Fig. 4.1
Mitral valve annulus by 3D – echocardiography and dedicated software, by comparison in a normal individual and a patient with dilated cardiomiopathy and secondary mitral regurgitation; A – Normal individual and no mitral regurgitation. A1 – Annular antero-posterior diameter (blue), annular area (yellow), and annular area fraction (red) are evaluated. Mitral annular area is displayed; A2 – Mitral Annulus antero-posterior diameter is displayed. B – Patient with dilated cardiomiopathy (DCM) and secondary mitral regurgitation. B1 – Increased antero-posterior diameter and area, with decreased annulus area fraction. Mitral annular area is displayed; B2 – Mitral Annulus antero-posterior diameter is displayed
B.
Among all patients with dilated cardiomiopathy (ischemic or non-ischemic), the group with LV dilation and SMR showeded the largest MVA area, larger antero-posteror diameter, and decreased annular area fraction, when compared to patients with LV dilation but no SMR [18]. MVA dilation seems to have a more symmetric pattern in patients with dilated cardiomiopathy [19] than in patients with ischemic MR.
Isolated MVA dilation does not seem to be sufficient to cause moderate or severe MR by itself [20], and is not correlated to LV dilation, as shown in a recent anatomical study [6]. To cause significant MR, MVA should be severely dilated, since the ratio between the leaflets’ and the annular areas is greater than 2 [21]. However, if the mechanism of SMR is simply type I Carpentier, with isolated annular dilation, and the leak is centrally directed into the atrium, or slightly posterior, (by “pseudo prolapse of anterior leaflet”, due to posterior leaflet restriction), it is likely that simple ring annuloplasty will fix the valve [22].
In all types of SMR, the presence of mitral regurgitation itslef leads to MVA and LV dilation, which begets MR, augmenting the central I type.
Type II Carpentier SMR
There are two relatively rare clinical entities in which SMR occurs as type II Carpentier: partial or complete rupture of a papillary muscle in acute myocardial infarction, and ischemic MR secondary to a transient active ischemic episode that causes transitory chordae elongation [14]. This is a particular form of MR, having organic changes of the mitral apparatus, and it is considered actually to be a primary MR. True ischemic MR is considered a chronic event, secondary to the initial myocardial damage, developed in parallel to LV dysfunction and remodeling, with apical displacement of the papillary muscles and tethering of the mitral leaflets [14].
Among the patients with ischemic MR who need MV surgery after an acute myocardial infarction, the incidence of infarcted papillary muscle is around 33 % (9 % with ruptured papillary muscle, and 24 % without) [23]. The rupture of a papillary muscle, usually the head of the postero-medial muscle (Fig. 4.2), represents a rare but severe mechanical complication of acute myocardial infarction [24], characterized by a high mortality rate if surgery is not immediately performed [25]. The consequences of type II Carpentier SMR depend on the severity of regurgitation, LV function, acuteness of the lesion and left atrial compliance [14].
Fig. 4.2
Mechanisms of type IIIb Carpentier secondary mitral regurgitation: Top – Four chamber view of the left ventricle (LV), with displacement of the papillary muscles, that causes restriction of the chordae, and apical displacement of the mitral leaflets, creating a tenting area. Middle – Apical long-axis view of the LV and left atrium (LA) shows a greater restriction of the posterior chordae (orange arrow), that causes a “pseudoprolapse” of the anterior mitral leaflet (blue arrow), resulting an eccentric mitral regurgitant jet. Bottom – In parasternal long-axis view, the coaptation distance can be measured from the mitral plane to the point of the leaflets coaptation
Type IIIB Carpentier SMR
Ischemic Mitral Regurgitation
Ischemic MR with type IIIb dysfunction is characterized by a systolic restriction of the mitral leaflets motion. It is the most common form of ischemic MR [2], encountered in approximately 70 % cases of MR following a myocardial infarction [23]. Ischemic MR with type IIIb Carpentier dysfunction occurs more frequently after inferior and lateral myocardial infarctions than anterior ones [26, 27], related to more severe geometric changes of mitral valve apparatus, due to local basal LV remodeling with greater displacement of posterior papillary muscle [28].
Despite previous studies have postulated that ischemic MR after a myocardial infarction was mainly caused by papillary muscle dysfunction [29–31]; more recent studies contradicted this theory, and proved that papillary muscle contractile dysfunction can actually decrease SMR, by reducing leaflet tethering [32, 33].
SMR due to post-infarction LV remodeling is actually considered a complex multifactorial entity, resulting from an unbalance between increased tethering forces and decreased closing forces [34], secondary to chronic LV dysfunction and remodeling.
Reduced closing forces that prevent effective mitral leaflet coaptation are represented by [14]:
decreased LV contractility [35]
reduced systolic annular contraction [18]
dyssynchrony between the two papillary muscles, and global LV dyssynchrony, particularly at basal segments [36–39], both at rest and during exercise [40]. Cardiac resynchronization therapy has been reported to improve SMR in several studies [41–45], while cessation of CRT lead to an acute worsening of MR [46].
The “chordae restriction”, which denotes the criteria for type IIIb Carpentier dysfunction, represents the actual phenomenon of “tethering”, which is considered one of the main mechanisms of SMR [47]. After a myocardial infarction, resulting wall motion abnormalities and LV remodeling lead to apical, posterior and lateral displacement of papillary muscles [10], which are key pathophysiological events in SMR. The displacement of the papillary muscles determines stretching of the inextensible chordae with traction on the mitral leaflets, resulting in apical displacement of the leaflets coaptation point. It results in a tent-like positioning of the mitral leaflets during systole, with loss of an efficient coaptation [48] (Fig. 4.2). Mitral tenting is therefore considered a major determinant of SMR, and is directly related to local LV remodeling [35]. Mitral tenting area measured with two-dimensional echo was the best predictor of MR severity measured as effective regurgitant orifice area (EROA) [49]. However, 3DE tenting volume has been reported to be an even better predictor of MR severity and of its relapse after restrictive annular surgery than 2D echo measures, such as tenting height or tenting area [13, 48].
In SMR, local LV remodeling and mitral valve apparatus deformation are the strongest predictors of the severity of SMR [50] and its late recurrence after a myocardial infarction [51]. Even after MV annuloplasty, the main predictor of MR recurrence or progression is not MVA dilation, but the increased mitral tenting, caused by the progressive LV remodeling with papillary muscle displacement [52] and chordae tethering [53].
Agricola et al. [54] hypothesized that patients with type IIIb ischemic MR can present at least two types of tethering (Fig. 4.3):
Fig. 4.3
Types of mitral tethering. Top and Bottom Left – Asymmetric Tethering. Schematic draw of the left ventricle (LV); predominant displacement of the postero-inferior papillary muscle with tethering of the posterior chordae. There is a retraction of the posterior mitral leaflet, with “pseudo-prolapse” of the anterior leaflet, creating a deficient coaptation point. It results an eccentric regurgitant jet of mitral regurgitation, directed mainly posterior into the left atrium (LA). Top and Bottom Right – Symmetric Tethering. Schematic LV with displacement of both papillary muscles. There is a symmetric tethering of the chordae of both mitral leaflets, which creates an inefficient coaptation point, displaced apical and central. The regurgitant jet is rather central into the LA
Asymmetric tethering, characterized by predominant posterior leaflet tethering, which is frequently seen in isolated infero-lateral myocardial infarction, and leads to an eccentric regurgitant jet.
Symmetric tethering, with an apical restriction of both leaflets, which occurs mostly after anterior or multiple myocardial infarction (multi-vessel disease), and leads to a central regurgitant jet.
The symmetric tethering pattern has been associated to a higher degree of global and local LV remodeling, dilation and sphericity, worse LV dysfunction and wall motion abnormalities. Patients belonging to the asymmetric group usually have a minor degree LV dysfunction and remodeling, conditions that are usually associated with a better prognosis.
SMR Due to Non-ischemic Dilated Cardiomyopathy
Initially, it was considered that the primary mechanism of SMR in patients with NIDCM was the global LV remodeling [55]. However, it has been later demonstrated that also local LV remodeling relates to MR severity [5]. In patients with NIDCM and SMR, tenting area, coaptation distance and inter papillary distance are related to the severity of the MR; even further, tenting area correlated to patients functional status, and both hospitalization and mortality rates [5].
When comparing the mechanismsms of SMR in ischemic heart disease with SMR in patients with NIDCM, LV remodeling, mitral apparatus deformity and incomplete closure of mitral leaflets were more accentuated in patients with ischemic SMR. Tenting area had the highest sensitivity and the regurgitant volume the highest specificity for the diagnosis of ischemic dilated cardiomiopathy [55, 56].
Treatment for Carpentier IIIb
While isolated restrictive annuloplasty addresses type I Carpentier SMR, the majority of patients with SMR have a mix mechanism type I and IIIb Carpentier. The latter may explain why simple restrictive annuloplasty has a MR recurrence of 30 % [57], urging the need of a more complex approach. Novel techniques that combine restrictive annuloplasty with surgical extension of the posterior MV leaflet had a better postoperative outcome, with only 10 % recurrence of severe MR at 2 years follow-up [57]. LV reverse remodeling after mitral valve repair was observed in approximately 50 % of all types of SMR [58] and lead to a longer repair durability and improved clinical outcome. Conversely, the ongoing of the LV remodeling process leads to increased recurrence of SMR after annuloplasty [53]. Careful indication and choice of the surgical procedure, as well as attention to technical details, contribute to improved results [59].
Other Types of Functional Classification for SMR
Fundaro et al. [60] Functional Classification
More recently, other types of SMR classifications were proposed in order to better address proper surgical treatment and reduce post-repair recurrence of the MR. Fundaro et al. [60] proposed a new classification taking into account three different characteristics: mechanism of regurgitation, indications for surgery, and prognosis (Table 4.1). MR is classified into type 1 and 2, based on global/regional ventricular – papillary muscle dysfunction, and in subtypes A, B and C, based on the presence of annular dilation or/and papillary muscle alterations (atrophy, elongation or displacement). It ignores the presence of isolated MVA dilation, (type I Carpentier), considered by the author as not existing in clinical practice.
Table 4.1
Types and subtypes of secondary mitral regurgitation
Chronic functional mitral regurgitation types and subtypes | ||
Ventricular – papillary dysfunction | ||
Regional = type 1 | Global = type 2 | |
Papillary muscles alterations (Atrophy, elongation, displacement) | ||
Subtype A | 1A | 2A |
Annular dilation | ||
Subtype B | 1B | 2B |
Both | ||
Subtype C | 1C | 2C |
Of note, the difference between “global” and “regional” is usually hard to be established (types 1 and 2), but it is useful because of the poorer prognosis of the severe LV remodeling. Also, there are rare pure subtypes A and B of MR, as both mechanisms usually coexist (subtype C).
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