(n)
3 years
4 years
5 years
10 years
Lamas et al. [3]
MR− (586)
87 %
CV surv
MR+ (141)
66 %
p
.0022
Grigioni et al. [4]
MR− (109)
61 ± 5 %
MR+ (194)
38 ± 5 %
p
<0.001
ERO 1–19 mm2
47 ± 8 %
ERO ≥20 mm2
29 ± 9 %
p
<0.0001
Bursi et al. [5]
MR− (387)
72 %
MR 1+ (297)
62 %
MR ≥2+ (89)
40 %
p
<0.0001
Surv HF free
MR− (387)
84 %
MR 1+ (297)
74 %
MR ≥2+ (89)
35 %
p
<0.0001
Grigioni et al. [6]
MR− (71)
69 ± 6 %
Surv HF free
MR+ (102)
30 ± 6 %
P
<0.0001
ERO 1–19 mm2
32 ± 9 %
ERO ≥20 mm2
22 ± 9 %
p
<0.0001
Aronson et al. [7]
MR− (642)
HF risk (HR)
MR mild (473)
2.9 (1.5–5.7)
MR ≥ mod (75)
4.6 (2.0–10.6)
p MR− vs MR mild
0.001
p MR− vs MR ≥ mod
<0.001
Death risk (HR)
MR− (642)
MR mild (473)
1.2 (0.8–1.8)
MR ≥ mod (75)
2.5 (1.3–3.9)
p MR− vs MR mild
0.43
p MR− vs MR ≥ mod
0.001
Agricola et al. [8]
MR mild (166)
64 %
Isch 76.5 %
MR mod (195)
50 %
Non-isch 23.5 %
MR sev (43)
49 %
p
0.03
CD free
MR mild (166)
94 %
MR mod (195)
57 %
MR sev (43)
55 %
p
0.003
Surv HF free
MR mild (166)
62 %
MR mod (195)
20 %
MR sev (43)
18 %
p
0.0001
Bursi et al. [9]
MR no/I (176)
82.7 %
Isch 36.2 %
MR II (87)
64.4 %
Non-isch 63.8 %
MR III (142)
58.5 %
Surv HTx free
MR IV (64)
46.5 %
p
<0.0001
Persson et al. [10]
MR ≤1+ (635)
70 %
ACS pts
MR >1+ (64)
30 %
HR
2.28 (1.67–3.12)
p
<0.0001
adjusted HR
2.08 (1.29–3.35)
p
0.003
Rossi et al. [11]
(1256)
MR− (27 %)
ERO 1–19 mm2 (49 %)
ERO ≥20 mm2 (24 %)
2.0 (1.5–2.6)
p
<0.0001
These studies do not solve, however, an important problem: when is severe FMR severe? Lamas et al. [3] stratified their patients using ventriculograms. This technique is now obsolete. In both papers by Bursi et al. [9] MR gradation is not clear. Aronson et al. [7] used the area of the regurgitant jet, but this method is not recommended by the European Society of Echocardiography (ESE) [12]. Agricola et al. [8] graded functional MR as organic MR, against ESE recommendations [12]. Persson et al. [10] used a method based on regurgitant flow intensity, at least difficult to reproduce. Better answers were given by other studies. Grigioni et al. [4] found lower 5-year survival when effective regurgitant orifice area (EROA) was ≥20 mm2 (Table 14.1). However the striking finding of this study was that any grade of ischemic FMR, independently from the ejection fraction (EF) (higher or lower than 40 %) was a risk factor for survival. In another study [6] the same Authors found that any grade of ischemic FMR was predictive of higher possibility of congestive heart failure (CHF) (RR 3.45 if EROA 1–19 mm2, p = 0.002, RR 4.42 if EROA ≥20 mm2, p = 0.001) or of the composite end point of death and CHF (RR 2.8 if EROA 1–19 mm2, p = 0.001, RR 3.42 if EROA ≥20 mm2, p 0.0006) These findings were confirmed by Rossi et al. [11]. Lancellotti et al. [13], using the same cutpoint, underlined as well the importance of stress echocardiography in patients with lesser grade of ischemic FMR, as an increase of EROA of 13 mm2 was predictor of adverse outcome. The ESE endorsed these conclusions and stated that “In functional ischaemic MR, an EROA ≥20 mm2 or a RVol ≥30 ml identifies a subset of patients at increased risk of cardiovascular events.” [12].
Surgical Indication
It seems evident that FMR severely affects survival and/or clinical outcome at a lower grade than organic MR, and EROA is the most used, and useful, method to stratify the consequences of FMR on patients’ prognosis.
It is then clear that the advent of FMR is associated with worse prognosis and higher incidence of heart failure. When MR is the only factor to influence LV volume changes, the sequence of events is well known.MR increases wall stress, eccentric LV hypertrophy follows, then enhanced ventricular compliance (compensated LV remodeling). At a certain stage, decompensated LV remodeling occurs. Compensatory hypertrophy changes to fibrosis and apoptosis, which causes myocite “drop- out” with hypertrophy of surviving myocites. Interstitial fibrosis increases and the LV, as a consequence, remodels into a hypocontractile, non compliant ventricle. This well known sequence cannot be adapted to FMR, which starts when the LV is already compromised. Decreased contractile function and LV dilatation occurs before FMR occurs. Is FMR then a variable which will cause further worsening or is it a marker of a worsened heart failure? This question was nicely answered by an experimental model by Beeri et al. [14], who, after having caused a myocardial infarction in dogs ligating the left anterior descending artery, built a LV–left atrium shunt, with a regurgitant volume of 30 %, mimicking a moderate FMR. Dogs with shunt had larger end systolic and end diastolic volumes and reduced contractility than dogs without shunt. This demonstrated, at least in an animal model, that FMR, even if simulated, caused early LV remodeling, worse than when FMR was not present.
Moderate or more FR has to be always treated. However we think than, in selected cases, when the mitral annulus is enlarged and the coaptation length is short, even mild FMR can be considered for surgical treatment.
Surgical Treatment and Results
There is general agreement that overreductive MV annuloplasty (MVA), proposed by Bolling et al. [15] is the technique of choice to correct FMR. Even if the same authors [16] were not able to demonstrate any benefit in survival when comparing treated and untreated patients, others [17, 18] found, in randomized trials, annuloplasty to improve the clinical status in patients with moderate FMR. Nevertheless, the evolution of MR after surgical correction is not always favorable. Due to the intrinsic characteristics of the disease, mostly related to ventricular events rather than to MV pathology, residual or recurrent MR is constantly shown in the follow up of surgical series. FMR in fact is a ventricular disease, because the mechanism of closure of the MV is affected by displacement of on e or both papillary muscles. Consequences of these changes are regurgitation of different grade and deepening of the CD.
MV anatomy, to be suitable for repair, needs two conditions: the AL has to be long enough to reach the PL and the AL has to be enough mobile to coapt with the PL. Excess of tethering of the PL or both AL and PL will limit the possibility of coaptation after overreductive MVA. Mitral prosthesis insertion (MPI) can be a solution of this problem. Many cut off values have been proposed to identify patients (Table 14.2) who will not benefit from repair. Our group first proposed a coaptation depth (the distance between the MV annular plane and the point where the two leaflets coapt) of 11 mm or higher as a simple and effective cut point to identify patients where MPI would be more beneficial than repair [19, 20]. There are many techniques described in the literature [25], ours included [20], which foresee the elimination of a triangle of AL and the attraction of the remnants of the AL toward the annulus using the prosthetic sutures (Fig. 14.1).
Table 14.2
Cut off values proposed to identify patients where restrictive MVA can be unsuccessful
CD >10 mm | Parasternal long axis, 2 and 4 | CD ≤10 mm MR post 1.2 ± 0.8 | |
Chambers view (mean value) | CD >10 mm MR post 2.5 ± 0.7 | ||
Magne et al. [21] | PL angle ≥45° | 4 chamber view, 9 days | MR ≤1 PL angle 33 ± 6 |
MR ≥2 PL angle 52 ± 5 | |||
Roshanali et al. [22] | PM distance >20 mm | Short axis 22 months | MR ≤1 distance 15.0 ± 4 |
MR ≥2 distance 26.5 ± 2.9 | |||
Gelsomino et al. [23] | AL angle ≥39.5 | Parasternal long axix
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