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Echocardiographic assessment of ischemic mitral regurgitation
Cardiovascular Ultrasound volume 12, Article number: 46 (2014)
Ischemic mitral regurgitation is an important consequence of LV remodeling after myocardial infarction. Echocardiographic diagnosis and assessment of ischemic mitral regurgitation are critical to gauge its adverse effects on prognosis and to attempt to tailor rational treatment strategy. There is no single approach to the echocardiographic assessment of ischemic mitral regurgitation: standard echocardiographic measures of mitral regurgitation severity and of LV dysfunction are complemented by assessments of displacement of the papillary muscles and quantitative indices of mitral valve deformation. Development of novel approaches to understand mitral valve geometry by echocardiography may improve understanding of the mechanism, clinical trajectory, and reparability of ischemic mitral regurgitation.
The mitral valve has a specific geometry designed to maintain leaflet coaptation and thereby prevent systolic regurgitation into the left atrium (LA). Mitral valve function must be conceptualized in terms of a holistic relationship with supporting ventricular structures, and thus derangements of any part of the mitral valve apparatus – including the mitral valve leaflets, but also the annulus, chordae tendinae, papillary muscles (PM), and left ventricle (LV) – can disrupt valvular coaptation and cause symptoms, physical examination findings, and echocardiographic manifestations of valvular incompetence. The concept of ischemic mitral regurgitation must be clarified in terms of possible mitral regurgitation (MR) mechanisms as well as by acuity of the insult causing MR (see Table 1). In acute coronary syndromes and early in the course of myocardial infarction, MR may occur due to PM ischemia or rupture due to infarction, ischemic LV dilation, and/or increased LV diastolic pressures.
The most common clinical situation encountered for MR arising post infarct, e.g. chronic ischemic mitral regurgitation (CIMR, also called “ischemic chronic secondary MR" by new guidelines ), is MR due to geometric changes of the LV and distortion of normal spatial relationships of the mitral apparatus, all secondary to remodeling from ischemic heart disease. CIMR is characterized mechanistically by incomplete mitral leaflet closure, namely displacement of the leaflet coaptation apically within the LV cavity . Although a spectrum of anatomic abnormalities of both LV and PMs exists, evidence points to a predominant role of “tethering” as the final common pathway in inducing CIMR. Post-infarct, outward displacement of PMs leads to stretching of the chordae tendinae and increased tethering forces on the mitral leaflets, which causes the apical coaptation and restricted closure. Annular dilatation may also contribute by stretching leaflets and causing incomplete closure. Accordingly, CIMR is classified as functional MR, or type IIIb in the Carpentier classification. Practitioners should also be mindful not to classify as CIMR those patients with mitral regurgitation and comorbid ischemic heart disease if there is any intrinsic mitral valve apparatus abnormality and/or there has not been a history of myocardial infarction.
This article will focus specifically on the echocardiographic characteristics of CIMR – given its importance in adverse prognosis (e.g. heart failure and mortality [4, 5]) and impact on evaluating treatment decisions including revascularization, annuloplasty, and cardiac resynchronization therapy. Echocardiography is the only reliable method available for clinical evaluation of CIMR because the physical examination reveals no audible murmurs in about one-third of CIMR patients with moderate or severe MR and half with mild MR .
Overview of echocardiographic assessment of CIMR
When assessing MR by echocardiography, the key inquiries are severity, delineation of pathology in the components of the mitral valve apparatus, overall mechanism of MR, and, based on the probable mechanism, consideration of treatment strategies to reduce MR. As applied to CIMR, the echocardiographer should:
confirm underlying chronic ischemic heart disease,
gauge the severity of MR,
exclude intrinsic pathology in the leaflets and chordae,
establish CIMR as the most likely etiology by assessing LV and PM displacement, and
characterize the phenotype of CIMR as either symmetric or asymmetric.
Echocardiographic assessment of CIMR should also include assessment of global and regional LV function, LV ejection fraction, LV dimensions, LV wall motion abnormalities, and pulmonary hypertension .
The prevalence of post-infarct MR has been reported to be as high as 50% in patient populations studied by echocardiography within 7 to 30 days post infarct [4, 5]. Thus echocardiography may be used to confirm sequelae of ischemic heart disease such myocardial scarring, wall thinning, and wall motion abnormalities. However, it is incumbent on the cardiologist and echocardiographer to be familiar with the patient’s history and other available diagnostic results including electrocardiography, nuclear perfusion tests, and angiography.
Concomitant with measuring severity of MR, one of the initial jobs of the echocardiographer is to ensure there is no other intrinsic pathology of the leaflets, chordae, and PMs; identifying such a finding could indicate the mechanism may not be CIMR. In general the pathologic processes underlying CIMR reflect ventricular and not leaflet pathology: adverse local and global remodelling of the LV changes the geometry of the PMs and the resultant dynamic vector forces exerted on the chordae-leaflet system. During systole, mitral leaflet closing is mediated by the interplay of closing forces  exerted by LV intracavitary systolic pressure on the ventricular surface of the mitral leaflets versus tethering forces, which restrict leaflet motion in systole by pulling apically away from the mitral annular coaptation plane. Tethering forces are applied by the LV, PMs, and annulus along apical, posterior, and lateral vectors  (Figure 1) and cause incomplete systolic mitral leaflet closure . Global LV dilatation will increase the distance from PM to the leaflet and cause tethering; similarly, a local area of infarction that distorts and outwardly displaces the myocardium underlying PM produces similar malposition. In part because of the more common single vessel supply of the posteromedial PM , tethering and resultant CIMR are more common with inferior infarcts than with anterior infarct . In addition, displacement of the anterolateral PM is more restricted due to the structural buttress afforded by the interventricular septum, and also because infarcts in the left coronary artery territory will more commonly produce apical dilatation as opposed to dilatation of territory subtended by the anterolateral PM.
The vector sum of forces applied to the mitral leaflet in CIMR generates an abnormal, ventricularly displaced coaptation shape of the mitral leaflets referred to as “tenting”. Two echocardiographic phenotypes of tenting in CIMR have been identified : asymmetric and symmetric (Figure 2), which depends on if the posterior or both leaflets are affected, which itself depends on the underlying LV and PM derangements. For example, global LV dilatation with radially outward and apical displacement of both PMs causes symmetric tenting of both leaflets. Inferoposterior infarction  with local adverse remodelling predominantly affects the posteromedial PM and restricts the posterior leaflet motion, causing a relative overriding of the coaptation zone by the non-tethered leaflet (“pseudoprolapse”). The coaptation zone, although more apically displaced in symmetric tethering, is less geometrically deformed than in asymmetric tethering. Regurgitant severity of CIMR is strongly affected by tethering phenotype, with higher degrees and more eccentric jets observed in asymmetric tethering (Figure 3). Symmetric tethering, despite more common association with worse LV dysfunction and dilatation, more frequently results in smaller non-eccentric central jets of MR. The characteristics of these phenotypes are summarized in Table 2.
In the following sections, transthoracic echocardiographic techniques will be discussed in tandem with reference to the underlying plausible mechanisms of CIMR and other etiologic contributors such as mitral annular dilatation.
Echocardiographic assessment of ischemic MR severity
Accurate grading of MR is central to clinical decision-making. MR should be graded using an integrative approach, incorporating multiple Doppler techniques for direct quantification as well as supportive data (left atrial size, LV chamber size, pattern of pulmonary vein flow) in the overall assessment . Color Doppler techniques include:
Distal jet area measures the high turbulent mosaic color Doppler pattern produced by the MR flow as it enters the left atrium, distal to the mitral valve leaflets. This color Doppler display is a surrogate measure of MR volume. It is measured as an absolute area, or also as a ratio relative to the left atrial area. The MR jet area is traced at its maximum in apical views and divided by the left atrial area traced in same frame (Figure 4). The advantage of jet area ratio is that it is a rapid, straightforward method, especially for centrally directed MR jets. Its disadvantages are that the distal MR jet varies with loading conditions, such as blood pressure, or technical factors such as machine color gain and frequency settings. In addition, the MR volume in eccentric jets is underestimated by the distal jet area method as the jet can be attenuated by the left atrial wall.B. Vena contracta (VC) measures the linear dimension of the neck of the MR jet as it enters the regurgitant orifice at the level of the leaflets. The VC is a simple linear measure of the regurgitant orifice and is relatively independent of loading conditions. The VC is measured in the parasternal long axis plane with the VC region magnified, and depth and sector size optimized for color Doppler resolution (Figure 5). Magnification is critical for accurate vena contracta grading, as small differences in measurement may change in grading category. Because reference ranges for VC have been defined in long axis planes, measurement of VC in the 2 chamber view should be avoided.
Proximal isovelocity surface area (PISA) or proximal flow convergence method calculates the effective regurgitant orifice area (EROA) and MR regurgitant volume (RVol) as follows:
where R is the radius of the hemispheric PISA zone (Figure 6)
The PISA method provides a quantitative method for MR grading. However, the calculation requires a geometric assumption of a hemispherical shape to the PISA region which is not always the case. Additionally, it can be technically challenging to measure the PISA radius accurately.
The pulsed Doppler volumetric method calculates MR RVol as mitral valve inflow minus aortic outflow. Although it provides a quantitative measure of MR, it has multiple measurement steps, each with potential for measurement variability and error. Additionally, this method requires two non-stenotic valves without important aortic insufficiency.
Tables 3 and 4 shows reference ranges for color Doppler criteria for MR grade based on 2003 American Society of Echocardiography guidelines ; however 2014 American College of Cardiology/American Heart Association guidelines propose a new classification scheme of valvular disease severity, based on a combination of echocardiographic and symptomatic parameters, with stages of “at risk” to “progressive” to “asymptomatic severe” to “symptomatic severe” . Recent consensus statements also endorse lower cut-off values for EROA for CIMR severity as compared to primary MR. In part this is due to 1) data that shows worse prognosis at smaller EROA in CIMR, likely reflecting the effects of the incremental volume load of lesser degrees of MR on an already dysfunctional ventricle, and 2) 2D echocardiographic underestimation of the flow convergence-method derived EROA due to “crescentic” orifice geometry in CIMR as opposed to a circular orifice .
In addition to semi-quantitative and quantitative Doppler techniques, it is important to integrate supportive and complementary data into the overall severity grading. Pulmonary venous flow reversal is specific for severe MR although of lower sensitivity (Figure 7). Chamber enlargement (LA and LV), dense continuous wave MR Doppler profile, and elevated E wave peak velocity >1.2 m/s are all suggestive of severe MR [11–13] (Figures 8 and 9).
3D echocardiography has been demonstrated to provide accurate and reproducible MR grading using 3D guided planimetry of the VC area, which is essentially equivalent to the direct measure of the EROA. An advantages of 3D measurement of the EROA is that it does not require geometric assumptions that are used for 2D EROA calculation. Disadvantages are the lower frame rates of 3D color Doppler, which can effect lateral resolution and hence may erroneously exaggerate the area measured .
Finally, CIMR is a dynamic process, and the echocardiographer must consider how ambient preloading and afterloading conditions such as patient’s volume status, systemic blood pressure, and medications may affect the observed degree of MR.
Echocardiographic assessment of global LV enlargement and dysfunction
Quantitative measures have attempted to correlate LV systolic dysfunction and LV dilatation with CIMR. Elegant experimental observations show that isolated LV systolic dysfunction (pharmacologically induced in a large animal model) does not produce significant MR [6, 15]. This is likely because without tethering forces, relatively little closing force is required to be generated by the LV to force the mitral leaflets toward the annular coaptation zone. However, in the same model of pharmacologic LV systolic dysfunction, when the LV was allowed to dilate by relieving an extrinsic pericardial restraint, MR was generated. This observation confirms as a key mechanism the apical and outward dilatation of PMs which create tethering forces on the leaflets.
In CIMR with symmetric tethering, LV end-systolic and end-diastolic volumes and the sphericity index correlate with the severity of MR. This is because the degree of LV dilatation directly relates to apical displacement of the PMs. For asymmetric tethering phenotypes the measures of global LV remodeling do not as robustly correlate with severity of MR because a small infarct can disrupt PM geometry and generate severe MR; the actual measures of mitral valve deformation are better predictors (see below). LV dilatation would therefore not be an independent predictor of CIMR severity in a population with mixed CIMR phenotypes.
Local LV remodelling and PM displacement
The normal orientation of the PMs is with their long axis parallel to that of the LV and perpendicular to the plane of the mitral annulus. A local infarct that disrupts myocardium underlying a PM can radically change the relationship of that PM relative to the other PM and to the valve apparatus. This asymmetric effect of the infarct on the posteromedial PM translates directly into creating asymmetry in mitral valve apparatus anatomy and function – by rotating the posteromedial PM, tethering the posterior leaflet, and deforming the posterior portion of the mitral annulus – which creates a substrate for eccentric CIMR (Figure 3 and Additional file 1). Several lines of experimental and echocardiographic evidence correlate post-infarct inferoposterior wall motion abnormality with severity of MR . Direct evidence that PM displacement generates CIMR was obtained in a sheep study of echocardiography-guided PM repositioning by an inflatable balloon external to the myocardium . In this study, a Dacron patch with an adjustable balloon was sewn epicardially over areas of infarct after circumflex artery ligation; inflation of the balloon could be tailored to reduce the ischemic dilatation of the inferior wall, thus re-approximating PM geometry, and reducing severity of MR without a change in measures of LV contractility.
In practice, echocardiographic measurement of PM displacement requires intracardiac landmarks. The anterior mitral annulus is anchored at the aortomitral fibrous curtain, and this point in the parasternal long axis or apical four chamber views can provide a reference for measurement of apical displacement of both PM heads (Figure 10B,C) . In a population of 128 LV systolic dysfunction patients, the strongest multivariate correlations with MR severity in a functional MR model were the apical displacement of the posteromedial PM and the inferoposterior displacement of the anterolateral PM . In the parasternal short axis view at the mid-ventricular level, PM body displacements may be referenced relative to the mathematical center of the LV. Agricola and colleagues constructed a “mid-septal perpendicular line,” bounded by the septal insertions of the right ventricle myocardium, from which to measure posterior displacements of the PMs (Figure 10D) . Lateral displacements of both PMs were measured from a second line constructed orthogonal to the mid-septal perpendicular line. Finally, a distance between the papillary body muscles was recorded. Regardless of CIMR phenotype, absolute value of each of these displacement measures is higher when compared to normal controls. In addition, the displacement measures will tend to be higher in symmetric versus asymmetric CIMR, but the magnitude of the changes between phenotypes is a few millimeters and thus not sufficient to differentiate them without other information on mitral valve deformation (Table 5). Some differences correlate with asymmetric phenotypes, e.g. the ratio of posterior displacements of the posteromedial:anterolateral PMs is about 1.2 in asymmetric CIMR but about 0.94 in symmetric CIMR or normal controls . 3D TTE permits additional insight into the geometric angles relating both PMs to the LV cavity long axis, with greater asymmetry in the angles in CIMR versus functional MR with a dilated cardiomyopathy . 3D TTE can be used to measure true spatial vector distances from the aortomitral curtain to the PM tips  and also characterize the spatial geometry of the PMs in relation to the annulus .
Wall motion abnormalities are critically important in gauging local LV dysfunction in CIMR: the echocardiographer should identify and quantify wall motion as part of a comprehensive assessment of a global assessment of ischemic burden. Indices of wall motion abnormalities underlying the posteromedial PM insertion are highly important in assessing CIMR. Novel methodologies, including LV basal rotation dynamics as assessed by speckle tracking, further highlight local differences between myocardial function in symmetric and asymmetric phenotypes . Normal systolic rotation may contribute to decreasing the distance from posterior PM head to leaflet and mitral annular contraction. In a multivariable model, impairment of basal rotation was a key predictor of CIMR severity after inferoposterior MI, likely because of less ability of myocardial rotation to reduce adverse tethering lengths and also a contribution to reduction of mitral annular contraction.
Ischemic and/or systolic PM dysfunction itself does not seem to contribute to CIMR on top of the contribution of PM displacement. Kaul first reported poor overall correlation of reduced PM thickening and MR severity in canines . In a sheep model of CIMR by left circumflex occlusion but with preserved PM blood supply via a perfusion catheter from the aorta, withdrawal of the perfusion catheter caused onset of papillary ischemia as measured by decreased strain rate but was correlated with diminished tethering distances and reduced MR . In humans, there is some evidence that PM dysfunction, as measured by longitudinal systolic strain, actually reduces MR observed after inferior myocardial infarction . Impairment of PM contraction presumably reduces tension on the chordae and paradoxically compensates for the tethering forces exerted by PM misalignment and/or LV dilatation. Novel protocols employing delayed enhancement cardiac magnetic resonance imaging confirmed that while PM infarct was observed in 30% of patients at 4 weeks after first myocardial infarction, neither partial nor complete PM infarct robustly correlated with CIMR . These observations reinforce the notion that geometric PM displacement, and not necessarily systolic function, is the key factor in determining CIMR.
Tethering and tenting of the mitral leaflets is the final common pathway mediating leaflet malcoaptation and incomplete closure in CIMR
The aggregate of the abnormal vector forces on the mitral leaflets manifest echocardiographically as incomplete mitral leaflet closure or tenting; as such it represents the common pathway of LV remodelling and PM displacement in CIMR. Various measures of quantifying tethering and tenting are available by routine 2D TTE techniques. The incomplete mitral leaflet closure pattern is often best appreciated in the apical four chamber view, because the mitral annular plane is defined in this view.A single linear measure of “tenting height” – the maximal mid-systolic distance from mitral leaflet tips to the annular plane – reflects the abnormal apical shift of the coaptation zone (Figure 10A). While this measure has been correlated with CIMR severity, tenting height understandably may be different when the tethering forces are directed posterolaterally versus apically for example because height alone it does not account for angle of tethering relative to the annular plane.
The tethering angles define the relationship of the base of the leaflets to the annulus: α represents the angle between annular plane and anterior mitral leaflet and β the angle between annular plane and posterior mitral leaflet . 3D TTE and TEE acquisition of volumetric data sets allows selection of particular imaging slices to calculate tethering angles . Though the exact values depend on methodology and imaging plane selected, higher ratios of posterior angle to anterior angle characterize the asymmetric tenting phenotypes, and also predicts increased MR severity .
Tenting area provides a more integrative measurement that is less dependent on a particular angle, and also accounts for the geometry of the entire leaflet and not just that at the annular attachment. Tenting area is calculated as the area bounded by the anterior and posterior leaflets and the mitral annular plane (Figure 10); this measurement is performed at mid-systole, when the tenting area would be at a maximum. In the VALIANT-Echo substudy of 341 patients with echocardiographic LV ejection fraction <35% after myocardial infarct, tenting area was the only independent predictor of progressively worsening CIMR based on followup TTE data to a median 24.7 months . Tenting area above a threshold of 4 cm2 predicted near 6 fold odds of having moderate or greater MR at the end of followup and an odds ratio of 3.6 for increase in the degree of MR. In patients with LV systolic dysfunction, tenting area was a major determinant of functional MR severity, independent of global LV function, LV volume, and spherical shape. Tenting area itself correlates with linear measures of apical or posterior PM displacements . Extending the analogy of assessment of tenting beyond tenting height and tenting area, tenting volume as defined by 3D echocardiography affords another level of comprehensive measurement of mitral valve deformation. However, the importance of the tenting phenotype must be considered, because even with the same indices of tenting height, area, or volume, an asymmetric CIMR phenotype will likely be associated with more significant MR (Figure 11).
Finally, secondary chordal attachments (basal or strut chordae) to the anterior mitral valve leaflet may exert additional geometric constraints on systolic MV configuration, most commonly manifesting as a bend, or an angle, between the distal and basal portions of the anterior mitral leaflet that further impairs coaptation. This angle can give a qualitative visual clue, assessed as a convexity or concavity in the configuration of the anterior mitral valve leaflet toward the left atrium in the parasternal long axis view in systole, with concavity indicating a bowing into the LV that strongly correlated with CIMR severity .
Mitral annular dilatation
The mitral annulus has a specialized 3D geometry likened to an ovoid saddle shape that reduces stresses on the leaflets and supports valvular competence . Dilatation of the annulus may occur secondary to either LV or LA dilatation, and while dilatation occurs primarily along the posterior annulus, even the fibrous anterior portion of the mitral annulus may dilate [31, 32]. Additionally, dilatation along the posterior annulus may be asymmetric, with a predilection for the region of the posterior commissure (P2 – P3 segment).
Annular dilatation can cause an incomplete coaptation pattern due to insufficient available leaflet area. However, the degree of dilatation does not necessarily correlate with the severity of CIMR. Distortion of the native 3D annular geometry to a “flattened” annulus may also contribute to CIMR by changing the leaflet motion. However in a study of lone atrial fibrillation patients with annular dilatation but normal LV chamber size, significant MR was not observed . This is because LV remodelling and dilatation is required to generate tethering forces, though the study did show a weak correlation between functional MR severity and annular area.
Annular dilatation can be measured by anterior and posterior dimensions, annulus area (apical four chamber mitral annulus dimension multiplied by apical two chamber mitral annulus dimension multiplied by π/4) and perhaps with more computationally sophisticated methods such as the MVQ software package (Mitral Valve Quantification, Phillips). Surveillance of mitral annular dilatation is a part of our practice because of a self-propagating cycle of annular dilatation → MR → LV dilatation → annular dilatation. Mitral annular contraction, equal to (diastolic annular area – systolic annular area)/diastolic annular area, has a negative correlation with MR severity in LV systolic dysfunction  and in post-infarct MR.
Mitral leaflet area
Work by Robert Levine at Massachusetts General Hospital has described 3D echocardiographic methods to compare the areas of the mitral leaflets to the “closing area” and the annular area [34, 35]. In human models of functional MR, the mitral leaflet areas are greater than in patients without dilatation or prior infarct. However, the ratio of the measured mitral leaflet area to the calculated “closing area” is decreased in functional MR. There may a threshold lower ratio which would be consistent with diagnosing a functional MR mechanism; it may be possible in the future to echocardiographically detect, measure and monitor this process as a means of assessing the remodelling response to CIMR. The biologic response that allows the valve to remodel by enlargement and thickening seems to be due to reactivation of embryonic development pathways occurring within the leaflet tissue .
Assessment of CIMR post-therapy
The mechanisms responsible for recurrence of CIMR after surgical revascularization and restrictive annuloplasty remain elusive. In some instances, the mechanism is ongoing adverse LV dilatation and spherical remodelling that worsens tethering [37, 38]. In a single center retrospective population of predominantly ischemic MR, preoperative LV end diastolic diameter indexed to body surface area with a cut-off of >3.5 cm/m2 predicted recurrence of MR . A greater degree of anterior mitral leaflet tethering angle α, specifically >36.9° (considered the moderate-to-severe or severe quintiles of anterior tethering), regardless of LV dilatation or geometry, conferred a multivariate OR of 3.6 for recurrent MR at 44.7 month follow-up of CIMR patients who underwent surgical revascularization and undersized ring annuloplasty . This is in accord previous results showing α ≥39.5° conferred OR of 3.1 for recurrent MR in a similar population of patients who underwent surgical revascularization and undersized ring annuloplasty . There was also a strong association (OR >4) for lack of LV reverse remodeling post-operatively. The results of this line of analysis underscores that preoperative echocardiography and tethering geometry does predict postoperative outcomes including MR recurrence, LV geometry, and outcome, and thus these should be part of preoperative assessment. Preoperative diastology may also impact postoperative outcome, with transmitral deceleration time <140 ms predictive of MR recurrence, and deceleration time and pulmonary vein systolic:diastolic flow ratio predictive of mortality .
Because annuloplasty shifts the coaptation zone more anteriorly, the posteromedial PM location can be further distorted and lie outside the annulus ring; the tethering effect on the posterior leaflet makes it less likely to coapt at the anteriorly shifted coaptation zone . In patients without continued global LV dilatation, recurrent MR is highlighted by adverse anterior leaflet tethering due to bending, as measured by anterior leaflet coaptation area .
Additional imaging techniques
Derangements in peak systolic longitudinal, radial, and circumferential strain measures mirror underlying wall motion abnormalities in both asymmetric or symmetric CIMR . In symmetric CIMR, peak systolic strain was reduced globally, while in asymmetric CIMR phenotypes there was more localized systolic strain derangements in the inferoseptal and inferior territories. While it is not yet clear how strain might add to the diagnosis of CIMR, it could assume a particular role in surgical planning: in a 61 patient CIMR cohort, strain did not improve after surgical revascularization and restrictive annuloplasty in the symmetric group, but did improve at one year in the asymmetric group .
Patients with mild (or “progressive”) rest CIMR may exhibit more severe inducible regurgitation as assessed by flow convergence methods , and this may represent the etiologies of exertional symptoms  and excess mortality seen with CIMR . Exercise physiology exerts multiple effects that bear on the mitral valve apparatus and degree of MR: inotropy increases which augments global and regional LV systolic dysfunction and has the potential to improve mitral valve coaptation geometry; against this, exercise contributes to increased LV systolic pressure and increased chronotropy with shortened systolic time, which contribute to augmented transmitral LV to left atrial pressure gradient . Additionally, exercise-induced ischemia could contribute to new or worsened WMA and tethering, or increased heart rate and altered loading conditions may result in worsening of ventricular mechanics which in setting of underlying akinesis or dyskinesis, result in increased MR. The net change in ischemic MR with exercise depends ultimately on which factor(s) represent the underlying mechanism of the ischemic MR: about one-quarter of CIMR patients show decrease ischemic MR with exercise , e.g. those with inferior myocardial infarction who can augment LV function with exercise and who would not have worsened ventricular mechanics.
Exercise may present a method to risk stratify patients with LV systolic dysfunction and mild rest CIMR at rest, as cardiovascular mortality at 19 month followup was predicted by worsening of mild rest CIMR (judged by an increase in EROA ≥13 mm2 on a symptom-limited semisupine bicycle exercise test for which beta blockers were held for 24 hours) . In another study of submaximal Bruce protocol treadmill exercise with patients on beta blockers, no rest echocardiographic parameters predicted severity of exercise-induced CIMR by EROA; instead only changes in exercise-induced mitral geometry measured by valve tenting area and coaptation distance represented the independent predictors of ischemic MR severity . Exercise echocardiography may be reasonable in patients with ischemic heart disease and suspected CIMR who report dyspnea disproportionate to rest MR and/or LV dysfunction or who experience pulmonary edema without explained cause, and for whom additional information would answer whether surgery would benefit [13, 46].
Transesophageal Echocardiography (TEE)
TEE can be a useful adjunct to TTE for characterizing the mechanism of MR (particularly for intrinsic leaflet pathologies) and mapping anatomic defects. It may help exclude an organic etiology when assessing the patient with CIMR, and also provide better spatial resolution of chordal and leaflet geometric relationships. The use of TEE intraoperatively and post-operatively in the evaluation of MR has been comprehensively reviewed by Sidebotham et al.  and Shakil et al. . TEE is important in assessment of patients undergoing surgical revascularization as it provides another opportunity to assess for CIMR. However, because of vasodilating effects of anesthesia, CIMR severity may be underestimated by intraoperative TEE. One proposed tactic to ensure appropriate severity grading is to administer vasopressors to mimic more physiologic afterload conditions. In a single study, the proxy for physiologic afterload was a systolic blood pressure of 160 mmHg though the exact target is debatable; concurrent with vasopressor administration, most patients’ pulmonary artery occlusion pressure rose and only a few patients were administered extra intravenous fluid to combat the venodilating effects of anesthesia .
Cardiac computed tomography and magnetic resonance
Non-echocardiographic cardiac imaging modalities are being deployed to study CIMR. These techniques may require the patient to remain immobile and flat and to perform breath holds – potential issues for patients with orthopnea due to cardiomyopathy or MR. Computed tomography implies a radiation exposure and magnetic resonance may require significant time as well as specialized equipment. Nevertheless, robust data sets with axial and three dimensional information may be derived which are suitable for a comprehensive classification of the interwoven geometry of the components of the mitral valve apparatus, for example augmented definition of annulus dimensions, annulus height, shape, and tenting height and angles [31, 52, 53] Delayed enhancement cardiac magnetic resonance and CT also offer alternative routes to more precise definition of region of PM and LV myocardial infarct , and are thus useful to establish the underlying ischemic etiology of MR and also define myocardial viability which may impact treatment decision-making . The role of computed tomography and magnetic resonance remains to be defined.
CIMR is the post-infarct pathophysiologic result of incomplete mitral valve coaptation due to global or local geometric deformity of the LV that generates apical displacement of normal mitral valve leaflets. Echocardiographic techniques can quantitate CIMR primarily by indices of leaflet tethering and tenting, effectively integrating the effects of multiple disparate forces. Because CIMR may beget CIMR through mechanisms of increased volume loading on the LV and annular dilatation, precise echocardiographic diagnosis and followup are essential. Improved echocardiographic assessments will augment our understanding of the etiologies CIMR, and translate to appropriate, mechanistically-targeted therapy. The typical therapy of CIMR has been restrictive mitral annuloplasty, but reshaping the annulus cannot alone solve the problem when the ultimate etiologic lesion is in ventricular geometry. This dilemma is appreciated in practice as it is not proven that current treatments of CIMR either boosts survival, helps LV reverse remodeling, or improves symptoms. Better definitions and improved phenotyping of CIMR will permit robust randomized controlled trials of surgical therapies , as well as refinements in percutaneous device therapies such as CRT (which reduces tethering and modifies timing of LV systolic forces)  and injectable polymers to reshape the posteromedial PM , novel surgical approaches (e.g. targeted surgical approaches such as LVplasty, annuloplasty and chordal cutting depending on the patient’s specific CIMR mechanism), and experimental devices to improve PM geometry .
JH is an associate professor of medicine at Harvard Medical School and the associate director of the echocardiography laboratory at Massachusetts General Hospital. She has participated on several writing group committees for American Society of Echocardiography guidelines, including those on valvular disease.
Chronic ischemic mitral regurgitation
Effective regurgitant orifice area
Guideline directed medical therapy
Proximal isovelocity surface area
Time velocity integral
Wall motion abnormalities.
Beaudoin J, Handschumacher MD, Zeng X, Hung J, Morris EL, Levine RA, Schwammenthal E: Mitral valve enlargement in chronic aortic regurgitation as a compensatory mechanism to prevent functional mitral regurgitation in the dilated left ventricle. J Am Coll Cardiol. 2013, 61: 1809-1816.
Nishimura RA, Otto CM, Bonow R, Carabello BA, Erwin JP, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM, Thomas JD: AHA/ACC Guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association task force on practice guidelines. Circulation. 2014, 129: e521-e643.
Godley RW, Wann LS, Rogers EW, Feigenbaum H, Weyman AE: Incomplete mitral leaflet closure in patients with papillary muscle dysfunction. Circulation. 1981, 63: 565-571.
Bursi F, Enriquez-Sarano M, Nkomo VT, Jacobsen SJ, Weston SA, Meverden RA, Roger VL: Heart failure and death after myocardial infarction in the community: the emerging role of mitral regurgitation. Circulation. 2005, 111: 295-301.
Perez De Isla L, Zamorano J, Quezada M, Almería C, Rodrigo JL, Serra V, García Rubira JC, Ortiz AF, Macaya C: Prognostic significance of functional mitral regurgitation after a first non-ST-segment elevation acute coronary syndrome. Eur Heart J. 2006, 27: 2655-2660.
He S, Fontaine AA, Schwammenthal E, Yoganathan AP, Levine RA: Integrated mechanism for functional mitral regurgitation. Leaflet restriction versus coapting force: in vitro studies. Circulation. 1997, 96: 1826-1834.
Agricola E, Oppizzi M, Maisano F, De Bonis M, Schinkel AFL, Torracca L, Margonato A, Melisurgo G, Alfieri O: Echocardiographic classification of chronic ischemic mitral regurgitation caused by restricted motion according to tethering pattern. Eur J Echocardiogr. 2004, 5: 326-334.
Voci P, Bilotta F, Caretta Q, Mercanti C, Marino B: Papillary muscle perfusion pattern: a hypothesis for ischemic papillary muscle dysfunction. Circulation. 1995, 91: 1714-1718.
Kumanohoso T, Otsuji Y, Yoshifuku S, Matsukida K, Koriyama C, Kisanuki A, Minagoe S, Levine RA, Tei C: Mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior myocardial infarction: quantitative analysis of left ventricular and mitral valve geometry in 103 patients with prior myocardial infarction. J Thorac Cardiovasc Surg. 2003, 125: 135-143.
Zito C, Cusma-Piccione M, Oreto L, Tripepi S, Mohammed M, Di Bella G, Falanga G, Oreto G, Lentini S, Carerj S: In patients with post-infarction left ventricular dysfunction, how does impaired basal rotation affect chronic ischemic mitral regurgitation?. J Am Soc Echocardiogr. 2013, 26: 1118-1129.
Zoghbi WA, Enriquez-Sarano M, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones MA, Rakowski H, Stewart MJ, Waggoner A, Weissman NJ: Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and doppler echocardiography. J Am Soc Echocardiogr. 2003, 16: 777-802.
Zeng X, Tan TC, Dudzinski DM, Hung J: Echocardiography of the mitral valve. Prog Cardiovasc Dis. 2014, 57: 55-73.
Lancellotti P, Moura L, Pierard LA, Agricola E, Popescu BA, Tribouilloy C, Hagendorff A, Monin J-L, Badano L, Zamorano JL: European Association of Echocardiography recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010, 11: 307-332.
Zeng X, Levine RA, Hua L, Morris EL, Kang YJ, Flaherty M, Morgan NV, Hung JMD: Diagnostic value of vena contracta area in the quantification of mitral regurgitation severity by color doppler 3D echocardiography. Circ Cardiovasc Imaging. 2011, 4: 506-513.
Otsuji Y, Handschumacher MD, Schwammenthal E, Jiang L, Song JK, Guerrero JL, Vlahakes GJ, Levine RA: Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry. Circulation. 1997, 96: 1999-2008.
Tenenbaum A, Leor J, Motro M, Hod H, Kaplinsky E, Rabinowitz B, Boyko V, Vered Z: Improved posterobasal segment function after thrombolysis is associated with decreased incidence of significant mitral regurgitation in a first inferior myocardial infarction. J Am Coll Cardiol. 1995, 25: 1558-1563.
Hung J, Guerrero JL, Handschumacher MD, Supple G, Sullivan S, Levine RA: Reverse ventricular remodeling reduces ischemic mitral regurgitation: echo-guided device application in the beating heart. Circulation. 2002, 106: 2594-2600.
Yiu SF, Enriquez-Sarano M, Tribouilloy C, Seward JB, Tajik AJ: Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: a quantitative clinical study. Circulation. 2000, 102: 1400-1406.
Veronesi F, Corsi C, Sugeng L, Caiani EG, Weinert L, Mor-Avi V, Cerutti S, Lamberti C, Lang RM: Quantification of mitral apparatus dynamics in functional and ischemic mitral regurgitation using real-time 3-dimensional echocardiography. J Am Soc Echocardiogr. 2008, 21: 347-354.
Otsuji Y, Handschumacher MD, Liel-Cohen N, Tanabe H, Jiang L, Schwammenthal E, Guerrero JL, Nicholls LA, Vlahakes GJ, Levine RA: Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation. J Am Coll Cardiol. 2001, 37: 641-648.
Hsuan C-F, Yu H-Y, Tseng W-K, Lin L-C, Hsu K-L, Wu C-C: Quantification of the mitral tetrahedron in patients with ischemic heart disease using real-time three dimensional echocardiography to evaluate the geometric determinants of ischemic mitral regurgitation. Clin Cardiol. 2013, 36: 286-292.
Zeng X, Nunes MCP, Dent J, Gillam L, Mathew JP, Gammie JS, Ascheim DD, Moquete E, Hung J: Asymmetric versus symmetric tethering patterns in ischemic mitral regurgitation: geometric differences from three-dimensional transesophageal echocardiography. J Am Soc Echocardiogr. 2014, 27: 367-375.
Gelsomino S, van Garsse L, Luca F, Parise O, Cheriex E, Rao CM, Gensini FS, Maessen J: Left ventricular strain in chronic ischemic mitral regurgitation in relation to mitral tethering pattern. J Am Soc Echocardiogr. 2013, 26: 370-380.
Kaul S, Spotnitz WD, Glasheen WP, Touchstone DA: Mechanism of ischemic mitral regurgitation. An experimental evaluation. Circulation. 1991, 84: 2167-2180.
Messas E, Guerrero JL, Handschumacher MD, Chow C-M, Sullivan S, Schwammenthal E, Levine RA: Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement. Circulation. 2001, 104: 1952-1957.
Uemura T, Otsuji Y, Nakashiki K, Yoshifuku S, Maki Y, Yu B, Mizukami N, Kuwahara E, Hamasaki S, Biro S, Kisanuki A, Minagoe S, Levine RA, Tei C: Papillary muscle dysfunction attenuates ischemic mitral regurgitation in patients with localized basal inferior left ventricular remodeling: insights from tissue Doppler strain imaging. J Am Coll Cardiol. 2005, 46: 113-119.
Chinitz JS, Chen D, Goyal P, Wilson S, Islam F, Nguyen T, Wang Y, Hurtado-Rua S, Simprini L, Cham M, Levine RA, Devereux RB, Weinsaft JB: Mitral apparatus assessemnt by delayed enhancement CMR: Relative impact of infarct distribution on mitral regurgitation. J Am Coll Cardiol Imaging. 2013, 6: 220-224.
Meris A, Amigoni M, Verma A, Thune JJ, Køber L, Velazquez E, McMurray JJV, Pfeffer MA, Califf R, Levine RA, Solomon SD: Mechanisms and predictors of mitral regurgitation after high-risk myocardial infarction. J Am Soc Echocardiogr. 2012, 25: 535-542.
Nesta F, Otsuji Y, Handschumacher MD, Messas E, Leavitt M, Carpentier A, Levine RA, Hung J: Leaflet concavity: A rapid visual clue to the presence and mechanism of functional mitral regurgitation. J Am Soc Echocardiogr. 2003, 16: 1301-1308.
Lang RM, Badano LP, Tsang W, Adams DH, Agricola E, Buck T, Faletra FF, Franke A, Hung J, Pérez de Isla L, Kamp O, Kasprzak JD, Lancellotti P, Marwick TH, McCulloch ML, Monaghan MJ, Nihoyannopoulos P, Pandian NG, Pellikka PA, Pepi M, Roberson DA, Shernan SK, Shirali GS, Sugeng L, Ten Cate FJ, Vannan MA, Zamorano JL, Zoghbi WA: EAE/ASE recommendations for image acquisition and display using three-dimensional echocardiography. J Am Soc Echocardiogr. 2012, 25: 3-46.
Kaji S, Nasu M, Yamamuro A, Tanabe K, Nagai K, Tani T, Tamita K, Shiratori K, Kinoshita M, Senda M, Okada Y, Morioka S: Annular geometry in patients with chronic ischemic mitral regurgitation: three-dimensional magnetic resonance imaging study. Circulation. 2005, 112 (Suppl 9): I409-I414.
Tibayan FA, Rodriguez F, Zasio MK, Bailey L, Liang D, Daughters GT, Langer F, Ingels NB, Miller DC: Geometric distortions of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation. Circulation. 2003, 108 (Suppl 1:II): 116-121.
Otsuji Y, Kumanohoso T, Yoshifuku S, Matsukida K, Koriyama C, Kisanuki A, Minagoe C, Levine RA, Tei C: Isolated annular dilation does not usually cause important functional mitral regurgitation: comparison between patients with lone atrial fibrillation and those with idiopathic or ischemic cardiomyopathy. J Am Coll Cardiol. 2002, 39: 1651-1656.
Chaput M, Handschumacher MD, Tournoux F, Hua L, Guerrero JL, Vlahakes GJ, Levine RA: Mitral leaflet adaptation to ventricular remodeling: occurrence and adequacy in patients with functional mitral regurgitation. Circulation. 2008, 118: 845-852.
Chaput M, Handschumacher MD, Guerrero JL, Holmvang G, Dal-Bianco JP, Sullivan S, Vlahakes GJ, Hung J, Levine RA: Mitral leaflet adaptation to ventricular remodeling: prospective changes in a model of ischemic mitral regurgitation. Circulation. 2008, 120 (11 Suppl): S99-S103.
Dal-Bianco P, Aikawa E, Bischoff J, Guerrero JL, Handschumacher MD, Sullivan S, Johnson B, Titus JS, Iwamoto Y, Wylie-Sears J, Levine RA, Carpentier A: Active adaptation of the tethered mitral valve: Insights into a compensatory mechanism for functional mitral regurgitation. Circulation. 2009, 120: 334-342.
Hung J, Papakostas L, Tahta SA, Hardy GA, Bollen BA, Duran CM, Levine RA: Mechanism for recurrent ischemic mitral regurgitation after annuloplasty: continued LV remodeling as a moving target. Circulation. 2004, 110 (Suppl II): 85-90.
Magne J, Pibarot P, Dumensil JG, Sénéchal M: Continued global left ventricular remodeling is not the sole mechanism responsible for late recurrence of ischemic mitral regurgitation after restrictive annuloplasty. J Am Soc Echocardiogr. 2009, 22: 1256-1264.
Lee LS, Kwon MH, Cevasco M, Schmitto JD, Mokashi SA, McGurk S, Cohn LH, Bolman RM, Chen FY: Postoperative recurrence of mitral regurgitation after annuloplasty for functional mitral regurgitation. Ann Thorac Surg. 2012, 94: 1211-1216.
van Garsse L, Gelsomino S, Lucà F, Lorusso R, Rao CM, Stefàno P, Maessen J: Importance of anterior leaflet tethering in predicting recurrence of ischemic mitral regurgitation after restrictive annuloplasty. J Thorac Cardiovasc Surg. 2012, 143: S54-S59.
Gelsomino S, van Garsse L, Lucà F, Lorusso R, Cheriex E, Rao CM, Caciolli S, Vizzardi E, Crudeli E, Stefàno P, Gensini GF, Maessen J: Impact of preoperative anterior leaflet tethering on the recurrence of ischemic mitral regurgitation and the lack of left ventricular reverse remodeling after restrictive annuloplasty. J Am Soc Echocardiogr. 2011, 24: 1365-1375.
Gelsomino S, Lorusso R, Billè G, Rostagno C, De Cicco G, Romagnoli S, Porciani C, Tetta C, Stefàno P, Gensini GF: Left ventricular diastolic function after restrictive mitral ring annuloplasty in chronic ischemic mitral regurgitation and its predictive value on outcome and recurrence of regurgitation. Int J Cardiol. 2009, 132: 419-428.
Hung J, Solis J, Handschumacher MD, Guerrero JL, Levine RA: Persistence of mitral regurgitation following ring annuloplasty: is the papillary muscle outside or inside the ring?. J Heart Valve Dis. 2012, 21: 218-224.
Levine RA, Schwammenthal E: Ischemic mitral regurgitation on the threshold of a solution: from paradoxes to unifying concepts. Circulation. 2005, 112: 745-758.
Szymanski C, Levine RA, Tribouilloy C, Zheng H, Handschumacher MD, Tawakol A, Hung J: Impact of mitral regurgitation on exercise capacity and clinical outcomes in patients with ischemic left ventricular dysfunction. Am J Cardiol. 2011, 108: 1714-1720.
Bigi R, Cortigiani L, Bovenzi F, Fiorentini C: Assessing functional mitral regurgitation with exercise echocardiography: Rationale and clinical applications. Cardiovasc Ultrasound. 2009, 7: 57-
Lancellotti P, Troisfontaines P, Toussaint AC, Peirard LA: Prognostic importance of exercise-induced changes in mitral regurgitation in patients with chronic ischemic left ventricular dysfunction. Circulation. 2003, 108: 1713-1717.
Giga V, Ostojic M, Vujisic-Tesic B, Djordjevic-Dikic A, Stepanovic J, Beleslin B, Petrovic M, Nedeljkovic M, Nedeljkovic I, Milic N: Exercise-induced changes in mitral regurgitation in patients with prior myocardial infarction and left ventricular dysfunction: relation to mitral deformation and left ventricular function and shape. Eur Heart J. 2005, 26: 1860-1865.
Sidebotham DA, Allen SJ, Gerber IL, Fayers T: Intraoperative transesophageal echocardiography for surgical repair of mitral regurgitation. J Am Soc Echocardiogr. 2014, 27: 345-366.
Shakil O, Jainandunsing JS, Ilic R, Mahmood F: Ischemic mitral regurgitation: an intraoperative echocardiographic perspective. J Cardiothorac Vasc Anesth. 2013, 27: 573-585.
Shiran A, Merdler A, Ammar R, Zlotnick AY, Aravot D, Lazarovici H, Zisman E, Pizow R, Lewis BS: Intraoperative transesophageal echocardiography using a quantitative dynamic loading test for the evaluation of ischemic mitral regurgitation. J Am Soc Echocardiogr. 2007, 20: 690-697.
Delgado V, Tops LF, Schuijf JD, de Roos A, Brugada J, Schalij MJ, Thomas JD, Bax JJ: Assessment of mitral valve anatomy and geometry with multislice computed tomography. J Am Coll Cardiol Imaging. 2009, 2: 556-565.
Beaudoin J, Thai W-E, Wai B, Handschumacher MD, Levine RA, Truong QA: Assessment of mitral valve adaptation with gated cardiac computed tomography: validation with three-dimensional echocardiography and mechanistic insight to functional mitral regurgitation. Circ Cardiovasc Imaging. 2013, 6: 784-789.
Acker MA, Parides MK, Perrault LP, Moskowitz AJ, Gelijns AC, Voisine P, Smith PK, Hung JW, Blackstone EH, Puskas JD, Argenziano M, Gammie JS, Mack M, Ascheim DD, Bagiella E, Moquete EG, Ferguson TB, Horvath KA, Geller NL, Miller MA, Woo YJ, D'Alessandro DA, Ailawadi G, Dagenais F, Gardner TJ, O'Gara PT, Michler RE, Kron IL: Mitral-valve repair versus replacement for severe ischemic mitral regurgitation. N Engl J Med. 2014, 370: 23-32.
Fukuda S, Grimm R, Song JM, Kihara T, Daimon M, Agler DA, Wilkoff BL, Natale A, Thomas JD, Shiota T: Electrical conduction disturbance effects on dynamic changes of functional mitral regurgitation. J Am Coll Cardiol. 2005, 46: 2270-2276.
Solis J, Levine RA, Johnson B, Guerrero JL, Handschumacher MD, Sullivan S, Lam K, Berlin J, Braithwaite GJ, Muratoglu OK, Vlahakes GJ, Hung J: Polymer injection therapy to reverse remodel the papillary muscles: efficacy in reducing mitral regurgitation in a chronic ischemic model. Circ Cardiovasc Interv. 2010, 3: 499-505.
Grossi EA, Patel N, Woo YJ, Goldberg JD, Schwartz CF, Subramanian V, Feldman T, Bourge R, Baumgartner N, Genco C, Goldman S, Zenati M, Wolfe JA, Mishra YK, Trehan N, Mittal S, Shang S, Mortier TJ, Schweich CJ, RESTOR-MV Study Group: Outcomes of the RESTOR-MV Trial (Randomized Evaluation of a Surgical Treatment for Off-Pump Repair of the Mitral Valve). J Am Coll Cardiol. 2010, 56: 1984-1993.
This work was supported in part by grant NIH/NHLBI R01 HL092101 (JH).
The authors disclose no competing financial or non-financial interests relevant to this manuscript.
DMD designed the paper, searched and interpreted published literature, prepared figures and tables, and drafted the manuscript. JH interpreted published literature, drafted and critically revised the manuscript, and prepared figures. Both authors read and approve the final manuscript and ensure the accuracy and integrity of the work.
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Additional file 1:TTE image of asymmetric CIMR developing after inferoposterior myocardial infarction. This video shows a TTE parasternal long axis loop taken from the same patient as described in Figure 3, and it demonstrates the inferobasal aneurysm and asymmetric tenting due to more severe tethering of the posterior mitral leaflet than the anterior mitral leaflet (the underlying rhythm is atrial fibrillation and the effects of variable heart rate must be appreciated by the echocardiographer as it may confound analysis). (ZIP 5 MB)
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Dudzinski, D.M., Hung, J. Echocardiographic assessment of ischemic mitral regurgitation. Cardiovasc Ultrasound 12, 46 (2014). https://doi.org/10.1186/1476-7120-12-46
- Chronic Ischemic mitral regurgitation
- Ventricular remodelling
- Papillary muscle displacement
- Mitral valve tethering
- Mitral valve tenting
- Tethering angles
- Tenting height
- Tenting area
- Mitral annulus dilatation
- Myocardial infarction