over the course of about 600 ms; contour tracking is an alternative approach for measurement of deformation without tagging.
Unlike LV strain, LV wall stress cannot be directly measured, and imaging-derived determinants or effects of LV wall stress are used to derive the parameter. Several models have been published for the assessment of LV wall stress (Figure 4). A common limitation is the assumption of idealized geometry and kinetics in most simple models; most use an ellipsoid to approximate the LV, which is a major limitation when investigating disease states that are known to involve abnormal geometry, such as ischemic heart disease. In addition, models of global geometry are unlikely to be sensitive tools for the investigation of regional dysfunction and remodeling. Finite element analysis—a technique where complex geometries are broken down into smaller and simpler components (the so called “finite elements”)—may go some way toward overcoming these issues. Finite element analysis generally involves creating a mesh of points, which when combined, form an anatomically correct representation of LV geometry. The way these representative points are connected and interact throughout a cardiac cycle is determined by a set of mathematical rules that govern the overall kinetic characteristics of the myocardium. Different rules can be imposed for different regions of the mesh, making it possible to model how different tissue types interact throughout the LV. Finite element models are heterogeneous, with different authors using different assumptions concerning cardiac kinetics, blood flow, and contractile fiber orientation (among many others). This heterogeneity, along with the lack of a satisfactory method to validate the measures, has limited the clinical utility of this parameter. The definition of a standard set of assumptions for finite element models is needed before results can be compared between different studies, as this is likely a key source of variation in values between studies. A further important issue relates to resolution. As sampled cardiac motion is used to solve the many equations governing a finite element model, it is intuitive that all components in the model must have motion data available. Although the number of “finite elements” needed to adequately describe global cardiac motion and geometry remains unclear, it seems likely that the limited resolution of 3-dimensional echocardiography (3DE) may be a barrier that might be avoided with CMR (20).
Inclusion of the changing orientation in myocardial contractile fibers should be included in models of LV wall stress. As stress distributions parallel wall tension, and the generation of wall tension is an active process, with changes in direction according to the position within the LV wall, it is highly likely that there is marked regional variation. The point during the cardiac cycle at which LV wall stress is measured at is also of importance. Assessing wall stress at end-systole may not be appropriate as various contributors (cavity dimensions, wall thickness, blood pressure [BP], and so on) are more favorable than during early ejection (21).
Sphericity index (SI) and conicity index (CI) are descriptors of LV shape that can be assessed using 2-dimensional echocardiography (2DE), 3DE, and CMR. SI characterizes LV geometry by providing a ratio of LV long axis to LV short axis, or LVEDV to the volume of a sphere with diameter equal to the measured LV long axis. SI is a measure of global geometry, namely globularity, and is fundamentally insensitive to regional changes in LV shape. CI was subsequently developed to address this problem by characterizing the shape of the apex, without reference to mid and basal regions (22,23). These indexes are on the basis of idealized LV geometries, and parameters such as LV curvature may afford a more robust assessment of LVr.
The measurement of changes in regional LV geometry using current volume- and shape-based methods has been difficult. However, assessment of LV curvature—a parameter that quantitatively describes how far a surface deviates from being flat—may provide a suitable metric for assessing changes in geometry (24) (Figure 5). LV curvature can be measured in both 2D and 3D, and is sensitive to small changes in shape. Although the variation in 2D measures of curvature is likely be high due to inconsistent contouring, foreshortening, and different imaging planes, 3D curvature is unaffected by these limitations and may provide a more robust method of characterizing regional shape. The main derivations of 3D curvature are Gaussian (intrinsic), and mean (extrinsic). As LVr invariably starts with regional changes, these assessments may give valuable prognostic information in various disease states. Importantly, algorithms for the automatic assessment of 3D meshes on the basis of 3DE and CMR output may be a very feasible method of tracking subtle changes in LV geometry (Figure 6). The intramodality variation of intrinsic measures of shape such as curvature are likely to be small using CMR. The difficulty in accurately assessing epicardial boundaries using echocardiography would imply that the variation in curvature values may be significant.
Assessment of Global and Regional LV Volume Using Cardiac Imaging
Clinical LVr is usually (but arbitrarily) defined as a 15% to 20% increase in LVEDV at follow-up. Although gross LVr has been well described qualitatively, the quantitative amount of LVr required to become clinically significant remains unclear, and HF can occur in the absence of current definitions of severe LVr. It may be that current definitions of LVr (generally on the basis of LV volumes) are inadequate to identify all people at risk of HF post-MI and that new methods are needed. Global volume change can be considered a result of myocardial dilation occurring in 1 or more LV segments. It hence may be more sensitive to approach LVr on a regional basis, as it may be that people with baseline myocardial damage (in the form of diabetic cardiomyopathy, hypertensive cardiomyopathy) are more susceptible to hemodynamic alterations resulting from regional ischemia and concurrent remodeling.
Regional LV volumes are usually expressed using a segmental model, which depends on the definition of a 3D LV axis of symmetry and anatomic landmarks (the apex, mitral annulus, and septum) (Figure 7). Different types of software use different definitions of the LV axis of symmetry. CT and CMR tend to use anatomic landmarks, whereas with echocardiography it is usually on the basis of center of mass. An important consequence of defining an axis of symmetry on the LV center of mass is that the orientation of this axis will change throughout the remodeling process, making longitudinal assessment of regional changes difficult. Anchoring the LV axis to the fibrous skeleton of the heart, such as the mitral annulus, may overcome this limitation (2).
Published data on regional LVr is extremely limited, and it is hence difficult to make a comment about normal values and variation. As global LVr would necessitate some degree of regional LVr, it is very likely that the 2 measures will significantly correlate, but it is currently not possible to make inferences about the strength of this correlation.
Further studies are needed to define the relationship between differing degrees of LVr and the development of clinical HF.
LV volumes have classically been approximated using Simpson’s biplane method applied to 2DE. The main limitations are related to the geometric assumptions necessary for calculation, off-axis imaging, and out of plane motion—all of which are problematic in remodeled ventricles. Additionally, 2DE systematically underestimates LV volumes compared with CMR (25). The coefficient of variation of repeated acquisitions of LVEDV is about 12% using 2DE (26), so follow-up measurements with this technique probably perform better across populations than within individuals.
3DE is not limited by geometric assumptions or apical foreshortening and has consistently been shown to be superior to 2DE for the quantification of LV volumes (27). Estimates of LV volume by 3DE closely parallel CMR-derived volumes, although a recent meta-analysis of 3,055 patients showed that 3DE continues to underestimate LV volumes by about 10 ml (28). The authors (28) showed that semiautomatic contouring reduced underestimation, whereas the presence of cardiac disease and female sex increased the underestimation. The accuracy of 3DE for LV volumes can be further improved through the use of tissue harmonic imaging (29), potentially by the use of contrast (25), and by appropriate method of volume calculation (28).
Although 3DE- and CMR-derived LV volumes correlate well on a cross-sectional basis, the correlation of the change in LV volumes between baseline and follow-up is substantially weaker (r = 0.47) (30). This may simply reflect the test-retest variation of both techniques, but specifically may reflect the inability of 3DE to completely image a large heart and poor image quality hindering 3DE estimations.
Few studies have assessed the ability of 3DE to track subtle regional LVr. Division of the LV into apical, mid, and basal sections using 3DE provides regional volumes that are not dependent on an axis of symmetry (31). This may be a feasible and simple strategy for tracking regional LVr post-MI, although sensitivity is likely lower than an approach based on smaller segmentation. Unfortunately, the use of a 16-segment model for measuring absolute volumes post-MI has shown only moderate correlations between 3DE and CMR, with attempts to follow changes in regional volumes being particularly problematic (2). In addition to endocardial tracking problems and poor spatial resolution, it is likely that a post-MI change in the LV centroid position may contribute to the difficulty of tracking subtle regional LVr (2).
A number of other barriers remain to the application of 3DE for following remodeling. There is a trade-off between temporal and spatial resolution, and the use of a single-beat acquisition—although avoiding the limitations of stitch artifacts due to inadequate breath-hold and rhythm problems—sacrifices spatial resolution, which may be critical in regional measurements. Different vendor approaches to post-processing may heighten the challenge of applying 3D deformation and volume data.
Cardiac magnetic resonance
The assessment of LV volumes with CMR has been validated against phantoms and explanted hearts with very strong correlations (r2 = 0.98) (32), leading this test to be the reference standard for quantification of LV volumes.
Regional LV volumes have also been validated by comparison with a CMR-compatible phantom (33). The average error of regional LV volumes was 0.2 ml, and subendocardial infarction was significantly associated with regional dilation, even though there was no increase in LVEDV. Interestingly, ACE inhibitors had no effect on the increment of regional volume. It remains to be seen which of 2 possible post-processing methods are optimal—1 that analyzes regional volumes on the basis of anatomical landmarks, or 1 on the basis of LV center of mass. It is expected that the landmark method for the calculation of regional LV volumes is likely a more accurate method of calculating regional volumes, as it is independent of a post-MI change in LV center of mass (2). Despite the diagnostic power of CMR, cost and availability have remained barriers to its adoption as a routine post-MI evaluation. CMR is not well suited to the imaging of critically ill patients.
Prediction of LVr
The prediction of both global and regional LVr may allow more timely and appropriate interventions to be targeted in this population. LV mechanics has already proved useful in this regard, with LV strain showing promise in the prediction of global LVr (34–48).
In addition to global longitudinal strain (GLS), radial strain, and global circumferential strain (GCS), speckle tracking also provides the possibility of measuring LV torsion (12,49). These global parameters are strengthened by spatial averaging, in contrast to individual regional strains, which are limited by artifact. Nonetheless, regional strain may be a sensitive marker of myocardial recovery and damage (50).
The longitudinally-arranged subendocardial fibers are most at risk of injury in MI, so GLS has been shown to be a sensitive marker and can hence identify patients at risk of adverse LVr (34–38) (Table 1). Normal GLS is approximately −20%, and GLS thresholds for high risk of LVr post-MI are consistent, being >−10 to −15%. In contrast to the subendocardium, midwall myofibers are orientated parallel to the short axis. As this area is less likely to be injured in MI, GCS may improve (due to circumferential compensation for poor longitudinal function) or remain normal in the initial stages of disease. As disease progresses, GCS may start to deteriorate, perhaps explaining the association of GCS with LVr at 2 years post-coronary revascularization (39). Unfortunately, GCS is susceptible to out-of-plane motion (51). Similarly, although LV torsion has been proposed as a sensitive marker of LV dysfunction and LVr risk post-MI (41), it remains technically challenging to measure the torsion distance by 2DE. Area strain (which incorporates longitudinal and circumferential function) has been used to predict LVr in a small (n = 61) post-non–ST-segment elevation myocardial infarction population (43). The preservation of circumferential function post-MI may limit the ability of area strain to detect subtle dysfunction.
It has been proposed that LV strain rate (GLSr, GCSr)—which accounts for the time course of contraction—may be a better parameter to use for the prediction of LVr post-MI, although the reported research is inconsistent. Hung et al. (40) showed that GCSr was predictive of outcome at 20-month follow-up post-MI, but that although GLSr had value in predicting all-cause mortality, it did not give information about LVr. In contrast, Zaliaduonyte-Peksiene et al. (35) showed no difference in baseline GCSr between patients with and without LVr at follow-up. The reasons for this discrepancy are unclear but may involve different enrolled populations, numbers of subjects enrolled (82 vs. 420), speckle tracking software (EchoPac [General Electric, Fairfield, Connecticut] vs. VVI [Siemens, Munich, Germany]), frame rates (80 frames/s vs. 30 frames/s), and follow-up times (4 months vs. 20 months).
To date, only 1 study of 66 first-time ST-segment elevation myocardial infarction patients has investigated the ability of strain to predict regional LVr (44). This work showed that assessment of baseline regional LS was significantly correlated with change in the respective LV subvolumes for irreversibly dysfunctional segments and all segments. They also showed that GLS could predict a change in subvolumes at follow-up. A very important limitation of this study was the measurement of regional volumes with 3DE, the problems with which have been previously described (2).
Sphericity and conicity
SI and CI give quantitative information about change in LV geometry throughout various cardiac diseases. The predictive power of SI remains unclear. It is predominately sensitive to increases in remote segment length, a characteristic of late LVr, and not infarct expansion, which is the predominant cause of early LVr (52). CI was proposed as a regional approach to quantifying altered LV geometry and is most often defined as the ratio of the apical axis to the short axis. CI has been shown to independently predict LVr at baseline post-MI (52,53). A notable limitation of this index is that it is not applicable to mid or basal segments. It has been proposed that increases in sphericity will act to decrease LV wall stress at the border zone (54), and that progressive LVr occurs when sphericity increases past a certain point.
Curvature is a geometric parameter that quantitatively describes how far a surface is from being flat and has units of inverse distance (Figure 5). LV curvature is greatest at the apex during systole and decreases throughout diastole in the normal heart. Global LV dilation decreases systolic and diastolic LV curvature, with systolic curvature thought to show the most marked difference from normal values (55). Curvature has also been shown to change in segments distal to a localized wall motion abnormality (WMA), with basal and inferior segments showing lower curvature in the presence of an anterior WMA (54–56). This may be representative of compensatory hyperkinesis. Interestingly, this was not found in apical segments in the presence of an inferior WMA (55). This may explain the different clinical courses experienced by patients with single-vessel versus multivessel disease, in addition to the increased risk of LVr with anterior infarction. Unfortunately, it is not clear whether these variations are somewhat dependent on the LV geometric model used—a consideration particularly important in 2D approximations of global LV geometry.
Curvature may prove useful in the investigation of regional LVr. Systolic curvature has been shown to be different in normal patients when compared with both DCM and chronic IHD (57). Segmental curvature changes seen in MI are contributors to the increased LV sphericity associated with poor prognosis, although it is unclear whether changes in curvature contribute to the progression of disease or are the result of other pathological processes (55). In patients investigated after a first anterior MI, the normal systolic increase in local curvature was lost and LV curvature increased at 3 weeks over the infarct zone (54); subsequent LVr was associated with anterobasal curvature. Similarly, Baur et al. (56) showed that patients with a first anterior MI showed an apical curvature that exceeded that of control subjects, and identified patients at risk of LVr. A decreased curvature will tend to increase LV wall stress, which may mediate the influence of curvature on LVr.
LV wall stress
Changes in LV wall stress correlate with the progression of LVr post-MI, although the chain of causality is hard to define. Unfortunately, the prognostic value of LV wall stress has been the subject of few studies to date.
In a small study of nonischemic patients, baseline regional and global LV wall stress has been shown to be significantly higher in patients showing LVr than control subjects, explained by a significant relationship between the extent of infarct and peak LV wall stress (58). Using a finite element model in post-MI patients, apical LV wall stress has been shown to be an independent predictor of LVr, with higher baseline LV wall stress associated with a higher chance of dilation. Importantly, this study also showed that full-dose ACE inhibition attenuated these effects (59).
The relative contributions of BP, left ventricular geometry, and wall thickness toward altered LV wall stress post-MI are unknown, but targeting interventions at reducing BP, reducing sphericity, and increasing wall thickness post-MI are all likely to be necessary to attenuate LV wall stress–induced LVr. Current post-MI treatments do not address distorted LV geometry and decreased wall thickness. This may explain the progressive LVr seen in some post-MI patients despite treatment.
LV volumes have been shown to hold significant prognostic value in post-MI populations, with increased volumes being linked to poor clinical outcomes (60). Baseline assessment of LV volumes may predict subsequent LVr post-MI, both in diastole (53,61,62), and systole (35,42,53,63). However, other studies have failed to show a prognostic role for baseline assessment of LV volumes (38,43–45,47), possibly reflecting the geometric challenges of measuring volumes as well as the confounding effects of other variables such as load. Further research is needed to clarify the role of baseline assessment of LV volumes in a post-MI population.
The outcomes associated with post-MI HF are still poor. LV strain and wall stress are able to predict global LVr, although their ability to predict regional LVr is not well established. This suggests that assessment of LV mechanics may improve risk assessment at baseline post-MI. However, although global LVr post-MI is well recognized as an adverse prognostic sign that can be accurately tracked using a variety of noninvasive clinical techniques, regional LVr is more difficult to investigate.
For additional mathematical formulas, please see the online version of this article.
Drs. D’hooge and Marwick have research collaborations with GE Medical Systems and Philips. Neither company had any role in the inception or preparation of this manuscript. Dr. Marwick has a research collaboration with Philips; and has received research grants from GE Medical Systems. Mr. D’Elia has reported that he has no relationships relevant to the contents of this paper to disclose.
- Abbreviations and Acronyms
- angiotensin-converting enzyme
- conicity index
- cardiac magnetic resonance
- global circumferential strain
- global longitudinal strain
- heart failure
- left ventricular
- left ventricular end-diastolic volume
- left ventricular remodeling
- myocardial infarction
- sphericity index
- 2-dimensional echocardiography
- 3-dimensional echocardiography
- Received June 22, 2015.
- Revision received September 30, 2015.
- Accepted October 8, 2015.
- 2015 American College of Cardiology Foundation
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