Fig. 2.1
The posterior mitral valve leaflet is tethered or restricted at P3 due to displacement of the posteromedial papillary muscle following an inferolateral myocardial infarction (Adapted from Chan et al. [5]. With permission from Elsevier)
Dilatation of the mitral annulus, both at the anterior fibrous trigone and the posterior muscular area, and flattening of its normal saddle shape, has been reported in functional ischaemic mitral regurgitation. These studies have largely been performed in animals and cadavers, and by echocardiography [6, 11–17]. Changes in the mitral annular geometry may be related to the degree of left ventricular remodelling and severity of mitral regurgitation in different patients, and may be related to the different stages of the cardiac cycle. Knowledge of this is important in the design of annuloplasty rings or bands, and in the practice of under-sizing the annuloplasty ring during surgery.
Functional ischaemic mitral regurgitation can also occur as a result of global left ventricular dilatation, usually following an anterior myocardial infarction, leading to displacement of both papillary muscles and tethering of both mitral valve leaflets [4, 9, 10, 18, 19]. However, it does not occur in all cases of ischaemic left ventricular dilatation, and further studies are needed to provide insights into this. It is possible that the development of functional ischaemic mitral regurgitation may be influenced by the degree and direction of papillary muscle displacement as a result of the dilated left ventricle, or an increased sphericity of the left ventricle, or decreased left ventricular contractility. Studies of the geometry, size, function and displacement of the papillary muscles and the left ventricle would provide valuable insights.
Animal studies have demonstrated that lateral displacement of papillary muscles occur in functional ischaemic mitral regurgitation [15]. Most echocardiographic studies have demonstrated lateral and posterior displacement of papillary muscles [7, 16, 19]. Some studies suggest that apical displacement of papillary muscles also occur [7, 19]. The role of papillary muscle dysfunction and infarction in the pathogenesis of functional ischaemic mitral regurgitation is also uncertain. It has been suggested that papillary muscle ischaemia or infarction may attenuate functional ischaemic mitral regurgitation as the loss of papillary muscle systolic contraction actually reduces leaflet tethering [8, 20–22]. The incidence of papillary muscle ischaemia or infarction is unknown.
Mitral Annular Geometry and Motion
The motion and geometry of the mitral annulus in the normal cardiac cycle is discussed in the previous chapter. In contrast to healthy subjects without functional ischaemic mitral regurgitation, in whom the mitral annular septolateral diameter decreased in size by about 15 % just before the start of left ventricular systole (phase VI of the cardiac cycle), and then increased in size towards the end of left ventricular systole just before leaflet opening (phase I of the cardiac cycle), the mitral annulus in patients with functional ischaemic mitral regurgitation remains a relatively constant size throughout the cardiac cycle (Fig. 2.2) [23–25].
In functional ischaemic mitral regurgitation, mitral annular function is impaired so that it fails to contract and reduce in size just before left ventricular systole. In normal subjects, the mitral annulus contracts and reduces in size just before left ventricular systole to increase the coaptation between the anterior and posterior mitral leaflets. This contractile function of the mitral annulus appears to be impaired in functional ischaemic mitral regurgitation and may be one of the mechanisms causing mitral incompetency [23, 24]. The mitral annulus is not necessarily dilated in functional ischaemic mitral regurgitation, although it may be. Rather, mitral annular function is impaired with reduced pre-systolic mitral annular contraction in its septolateral dimension. As a result, the mitral annulus is enlarged in the septolateral dimension at the onset of left ventricular systole, reducing leaflet coaptation.
The excursion of the mitral annulus towards the left ventricular apex during left ventricular systole in patients with functional ischaemic mitral regurgitation (phase I of the cardiac cycle) is significantly less than the corresponding values in healthy subjects [23, 24]. This finding again confirms reduced mitral annular function in functional ischaemic mitral regurgitation, although in this case, impaired left ventricular function is the likely contributing factor. The reduced excursion of the mitral annulus towards the left ventricular apex during left ventricular systole increases the tension on the mitral subvalvular apparatus during systole resulting in increased tethering of the mitral leaflets. This may be another mechanism contributing to mitral incompetency in functional ischaemic mitral regurgitation.
The mitral annulus in functional ischaemic mitral regurgitation shows impaired function with reduced septolateral contraction and reduced excursion towards the left ventricular apex and consequently, reduced recoil back towards the left atrium [24]. The mitral annulus in functional ischaemic mitral regurgitation is not necessarily dilated, at least in patients with less than severe functional ischaemic mitral regurgitation. Rather, the loss of pre-systolic mitral annular contraction results in a larger mitral annulus in the septolateral dimension at the onset of left ventricular systole, which may be an important mechanism reducing the surface of coaptation of the mitral valve leaflets [24]. Decreased mitral annular contraction in functional ischaemic mitral regurgitation has previously been documented using echocardiography [7, 16]. Some studies report that the mitral annulus is dilated in the septolateral direction but these studies did not analyse the mitral annular size throughout the cardiac cycle and it is possible the images were acquired at early systole [6, 16, 26]. It is also possible that patients in those studies had more severe mitral regurgitation and therefore more advanced disease.
In patients with more advanced disease with greater left ventricular dilatation, in addition to a loss of pre-systolic contraction, the mitral annulus may also dilate. Cadaveric studies have reported dilatation of both the anterior and posterior mitral annulus in advanced ischaemic cardiomyopathy [12]. Animal studies have also reported an increase in the septolateral mitral annular diameter in functional ischaemic mitral regurgitation, although the left ventricular remodelling in these animal models are likely to be more significant and exaggerated, compared to functional ischaemic mitral regurgitation patients, as the models involved complete acute ligation of the circumflex coronary artery [13, 15].
These findings lend support to the use of an under-sized complete rigid or semi-rigid annuloplasty ring for functional ischaemic mitral regurgitation, which reduces the size of the mitral annulus at the septolateral dimension and fixes its position in systole.
The excursion of the mitral annulus towards the left ventricular apex during left ventricular systole is also significantly reduced in patients with functional ischaemic mitral regurgitation compared to controls [24]. This observation has also been reported in another study using echocardiography [27]. As discussed in Chap. 1, the mitral annulus in normal subjects moves towards the apex of the left ventricle during left ventricular systole, and the left ventricle along with the papillary muscles it supports, moves towards the mitral annulus. Papillary muscle contraction occurs during this time to maintain mitral leaflet competency and prevent leaflet prolapse. The reduced excursion of the mitral annulus towards the left ventricular apex in functional ischaemic mitral regurgitation would have the effect of increasing tethering on the mitral valve leaflets. This is possibly an added mechanism contributing to functional ischaemic mitral regurgitation.
Mitral Leaflet Geometry and Motion
Leaflet restriction during systole, particularly of the posterior mitral leaflet at P3 is typical, although anterior leaflet restriction also occurs. In many cases, restriction of P2 is also present. Restriction of both the anterior and posterior mitral leaflets during left ventricular systole is present in most patients, with the most common scallops involved being A2-P2 and A3-P3. There is also restriction of leaflet mobility with the maximal separation of the mitral leaflets during diastole (in phase II of the cardiac cycle) being significantly less than that in healthy subjects [23, 24]. It was demonstrated in Chap. 1 that recoil of the mitral annulus towards the left atrium during atrial systole further increases leaflet separation. The reduced systolic excursion of the mitral annulus during left ventricular systole and resulting reduced atrial recoil of the annulus at the end of left ventricular systole may explain the reduced maximal separation of the mitral leaflets in functional ischaemic mitral regurgitation.
Restriction of the leaflets during systole results in an increase in the tethering distance and tethering area [26]. Most authors measure the tethering distance, which is the distance between the mitral annular plane and the point of coaptation of the mitral leaflets (Fig. 2.3). However, the difference between the tethering distance in functional ischaemic mitral regurgitation patients and healthy subjects may not always be large, and it may be better to measure the tethering area instead which gives a more reliable indicator of the degree of tethering throughout the mitral valve leaflets, rather than just at its coaptation point (Fig. 2.4) [24]. There is an increased tethering area and tethering distance between the plane of the mitral annulus and the mitral leaflets during systole. The size of the tethering area is correlated with left ventricular volumes; bigger left ventricles were associated with larger tethering areas [24].
Fig. 2.3
The tethering distance is measured from the mitral annular plane to the coaptation point of the mitral leaflets
Fig. 2.4
The tethering area is measured as the area bounded by the mitral leaflets and the mitral annular plane
The mitral leaflet in functional ischaemic mitral regurgitation shows restricted motion at systole with significant tethering away from the mitral annulus. Furthermore, the maximal separation of the mitral leaflets in diastole (Phase II of the cardiac cycle) is reduced, possibly due to decreased recoil of the mitral annulus in these patients [24]. As discussed in Chap. 1, recoil of the mitral annulus towards the left atrium may pull the mitral leaflets further apart. The maximal separation of the mitral valve leaflets during left ventricular diastole is decreased and may be related to impaired mitral annular function. Recent studies have also suggested that cellular changes occur in the mitral leaflet in mitral regurgitation with an increase in collagen synthesis and leaflet thickness, and it is possible that this may also contribute to its reduced motion and separation [28, 29].
Papillary Muscle Geometry, Function and Viability
Lateral and Posterior Displacement
During both left ventricular systole and diastole, the inter-papillary muscle distance (i.e., the distance between the anterolateral and posteromedial papillary muscles, Fig. 2.5), the posterior displacement of the posteromedial papillary muscle from the septum, and the lateral displacement of the posteromedial papillary muscle from the long axis midline of the left ventricular chamber are significantly greater in functional ischaemic mitral regurgitation compared to healthy subjects [23, 24].
Fig. 2.5
Inter-papillary muscle distance
These findings strongly demonstrate that in functional ischaemic mitral regurgitation, the geometry of the papillary muscles is altered with lateral displacement of the papillary muscles away from each other and from the midline of the left ventricular chamber, and posteriorly away from the LV-RV septum. This altered geometry of the papillary muscles is most marked at the end of left ventricular systole. The effect of such alterations in papillary muscle geometry would be to increase the tension on the chordae and the mitral leaflets during leaflet closure at the onset of left ventricular systole (phase VI of the cardiac cycle) resulting in increased mitral leaflet tethering. The cause of such alteration in the papillary muscle geometry may be related to increased left ventricular size and impaired left ventricular function, and to local remodelling of the left ventricle at the region of papillary muscle insertion.
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