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The basic mechanism of ischemic mitral regurgitation (MR) is believed augmented leaflet tethering due to the outward displacement of the papillary muscles by left ventricular (LV) remodeling or dilatation. Annular dilatation and LV dysfunction may not be the central mechanism, but contribute to the development of MR in the presence of augmented tethering. Papillary muscle dysfunction was initially expected to cause leaflet prolapse and MR. However, multiple studies have confirmed that papillary muscle dysfunction per se does not usually cause ischemic MR and recent studies further suggest that papillary muscle dysfunction may occasionally attenuate tethering and MR. Although surgical annuloplasty is usually effective to treat ischemic MR, occasional patients with persistent or recurrent ischemic MR after surgical ring annuloplasty even with advanced downsizing suggest the need for approaches to address tethering. Finally, leaflet tethering in patients with ischemic MR can be heterogeneous, indicating the need for individualized approaches to correct ischemic MR in affected patients.
Ischemic mitral regurgitation (MR) develops in approximately one fifth of patients following acute myocardial infarction (MI) and one half of those with congestive heart failure [
]. Due to the large number of patients with acute MI, the incidence of ischemic MR is also high. Ischemic MR affects patients’ prognosis and doubles mortality following myocardial infarction and heart failure [
], suggesting the specific need to treat mild MR in this etiology. In most patients, the grade of ischemic MR is usually mild and its murmur is soft or occasionally inaudible, so its importance may often be unrecognized by physicians. In addition, treatment strategy is not established. Surgical as well as non-surgical interventions are effective, but considerable numbers of patients with ischemic MR can often present with persistent or recurrent MR even after therapeutic interventions. Therefore ischemic MR presents a vexing clinical problem that requires established therapeutic strategies based on mechanistic understanding.
MR is likely associated with separation or weak coaptation between the anterior and posterior leaflets, which may reflect a morphological change of the leaflets. Because leaflets and chordae are largely avascular tissue and resistant to ischemia, changes in other structures or hemodynamics may cause leaflet deformation and regurgitation. Potential changes that could affect leaflet function include alterations in the mitral annulus, the left ventricular (LV) free wall, the PM, and the pressure or flow around the leaflets. Therefore steps to explore the mechanism of ischemic MR can include evaluation of the morphological characteristics of the leaflets and their correlation with alterations in other structures or hemodynamics.
Insights from mitral leaflet configurations: importance of leaflet tethering
Apical displacement of mitral leaflets relative to the annulus is an important morphological characteristic of the leaflets. Apical displacement of the leaflets and the coaptation relative to the annulus in patients with ischemic MR was initially observed by Ogawa et al. and by Godley et al. (Fig. 1) [
]. The spatial position of the systolic leaflets and the coaptation can be determined by two superimposing and opposing forces acting on the leaflets. Increased LV pressure acts to push the leaflets toward the left atrium, while tethering force of the chordae pulls the leaflets toward papillary muscles and prevent leaflet prolapse into the left atrium. Therefore, systolic position of leaflets can be determined by the balance of these two forces (Fig. 2). Apical displacement of the leaflets and coaptation result from greater tethering force either by reduced closing force and/or augmented tethering force. The tethering force is directly related to the position of the PMs, and outward displacement of the PMs can augment tethering force. Because anterior annulus is spatially fixed at the aortic root, the distance between the anterior annulus and the PM tips can be used as a measure to express the outward displacement of the PMs and tethering [
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
] (Fig. 2). Measurement of the distance between the PM tip and the anterior annulus with apical views using two-dimensional echocardiography can be practical in clinical patients (Fig. 3) [
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.
Figure 1Apically displaced mitral leaflets in patients with ischemic mitral regurgitation (MR). Normal mitral leaflets (white arrows) close at the annular level (red arrows). However, leaflets in patients with ischemic MR coapt at an apically displaced position (yellow arrows) and cannot reach the annular level and (red arrows). LV: left ventricle, LA: left atrium and Ao: aorta.
Figure 2Mitral leaflets closing position can be determined by two superimposing and opposing forces on the leaflets. Greater tethering force either by reduced closing force and augmented tethering force may result in apically displaced leaflets and mitral regurgitation (MR). LV: left ventricle, LA: left atrium and Ao: aorta.
Figure 3A method to measure papillary muscle (PM) tethering distance by routine echocardiography. In the apical 4- and 2-chamber views, distances between PM tip and the contralateral anterior annulus express outward displacement of the lateral and medial PM relative to the anterior annulus, respectively. LV: left ventricle and LA: left atrium.
]. This proposal was based on observations that most patients with ischemic MR have LV dysfunction. Further, experimentally created LV dysfunction has demonstrated apical displacement of the leaflets [
]. However, these observations have been performed in association with LV dysfunction and LV dilatation. Therefore, separation of LV dysfunction from dilatation is necessary to understand the relationship between these factors and ischemic MR with the apical displacement of the leaflets.
In vitro model can offer unique opportunities to evaluate effects of LV dilatation on mitral leaflets without changing other factors. He et al. developed an in vitro mitral valve model and observed that outward displacement of the PM caused MR with apical displacement of the leaflets in the absence of reduced closing force or LV pressure [
]. Schwammenthal further created an in vivo model to separate LV dysfunction from dilatation. He created severe LV dysfunction by beta-blockade with LV ejection fraction below 20% and controlled LV dilatation by pericardial restraint and decreasing preload with roller pump. This investigator then observed that severe LV dysfunction without significant LV dilatation failed to cause apical displacement of the leaflets and MR, while the combination of LV dysfunction and dilatation resulted in apical displacement of the leaflets with ischemic MR [
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
]. The increase in the tethering distance between the PMs and the anterior annulus was proportional to the degree of the ischemic MR in this investigation. This study strongly suggests that augmented PM tethering secondary to LV dilatation is the main cause of ischemic MR.
This concept is consistent with data by other investigators [
Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation.
], including a report by Yiu et al. that characterized the relationship between PM tethering, leaflet tenting, and severity of ischemic MR in clinical patients [
]. The importance of LV sphericity in the development of ischemic MR also supports the tethering concept as a mechanistic explanation for ischemic MR [
It is of note that PM tethering is not necessarily proportional to LV dilatation. Discrepancies between LV dilatation and the degree of associated MR are frequently observed in clinical practice. The most common discrepancy is the higher incidence of ischemic MR in patients with inferior myocardial infarction compared to those with anterior infarction and larger LV [
Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography.
]. Gorman et al. have demonstrated that LV dilatation without prominent geometric changes in the mitral valve apparatus with anteroseptal MI does not cause ischemic MR, while posterior MI, with mitral valve annular and posteromedial PM geometric changes, causes MR in a sheep model (Fig. 4) [
]. Kumanohoso et al. further reported that inferior MI causes less global LV dilatation but greater displacement of the medial PM in clinical patients [
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.
]. Therefore, ischemic MR is proportional to the degree of deformity of the mitral valve complex, especially the outward displacement of the PMs, rather than to global LV dilatation.
Figure 4Mechanism for the higher incidence of ischemic mitral regurgitation in inferior versus anterior myocardial infarction (MI). Global LV remodeling in anterior MI may involve broader LV but without causing major alterations in the mitral valve complex. In contrast, LV remodeling in inferior MI may involve less global remodeling but with major alterations in the mitral valve complex. LV: left ventricle, LA: left atrium and Ao: aorta.
Because augmented tethering seems to be the main cause of ischemic MR, procedures to reverse tethering would be expected to attenuate MR. Liel-Cohen et al. created an animal model of chronic ischemic MR with apical displacement of leaflets due to postero-lateral wall bulging underlying the medial PM. By plicating the bulging wall, the outward displacement of the medial PM was corrected, and the MR was also eliminated [
]. Hung et al. have applied a localized patch containing an epicardial balloon over inferior infarcts with ischemic MR in a sheep model. Injection of saline into the balloon repositioned the underlying wall and PM and eliminated MR with leaflet tenting [
Papillary muscle sling: a new functional approach to mitral repair in patients with ischemic left ventricular dysfunction and functional mitral regurgitation.
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation.
]. However, there are evidences to support the role of reduced closing force as a supplemental factor leading to ischemic MR in the presence of augmented tethering force. In an in vivo model of ischemic MR caused by fixed outward displacement of the PM and constant annular dilatation, He et al. investigated the effects of LV pressure rise on the mitral regurgitation. Increase in systolic LV pressure in this model with fixed mitral valve geometry paradoxically reduced the apical displacement of the leaflets as well as the regurgitant fraction [
]. Schwammenthal et al. further have found that the instantaneous severity of ischemic MR dynamically changes within a cardiac cycle, with the severity maximal in early and late systole and minimal in mid-systole with maximal LV pressure (Fig. 5) [
Dynamics of mitral regurgitant flow and orifice area. Physiologic application of the proximal flow convergence method: clinical data and experimental testing.
]. Hung et al. confirmed such dynamic MR even in patients with fixed annular size by surgical ring plasty, confirming the importance of closing force [
Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: physiologic insights from the proximal flow convergence technique.
]. Breithardt et al. have demonstrated that acute reduction in ischemic MR following cardiac re-synchronization treatment prior to chronic reverse LV remodeling is associated with increase in the leaflet closing force (LV + dP/dt) [
]. These data suggest that, although closing force is not the primary determinant of ischemic MR, it may be a significant and supplemental factor, especially in the presence of augmented leaflet tethering due to PM displacement.
Figure 5Phasic changes in the instantaneous degree of ischemic mitral regurgitation (MR) expressed by proximal isovelocity surface area (PISA) during one cardiac cycle. While MR is maximal in early and late systole, it is minimal in mid-systole (pink arrows) with maximal closing pressure, suggesting that reduced closing force augment MR in early and late systole (blue arrows). LV: left ventricle and LA: left atrium.
The concept of PM dysfunction was proposed by clinical observations that ischemic MR frequently occurred after inferior myocardial infarction with medial papillary muscle dysfunction [
]. Ischemic MR was expected to result from leaflet prolapse due to the reduced longitudinal contraction of the PMs secondary to ischemic dysfunction (Fig. 6). However, multiple experimental studies have reported that isolated PM dysfunction did not cause ischemic MR [
Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography.
]. Therefore, it may be clear that PM dysfunction does not cause MR but there can be a significant relationship between PM dysfunction and ischemic MR due to their close anatomical continuity, which remains unclear.
Figure 6Concept of papillary muscle (PM) dysfunction to cause ischemic mitral regurgitation (MR). PM dysfunction with reduced PM longitudinal shortening was expected to induce leaflet prolapse and ischemic MR. LV: left ventricle, LA: left atrium and Ao: aorta.
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
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.
Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation.
]. Therefore, it is reasonable to view the effects of PM dysfunction on the mitral valve function from the standpoint of leaflet tethering. In this context, LV remodeling in the wall adjacent to the PM may result in augmented tethering and secondary MR (Fig. 7). This can be expressed as associated effects of PM dysfunction to augment tethering and ischemic MR. Alternatively, in the presence of LV remodeling in the adjacent wall, PM dysfunction per se may attenuate longitudinal PM shortening and tethering. This can be expressed as direct effects of PM dysfunction to attenuate tethering and MR.
Figure 7Two superimposing and opposing effects of papillary muscle (PM) dysfunction. Associated effects of PM dysfunction by remodeling of the adjacent wall may augment tethering and mitral regurgitation (MR). In contrast, direct effects of PM dysfunction reduced PM longitudinal shortening may reduce tethering and ischemic MR. LV: left ventricle and LA: left atrium.
Messas et al. addressed this concept and created an animal model of ischemic MR induced by basal posterior myocardial infarction with maintenance of PM perfusion to assure normal PM function. The investigators observed that addition of PM dysfunction with ischemia attenuated leaflet tethering and MR [
Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement.
]. Associated LV adjacent wall remodeling to augment tethering may modulate direct effects of PM dysfunction to attenuate tethering and MR in clinical patients. In this case, PM dysfunction may be associated with less MR in selected patients with a similar degree and location of LV remodeling. With this hypothesis, the investigators selected patients with significant LV remodeling due to inferior myocardial infarction and without other lesions, therefore, similar degree and location of LV remodeling. In these selected patients with similar LV remodeling, PM dysfunction was associated with less MR and less leaflet tenting. These data indicate that PM dysfunction is not the primary cause of ischemic MR and that it may result in attenuated tethering and MR.
Accumulated evidences suggest that PM dysfunction does not generally cause ischemic MR, however, mitral valve prolapse with MR may occasionally develop in patients with ischemic heart disease or in animal models [
Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography.
]. Such patients with myocardial infarction have leaflet prolapse with PM elongation or a short distance between the PM and the mitral annulus due to a hypercontractile LV. Further, the secondary MR responds to PM shortening or leaflet reduction [
]. These observations, rather than disproving the tethering mechanism, actually confirm that the tethering distance from the PM tip to the mitral annulus is the final common pathway that determines the level of leaflet coaptation.
PM dyssynchrony can potentially worsen ischemic MR. Investigators have observed association of ischemic MR and PM dyssynchrony [
A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: insights from mechanical activation strain mapping.
]. These investigations require further study to separate effects of PM dyssynchrony from other factors such as LV dilatation, dysfunction and others.
Annular dilatation
From the structural characteristics of the mitral valve complex, annular dilatation is expected to worsen ischemic MR. The unclear point is whether it is a major determinant of the MR or not.
Mitral annulus is consistently dilated in patients with ischemic MR compared to normal subjects [
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.
Annular geometry and motion in human ischemic mitral regurgitation: novel assessment with three-dimensional echocardiography and computer reconstruction.
]. Therefore, it is not clear whether annular dilatation is a major determinant of ischemic MR or not.
Annular dilatation is usually associated with LV dilatation in patients with the MR, which can cause difficulty in characterizing the role of annular dilatation in the development of ischemic MR. In order to avoid this difficultly, we studied patients with lone atrial fibrillation, who often have left atrial dilatation without LV dilatation [
]. Because the mitral annulus is positioned in between the left atrium and the LV, lone atrial fibrillation may cause isolated annular dilatation without LV dilatation, which may offer a unique opportunity to investigate effects of annular dilatation on mitral valve function. We have found that annular dilatation in patients with lone atrial fibrillation was comparable to the annular dilatation in those with ischemic or idiopathic cardiomyopathy. Further, the annular dilatation in patients with lone atrial fibrillation was not associated with moderate to severe MR, while the same degree of the annular dilatation in those with cardiomyopathy was frequently associated with significant MR (Fig. 8) [
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.
]. These data demonstrate that isolated annular dilatation, even with the same degree to patients with cardiomyopathy and significant MR, failed to cause significant MR. These suggest that annular dilatation is not a major determinant of MR in the absence of leaflet tethering due to LV dilatation. However, annular dilatation may exert an effect on development of MR in the presence of leaflet tethering. For example, He et al. reported a greater increase in MR in response to annular dilatation in the presence of PM displacement in an in vitro model [
Figure 8Discrepancies between annular dilatation and the grade of mitral regurgitation (MR). The left panel shows that annular dilatation in a patient with lone atrial fibrillation (Af) without left ventricular (LV) dilatation fails to cause leaflet tenting and significant MR. The right panel shows that the same degree of mitral annular dilatation in a patient with dilated cardiomyopathy (DCM) is associated with apically displaced leaflets and significant MR. LV: left ventricle, LA: left atrium, Ao: aorta and RV: right ventricle.
], which may increase the distance between the commissural points and the PMs, potentially increasing tethering. Based on this concept, several groups have attempted to determine the effect of a modified ring shape on tethering and MR. Reduction in systolic contraction of the annulus may also contribute to the development of ischemic MR.
Effects of annuloplasty on ischemic MR
Multiple experimental and clinical studies seem to indicate that annular dilatation is not of critical importance to the development of ischemic MR [
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
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.
Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: physiologic insights from the proximal flow convergence technique.
], is usually effective in eliminating ischemic MR. Development of ischemic MR due to leaflet tethering by outward displacement of the PMs can result from consumption of the physiological coaptation zone between the anterior and posterior leaflet (Fig. 9). Annular size reduction may not relieve tethering of the leaflets but does shift the posterior annulus and leaflet anteriorly so that the consumed coaptation zone can be restored (Fig. 9) [
]. Thus, while surgical annuloplasty is effective in reversing ischemic MR, the procedure does not necessarily address tethering. Therefore, advanced tethering may result in persistent ischemic MR even after ring annuloplasty with or without down sizing [
Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: physiologic insights from the proximal flow convergence technique.
Figure 9Mechanism of beneficial surgical ring annuloplasty on ischemic mitral regurgitation (MR). The middle panel shows that development of the ischemic MR is related to the consumption of physiological coaptation between the anterior and posterior leaflets. Surgical ring annuloplasty can shift the posterior annulus and leaflet anteriorly so that the coaptation can be restored even with maintained tethering. LV: left ventricle, LA: left atrium and Ao: aorta.
Because leaflet tethering due to outward displacement of the PMs appears to be the main cause of the ischemic MR and the geometric relationship between the PMs and the chordal attachment at the leaflet can be heterogeneous, leaflet tethering can vary within a single patient as well as among multiple patients.
One such example is the augmented tethering that occurs at the mid-portion of the anterior leaflet with basal or strut chordal insertion (Fig. 10). While anterior leaflet in the echocardiographic long axis view is convex toward the left atrium in normal subjects, it is concave in patients with ischemic MR. This suggest that the middle portion of the anterior leaflet is more tethered compared to the leaflet tip [
]. Based on these observations, Messas et al. reported that cutting of the basal chordae in an animal model of ischemic MR eliminated the MR by restoring the physiological convex configuration of the anterior leaflets toward the left atrium [
Figure 10Regional difference in tethering at the middle portion of anterior mitral leaflet. Although apical displacement of leaflets involves whole anterior and posterior leaflets, the displacement is regionally augmented in the middle portion of the anterior leaflet (yellow arrows). LV: left ventricle, LA: left atrium, Ao: aorta and RV: right ventricle.
The degree and direction of outward displacement of the PMs can vary between patients, which suggest that leaflet tethering pattern may also vary between patients with ischemic MR. Kwan et al. reported that the medial side of the mitral leaflets is more apically displaced compared to lateral side of the leaflets in patients with ischemic MR due to inferior myocardial infarction, while the displacement was approximately symmetric when comparing the medial and lateral side in patients with MR due to dilated cardiomyopathy [
Real-time three-dimensional echocardiography study. Geometric differences of the mitral apparatus between ischemic and dilated cardiomyopathy with significant mitral regurgitation: real-time three-dimensional echocardiography study.
]. The medial and lateral PM displacement was also asymmetric, with a predominance for the medial PM in patients with ischemic MR due to inferior myocardial infarction [
]. It is, however, controversial whether asymmetric PM displacement causes asymmetric leaflet tenting or not. Watanabe et al. have observed approximately symmetric leaflet tenting in patients with inferior myocardial infarction with potentially asymmetric PM displacement [
Geometric differences of the mitral valve tenting between anterior and inferior myocardial infarction with significant ischemic mitral regurgitation: quantitation by novel software system with transthoracic real-time three-dimensional echocardiography.
Surgical ring annuloplasty may also cause heterogeneous mitral leaflet tethering. Surgical ring annuloplasty, which reduces the antero-posterior dimension of the mitral annulus, displaces the posterior annulus anteriorly. However, the anterior annulus remains fixed at the aortic root, which can result in augmented tethering of the posterior leaflet while maintaining tethering of the anterior leaflet. This predominant tethering of the posterior mitral leaflet can be observed in the echocardiographic long axis view. Fig. 10 shows usual leaflet tethering due to dilated cardiomyopathy that results in approximately symmetric tethering of the anterior and posterior leaflets with increased angles between the leaflets and the line connecting the annuli. However, this angle becomes highly asymmetric following surgical annuloplasty for ischemic MR (Fig. 11). This asymmetric tethering of the posterior leaflet can be associated with persistent or recurrent ischemic MR after the surgery [
Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase following surgical annuloplasty: Importance of augmented posterior leaflet tethering.
Figure 11A patient with recurrent functional mitral regurgitation (MR) following mitral annuloplasty (aortic valve replacement [AVR] was also performed). The mitral annuli are connected with a white line. The left ventricle (LV) is dilated, the anterior leaflet is tethered (larger white arrow), and the posterior leaflet is extremely tethered (yellow arrow), resulting in more posterior coaptation (pink arrow) than posterior annulus (thinner yellow arrow). LA: left atrium and RV: right ventricle.
Further variability in mitral leaflet tethering may occur in the context of individually heterogeneous deformation of the mitral valve complex in patients with ischemic MR. A global and three-dimensional approach may allow for comprehensive evaluation of the tethering of the whole leaflets and help guide surgery [
Basic mechanism of ischemic MR is geometric deformity of the mitral valve complex with outward displacement of papillary muscles. Current therapeutic approaches may not fully address such geometric abnormalities. Comprehensive evaluation of the geometry of the mitral valve complex may allow better understanding of the pathophysiology, leading to therapeutic approaches that address fundamental mechanism of the disease.
References
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Gardner L.H.
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Outcome of patients sustaining acute ischemic mitral regurgitation during myocardial infarction.
Insights from three-dimensional echocardiography into the mechanism of functional mitral regurgitation: direct in vivo demonstration of altered leaflet tethering geometry.
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.
Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation.
Mechanism of mitral regurgitation in patients with myocardial infarction: a study using real-time two-dimensional Doppler flow imaging and echocardiography.
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.
Papillary muscle sling: a new functional approach to mitral repair in patients with ischemic left ventricular dysfunction and functional mitral regurgitation.
Dynamics of mitral regurgitant flow and orifice area. Physiologic application of the proximal flow convergence method: clinical data and experimental testing.
Mechanism of dynamic regurgitant orifice area variation in functional mitral regurgitation: physiologic insights from the proximal flow convergence technique.
Paradoxic decrease in ischemic mitral regurgitation with papillary muscle dysfunction: insights from three-dimensional and contrast echocardiography with strain rate measurement.
A mechanism for immediate reduction in mitral regurgitation after cardiac resynchronization therapy: insights from mechanical activation strain mapping.
Annular geometry and motion in human ischemic mitral regurgitation: novel assessment with three-dimensional echocardiography and computer reconstruction.
Real-time three-dimensional echocardiography study. Geometric differences of the mitral apparatus between ischemic and dilated cardiomyopathy with significant mitral regurgitation: real-time three-dimensional echocardiography study.
Geometric differences of the mitral valve tenting between anterior and inferior myocardial infarction with significant ischemic mitral regurgitation: quantitation by novel software system with transthoracic real-time three-dimensional echocardiography.
Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic phase following surgical annuloplasty: Importance of augmented posterior leaflet tethering.
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