Mechanism Of Ischemic Mitral Regurgitation Research Articles

Correlation between echocardiographic severity of ischemic mitral valve regurgitation following acute myocardial infarction and its electrocardiographic location

Introduction: Ischemic mitral regurgitation (IMR) is common after acute myocardial infarction (AMI) which is associated with long-term cardiovascular mortality. Size, transmurality and location of the myocardial infarction (MI) has role on the development of IMR. In this study we evaluated the severity of IMR after different types of MI. Methods: One-hundred patients with the first AMI were recruited and according to echocardiographic findings were categorized to have moderate to severe IMR (case group, n=50) or trivial or no IMR (control group, n=50). Demographic and echocardiographic findings and MI location were compared between groups. Results: Case group compared to control group had significantly higher Killip class, more cases with left ventricular ejection fraction (LVEF) <30% and inferolateral STEMI. They had significantly higher left ventricular (LV) and right ventricular (RV) diastolic dysfunction. Mechanism of IMR was mono leaflet tethering in 88%, both leaflets tethering in 12% and ring dilatation in 62%. MR jet origin-direction was medial commisure-posterior in 66%, lateral commisure-anterior in 11 22% and both commisure-central direction in 12%. Conclusion: IMR is common after AMI, especially in cases with inferior MI. The echocardiographic findings are indicative of left ventricular remodeling and abnormality of mitral valve apparatus.

Ischemic Mitral Regurgitation: Unusual Approaches for Correction

Ischemic mitral regurgitation (MR) results from ischemic left ventricular distortion with tethering of the mitral leaflets. The standard surgical therapy for ischemic MR is mitral ring annuloplasty, often performed at the time of coronary artery bypass surgery. However, ring annuloplasty is associated with an up to 30% recurrence rate of MR, as it does not directly address ventricular distortion and tethering of the mitral leaflets and there is often further ventricular remodeling following bypass surgery. This article reviews the background and mechanism of ischemic MR and unusual approaches to this important yet difficult to treat valvular problem.

Mechanism of ischemic mitral regurgitation

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.

Mechanism of Ischemic Mitral Regurgitation

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.

Different Mechanisms of Ischemic Mitral Regurgitation in Patients With Inferior and Anterior Myocardial Infarction

Background. Basic mechanism of ischemic mitral regurgitation (MR) is displacement of papillary muscles (PMs) due to left ventricular (LV) remodeling. Variability in LV remodeling can potentially cause heterogeneous PM displacements. The aim of this study is to compare the mitral valve complex geometry in patients with ischemic MR due to inferior and anterior myocardial infarction (MI).Methods. In 33 patients with prior inferior MI, 61 with anterior MI, and 22 controls, LV volume, mitral annular area, PM tethering distance, and MR were quantified by echocardiography.Results. Significant MR (MR fraction > 20%) was observed in 12 of the 33 with inferior MI and 7 of the 61 with anterior MI. In patients with MR due to inferior MI, tethering distance was significantly longer in medial compared to lateral PM (42.6 ± 4.9 vs. 36.1 ± 1.7 mm, p Conclusions. Although patients with ischemic MR due to inferior MI have asymmetrically predominant medial PM displacement, those with ischemic MR due to anterior MI have symmetric bilateral PM displacements.

Echocardiographic classification of chronic ischemic mitral regurgitation caused by restricted motion according to tethering pattern.

Although the mechanism of ischemic mitral regurgitation (MR) is understood, the echocardiographic picture of ischemic MR is not homogeneous. Ninety-two consecutive patients with chronic ischemic MR due to restricted motion were divided into two groups according to tethering pattern: the asymmetric group with predominant posterior tethering of both leaflets (54 patients) and the symmetric one with predominant apical tethering of both leaflets (38 patients). The mitral deformation indexes, LV global (volume, function and sphericity) and local (papillary muscle displacements and regional wall motion score index) remodeling were evaluated. All indexes of global LV remodeling were significantly higher in the symmetric than asymmetric group (all p < 0.0001), such as the posterior and lateral displacement of the anterior papillary muscle (both p < 0.04), the papillary muscle separation and the anterior papillary muscle wall motion index (both p < 0.0001). The origin as well as the direction of the jet was central in all patients of the symmetric group. In the asymmetric one the origin was central in 78% of the cases and arising from the medial commissure in 22% whereas the jet direction was posterior and central in 83% and 17% of patients, respectively. Therefore, it is possible to distinguish at least two subgroups of patients with ischemic MR due to restricted motion on the basis of tethering pattern, different degree of local and global LV remodeling and characteristics of the regurgitant jet.

Cirugía de la insuficiencia mitral isquémica

Ischemic mitral regurgitation (IMR) is a severe condition which may be best treated by surgery, notwithstanding a relatively high mortality rate. To evaluate the results of mitral valve replacement or repair in patients with IMR. Retrospective review of the clinical records in 29 patients with IMR who were surgically treated from 1990 to 1999. They represent 8% of surgical procedures on the mitral valve. Mean age was 67 +/- 9 years. Surgery was performed urgently in 19 patients (66.5%). NYHA functional class was 3.4 +/- 0.8. The mechanism of IMR was annular dilatation and spreading of papillary muscles in 18 patients, papillary muscle rupture in 9 and fibrosis in 2. Mitral valve replacement was performed in 14 patients and mitral valve repair in 15. Twenty four patients (83%) had concomitant myocardial revascularization. Overall surgical mortality was 24%; 26% for mitral replacement and 13% for mitral valve repair (p = 0.215). On follow up of 26 +/- 33 months, one year survival was 76 +/- 0.8% and 5 years survival was 59 +/- 12%. Excluding in hospital mortality, survival was 100% at one year and 78 +/- 14% at 5 years. Functional class improved in all survivors, to 1.4 +/- 0.5. Late echocardiographic evaluation of patients with mitral valve repair showed absence of mitral regurgitation in 58%, 1+ MR in 17% and 2+ MR in 25%. In spite of a high perioperative mortality, surgery for IMR is a valuable procedure for patients with an otherwise highly lethal disease.

Mechanism of ischemic mitral regurgitation with segmental left ventricular dysfunction: three-dimensional echocardiographic studies in models of acute and chronic progressive regurgitation

OBJECTIVESThis study aimed to separate proposed mechanisms for segmental ischemic mitral regurgitation (MR), including left ventricular (LV) dysfunction versus geometric distortion by LV dilation, using models of acute and chronic segmental ischemic LV dysfunction evaluated by three-dimensional (3D) echocardiography.BACKGROUNDDysfunction and dilation—both mechanisms with practical therapeutic implications—are difficult to separate in patients.METHODSIn seven dogs with acute left circumflex (LCX) coronary ligation, LV expansion was initially restricted and then permitted to occur. In seven sheep with LCX branch ligation, LV expansion was also initially limited but became prominent with remodeling over eight weeks. Three-dimensional echo reconstruction quantified mitral apparatus geometry and MR volume.RESULTSIn the acute model, despite LV dysfunction with ejection fraction = 23 ± 8%, MR was initially trace with limited LV dilation, but it became moderate with subsequent prominent dilation. In the chronic model, MR was also initially trace, but it became moderate over eight weeks as the LV dilated and changed shape. In both models, the only independent predictor of MR volume was increased tethering distance from the papillary muscles (PMs) to the anterior annulus, especially medial and posterior shift of the ischemic medial PM, measured by 3D reconstruction (r2= 0.75 and 0.86, respectively). Mitral regurgitation volume did not correlate with LV ejection fraction or dP/dt.CONCLUSIONSSegmental ischemic LV contractile dysfunction without dilation, even in the PM territory, fails to produce important MR. The development of MR relates strongly to changes in the 3D geometry of the mitral apparatus, with implications for approaches to restore a more favorable configuration.

Mechanism of Ischemic Mitral Regurgitation With Ventricular Remodeling After Myocardial Infarction: Demonstration of Leaflet Tethering by Three-dimensional Echocardiography

Mechanism of Ischemic Mitral Regurgitation With Ventricular Remodeling After Myocardial Infarction: Demonstration of Leaflet Tethering by Three-dimensional Echocardiography

Mechanism of ischemic mitral regurgitation with ventricular remodeling after-myocardial infarction: demonstration of leaflet tethering by three-dimensional echocardiography

Mechanism of ischemic mitral regurgitation with ventricular remodeling after-myocardial infarction: demonstration of leaflet tethering by three-dimensional echocardiography

Mechanism of ischemic mitral regurgitation. An experimental evaluation.

Papillary muscle dysfunction (PMD) has been implicated in the pathogenesis of ischemic mitral regurgitation (MR). We hypothesized that ischemic MR is not caused by PMD and/or dysfunction of the myocardial regions from where the papillary muscles arise but is related to reduction in global left ventricular (LV) function. To test this hypothesis, three groups of dogs were studied. In group 1 dogs (n = 8), varying degrees of regional and global LV dysfunction were produced. In group 2 dogs (n = 7), the circulation to the papillary muscles was isolated from that of the rest of the LV. Dysfunction of one or both papillary muscles was produced without producing global LV dysfunction. Global LV dysfunction was also produced while keeping papillary muscle function intact. The degree of MR (assessed using contrast echocardiography) was correlated in both groups of dogs with thickening of the papillary muscles and regional and global LV function. In the group 3 dogs (n = 6), the spatial distribution of blood flow within each papillary muscle was determined during ischemia by using radiolabeled microspheres. Thickening of the papillary muscles was assessed at three different levels along their lengths and was correlated with average blood flow at these levels. In group 1 dogs, MR was noted only when global LV function was affected and its severity correlated inversely with global LV function (r = -0.84 with peak positive LV dP/dt and r = -0.95 with global LV thickening, respectively). In comparison, there was poor correlation between MR and anterior and posterior papillary muscle thickening (r = -0.38 and r = -0.49, respectively). In group 2 dogs, MR did not occur in the presence of either PMD or akinesia of the immediately adjacent LV myocardium. MR occurred only when global LV dysfunction was produced (with the papillary muscle function intact), and its severity correlated inversely with global LV function (r = -0.92 with LV dP/dt and r = -0.86 with global LV thickening, respectively). There was poor correlation between the degree of MR and thickening of the anterior and posterior papillary muscles (r = -0.24 and r = -0.38, respectively). In both groups of dogs, MR was associated with incomplete mitral leaflet closure (IMLC), and the severity of MR correlated linearly with the degree of IMLC (r = 0.98). MR was never associated with mitral valve prolapse. In the group 3 dogs, despite more inhomogeneous flow during ischemia to the anterior compared with the posterior papillary muscle, mean thickening of these muscles was similar (3 +/- 10% and 3 +/- 4%, respectively). Furthermore, there was minimal variability in thickening between different parts of the muscles (3 +/- 2% and 5 +/- 3%, respectively). It is concluded that PMD and/or dysfunction of the immediately adjacent LV myocardium does not result in MR. MR occurs during ischemia only when global LV function is affected, even when thickening of the papillary muscles and the immediately adjacent LV remains intact. MR in this situation is related to IMLC; the greater the degree of IMLC, the greater the MR. These findings suggest that the mechanism of ischemic MR is not related to PMD. There may also be important therapeutic implications of these findings.