Correctly identifying the mechanism of MR as functional and ischemic and correctly evaluating its severity can be surprisingly challenging. It is therefore fundamental to success that the echocardiologist has an in-depth understanding of the normal morphology and physiology of the mitral valve-LV complex [10]. The term “mitral valve-LV complex includes the leaflets, annulus, chordae, papillary muscles and supporting left ventricular myocardium, and the exact geometry required to produce perfect leaflet coaptation may be disrupted by abnormalities of any one of these components. Transthoracic echocardiography (TTE) may in many cases prove sufficient to confirm the diagnosis, but transesophageal echocardiography (TEE) is needed in cases where the ischemic mechanism is unclear and is also a useful adjunct for delineating the mechanism and quantifying morphological parameters in the pre- and perioperative patient thus allowing for advanced planning of individually-tailored intervention [11]. Guidelines state that all patients being considered for mitral intervention should undergo transesophageal echocardiography [19].

Many, but not all, patients will give a definite history of myocardial infarction and/or coronary artery disease. Before assessing the mitral valve itself, the echocardiographer must first make a thorough assessment of the left ventricle (LV), including wall thickness and diastolic and systolic chamber dimensions and volumes, either from 2-dimensional or 3-dimensional imaging (Fig. 3.3). The abnormality of the ventricle may be global dilatation or regional/segmental dysfunction (Fig. 3.4). Differentiation between the two is key to classification of the FIMR. Identification of a segmental wall motion abnormality suggesting previous infarction is often the key finding and the typically-affected segments are the basal and mid inferior and/or inferolateral segments [12]. These regional abnormalities can be very subtle, particularly if the infarct is subendocardial. In addition, in the presence of moderate or severe MR, the resulting hyperdynamic wall motion of other segments will tend to mask mild segmental abnormalities. The key is to have a high degree of suspicion in any patient with a history of CAD or significant risk factors and to look for abnormalities of thickening rather than motion. Newer techniques such as analysis of basal rotational dynamics and segmental layered strain analysis by speckle-tracking echocardiography can be a useful adjunct if there is doubt about the presence of a segmental wall motion abnormality [13]. Cardiac magnetic resonance imaging has also proved to be helpful in these situations, in that late-enhancement with gadolinium contrast agents can identify areas of segmental partial thickness infarction, which may be revealed even in patients who do not have a confirmed history of myocardial infarction (Fig. 3.5) [14]. As infarction of the basal inferior and inferolateral segments is a predictor of recurrent MR after mitral ring annuloplasty this author recommends cardiac MRI in any patient with valve morphology consistent with FIMR but no history or obvious regional wall motion abnormality.

Leaflet tethering or restriction (the terms are used interchangeably) due to displacement of one or both papillary muscles (PM) is the key echocardiographic finding in FIMR. Tethering may be symmetrical, affecting both leaflets, when it is also referred to as “tenting” (Fig. 3.6) or asymmetrical, affecting only one leaflet (Fig. 3.7a) [15]. If only one leaflet is affected, it is more often the posterior leaflet, as the posteromedial papillary muscle tends to have a single-vessel blood supply and so inferior or inferolateral infarction is more likely to cause asymmetric tethering than anterior infarction – the P3 scallop can be restricted almost in isolation if an infarct is limited and well-circumscribed. The result is that the anterior leaflet coaptation zone or rough zone apposes the body of the posterior leaflet rather then its corresponding coaptation zone. This reduces the coaptation length and produces an eccentric jet of mitral regurgitation – directed towards the restricted leaflet ie most commonly posteriorly-directed (Fig. 3.7b).

If the area of myocardial dysfunction is large and involves several segments, or if there is extensive ventricular remodeling, then LV dilatation may be global. The resulting apical displacement and increased separation of the papillary muscles causes both leaflets of the mitral valve to be tethered or tented into the LV. In these cases, the LV function is usually more severely impaired and the resultant mitral regurgitant jet is more central – though it is rarely absolutely central. There have been numerous studies investigating possible relationships between LV systolic dysfunction, dilatation and severity of FIMR. In an animal model it has been shown that systolic dysfunction in isolation does not cause MR, presumably because without the additional forces tethering the leaflets into the ventricle there is still sufficient force generated to produce sufficient leaflet coaptation. However, in the same model, when the LV was allowed to dilate, causing tethering of one or both leaflets, the result was MR. This confirms that the outward and apical displacement of the PMs is the key mechanism of FIMR. Other work in animal models suggests that ischemia or infarction of the PMs without displacement is not directly related to severity of FIMR. In a canine model there is poor correlation between reduced PM thickening and MR severity, and in another study FIMR was modeled by occlusion of the left circumflex artery in sheep. Ischemia and dysfunction of the PM in the ovine model correlated with reduced rather than increased MR, presumably due to reduction in tethering forces acting on the posterior leaflet. It is also recognized in humans that following inferior infarction, “waisting” or elongation of the posteromedial PM may prevent the occurrence or reduce the severity of FIMR. Gadolinium-enhanced cardiac MRI has also shown no firm correlation between PM infarction and FIMR.

The most important distinction to make is whether leaflet tethering is symmetrical or asymmetrical. In the context of limited inferior or inferolateral infarction, affecting one or two myocardial segments only, the outward displacement of the affected segments and distortion of the posterior annulus tethers only the posterior leaflet – often the P3 scallop is severely affected – and this produces a characteristic appearance which may be mistakenly interpreted by the less-experienced as “prolapse of the anterior mitral valve leaflet tip”. In reality, the coaptation point does not come above the annulus, but failure of the tethered posterior leaflet to move upwards towards the annular plane results in the tip of the AMVL meeting the body of the PMVL. The resulting coaptation is highly inefficient and produces a highly-eccentric jet of IMR directed towards the tethered leaflet i.e., posteriorly around the posterior wall of the left atrium (LA). Tenting height, tenting area and tenting angles should also be measured in the parasternal long axis (PLAX) view or apical four chamber (A4Ch) view (Fig. 3.6). Tenting height (or depth – the terms are used interchangeably) is usually measured in the A4Ch view as the maximum mid-systolic distance from the coaptation point to the annular plane. This gives an assessment of the degree of apical shift of the coaptation point and reduction in coaptation length. The term “tenting angles” refers to the relationship between the base of the leaflets and the annular plane. The anterior leaflet angle is termed “α” and the posterior leaflet angle “β”. Slices may be selected from 3D volumetric datasets to calculate tethering angles, but unfortunately these angles do vary depending on the exact slice selected and there is as yet no defined standard for how this should be done. In general terms, the greater the ratio of posterior leaflet angle to anterior leaflet angle, the greater the degree of asymmetric tethering, and increased asymmetry of tethering is associated with increased MR severity. A posterior leaflet angle of >45° is also important as a predictor of an unsatisfactory result after ring annuloplasty (see below). Tenting area is probably the most reproducible measurement as it is not dependent on delineation of one particular angle. It is defined as the area bounded by the anterior and posterior leaflets and the annular plane, usually in the PLAX view, and should be measured in mid-systole when the area is at a maximum. A tenting area of ≥ 4 cm² has been shown to be a predictor of moderate-severe FIMR over a 2-year period, and also of worsening of FIMR. In patients with systolic dysfunction, tenting area is a major determinant of FIMR severity, independent of global LV function or sphericity. This is probably because tenting area correlates with linear measures of PM displacement and thus acts as a surrogate marker for the severity of posterior and apical PM displacement. 3D volumetric datasets can be used to measure tenting volumes. However whether tenting areas or volumes are measured, it should be noted that for any given value of tenting area or volume, a greater degree of asymmetric tethering will be associated with more severe FIMR.

In addition to tethering of the leaflets due to PM displacement, the body of the anterior leaflet may also be tethered by its secondary chords, causing it to fold into a slight “V” shape in systole – sometimes called the “seagull sign”, referring to the silhouette of a seagull’s wings in flight. This form of asymmetric tethering is also associated with more severe FIMR.

Dilatation of the annulus is often found in association with FIMR, as it can be caused by global LV dilatation or regional remodeling and exacerbated by increased LA size due to either chronically increased filling pressures or atrial fibrillation. Determining the size of the annulus is useful to the surgeon or interventionist and should be measured in at least two planes – across the commissures and in the antero-posterior direction. These are best appreciated from the 60° and 120° lower esophageal views by TEE (Fig. 3.8). Annular area can also be calculated assuming an elliptical shape by the formula π(d/2) _A x (d/2) _B where A is the diameter of the long axis of the ellipse (ie across the commissures) and B is the short axis (anteroposterior diameter) or by using one of the widely available software analysis packages for quantification of the mitral valve. After infarction, reduced annular contraction correlates with increased MR severity.

Although it is usually asserted that FIMR is a condition of the ventricle and not the valve itself, and that the leaflets are “normal”, some work has suggested that over time, the leaflets do change in size and shape. In one study using 3D echocardiography to measure leaflet areas in humans, it was shown that total mitral leaflet area is greater in patients with FIMR than in patients without LV dilatation or previous infarction. However, the ratio of the total area to the “closing area” was decreased [16]. It has been postulated that the adaptation of the leaflets over time is due to reactivation of embryonic development pathways which allow the leaflets to enlarge and thicken, thus effectively remodeling the valve. Leaflet area can be appreciated well from 3-dimensional TOE datasets reconstructed using widely-available commercial analysis packages.

The dimensions and contractility of the LV can give the first clue to the severity. A reduced end-systolic dimension or volume is an indicator of hyperdynamic function due to a high degree of off-loading into the left atrium (LA) in severe MR. However, this can be confounded in the presence of severe ischemic impairment of LV function – infarcted myocardium is unable to contract so dimensions may not reflect the severity of MR. Annular size should always be measured and as this changes throughout the cardiac cycle, mid-systole is a reasonable point to do this. Dilatation of the annulus is a common finding in functional MR. The degree of tethering of the leaflet should be estimated and this is done by tracing the area bounded by the leaflets at end-systole and the annular plane. This “tenting area” is directly related to the chance of successful repair and so is vital information for the surgeon. The coaptation point and length should be measured. Only when the morphology of the valve has been fully delineated should other methods of echocardiography be used.

Whilst the echocardiographic diagnosis of MR depends on the demonstration of a jet of mitral regurgitation on color flow Doppler imaging, this is not a good method of assessing severity. Nevertheless, there are some important clues which can be gained from an assessment of color flow.