The term functional mitral regurgitation is used to describe mitral regurgitation in the absence of any “organic” lesions of the mitral valve. It includes mitral regurgitation (MR) that results from dilated cardiomyopathy and also mitral regurgitation caused by ischemic dysfunction of the ventricle and subvalvular apparatus. Using the Carpentier pathophysiologic triad ischemic MR has an etiology of known coronary artery stenosis with evidence of prior myocardial infarction with regional or global left ventricular dysfunction. The primary lesion causing regurgitation in this setting is tethering of the mitral valve leaflets often combined with some degree of annular dilation. The resulting dysfunction in the case of chronic ischemic MR is most frequently Carpentier type IIIb dysfunction caused by restricted leaflet motion which occurs in response to ventricular remodeling after myocardial infarction. Carpentier type I dysfunction, or MR resulting from annular dilation with a lack of leaflet coaptation despite normal leaflet motion, may occur in the setting of basal infarction but accounts for less than 10 % of ischemic MR cases and should be easily repairable with a reduction ring annuloplasty. Carpentier type II dysfunction, or leaflet prolapse, may occur with complete or partial rupture of the posteromedial papillary muscle but is rare in the current era of percutaneous early revascularization for myocardial infarction.

The normal mitral valve function involves a complex interaction among the valve leaflets, annulus, subvalvular apparatus, and left ventricle. In ischemic mitral regurgitation, the leaflets are spared but each of the other components of the normally functioning mitral valve are differentially affected. Annular dilation and distortion is present, dilation and increased sphericity of the ventricle occurs, and with these changes the papillary muscles of the subvalvular apparatus are displaced. All of these changes combine to cause leaflet tethering and therefore poor coaptation, creating a regurgitant valve. It is commonly and accurately stated that ischemic mitral regurgitation is a disease of ventricle, not a disease of the valve, and understanding it in this manner is necessary when pursuing effective and durable repair techniques.

Breaking down the changes in the valve components that lead to the final common pathway of Carpentier IIIb MR caused by leaflet tethering we can start with the most important changes which occur in the left ventricle. Myocardial ischemia or infarction with remodeling leads to regional distortion and ultimately poor leaflet coaptation. Watanabe and colleagues have shown that in patients with inferior infarction, tethering was more localized in the medial posterior leaflet, while anterior infarction results in more widespread tethering of both leaflets [1]. This observation confirms the crucial role that regional ventricular geometry and function play in the pathophysiology of ischemic MR and helps explain why some patients with only mildly impaired LV function develop severe ischemic MR. Indeed, the geometry of ventricle as it remodels in response to ischemia and infarction seems to be more important determinant of ischemic MR than the LV volume or ejection fraction.

Annular dilation is common in chronic ischemic MR however the degree of annular dilation does not necessarily correlate with the degree of MR. Some patients have severe MR with very little annular dilation while others with significant annular dilation have only mild regurgitation. Several studies have noted that the degree of septolateral (SL) dilation seems more important in the pathophysiology of ischemic MR than the commisure-commisure (CC) dilation [2, 3]. In severe cases of ischemic MR the SL dimension can approach the CC dimension which results in a circular annulus instead of the usual elliptical one. Most often, the majority of the dilation occurs in the posterior annulus, particularly in the region of the posterior commissure [4, 5].

When examining the role of the subvalvular apparatus, it is clear that papillary muscle displacement plays a critical role in the development of ischemic MR. On the contrary, papillary muscle dysfunction itself does not seem to significantly contribute to ischemic MR [6, 7]. Carpentier and colleagues demonstrated in sheep studies in the 1980s that formaldehyde injection in the posterior papillary muscle did not produce MR [8]. Instead, MR could only be produced by extending formaldehyde injection into the adjacent myocardium resulting in regional wall motion abnormality. The pattern of papillary muscle displacement necessary to yield ischemic MR is complex and involves displacement of the muscle tips posterolaterally and apically away from the anterior annulus and away from each other. The tethering distance has been shown experimentally to correlate with the severity of ischemic MR [9]. Displacement of both papillary muscles is likely necessary to induce severe MR but particularly displacement of the posteromedial muscle usually predominates.

The combination of regional LV dysfunction and sphericity, annular dilation, and papillary muscle displacement all create a tethering force that leads to apical tenting of the mitral valve leaflets and Carpentier IIIb MR. Tethering of the primary chordae leads to restricted motion of the free margins of the leaflets which prevents them from rising to the plane of the annulus during systole with resultant poor coaptation and regurgitation. In addition, tethering of the secondary chordae can result in deformation of the body of the leaflet which also contributes to impaired coaptation.

Therapeutic targets for correction of ischemic MR include the coronary arteries, mitral annulus, subvalvular apparatus, valve leaflets, and the ventricle itself. Any surgery for ischemic MR should include full coronary artery revascularization. To date, the most common surgical treatment for ischemic MR involves coronary revascularization and a reduction ring annuloplasty which restores leaflet coaptation but fails to address the underlying tethering component in the pathophysiology of ischemic MR. This failure may explain why about a third of patients develop recurrent MR within a year of successful reduction annuloplasty. The remainder of this chapter will focus on surgical approaches to management of the subvalvular apparatus via varying techniques of papillary muscle relocation and several techniques of chordal modification in an effort to obtain a more durable correction of ischemic MR that is more resistant to continued ventricular remodeling and tethering. In rare cases, a simultaneous ventricular remodeling procedure such as a Dor operation may be indicated or necessary but this will be discussed elsewhere.

To determine which patients are appropriate candidates for mitral valve repair with the employment of adjunctive subvalvular techniques, a thorough understanding of the latest data on ischemic MR is necessary. Traditional mitral valve repair for ischemic MR involves revascularization of ischemic myocardium along with a reduction ring annuloplasty as first described by Bolling and Bach in 1995 [10]. This repair technique is simple and has demonstrated a large degree of success over the past two decades but as alluded to earlier, this approach addresses the annulus only and ignores the underlying contributions of ventricular dysfunction and changes in geometry of the subvalvular apparatus to the development of ischemic mitral regurgitation. Not surprisingly, the rates of recurrent MR after reduction ring annuloplasty have been shown to be higher than 30 %.

As mentioned previously, results from the recent Cardiothoracic Surgical Trials Network (CTSN) randomized study on mitral valve repair versus replacement for severe ischemic MR [11] suggest that this approach alone is inadequate for some patients. In this trial, 251 patients with severe ischemic MR were randomized to mitral valve repair or chordal-sparing mitral valve replacement with a primary endpoint on left ventricular end-systolic volume index (LVESVI) and secondary endpoints of major adverse cardiac and cerebrovascular events, mortality, degree of residual MR, functional status, and quality of life. The vast majority of mitral valve repairs in this trial were done with reduction ring annuloplasty of 1–2 sizes. At 1 year, there was no significant difference between repair and replacement in either the primary or any secondary outcome. Notably, the rate of recurrent moderate or severe MR at 1 year in the repair group was 32.6 % vs. only 2.3 % in the replacement group (P < 0.001). Of those undergoing repair, the LVESVI was 64.1 ± 23.9 ml/m² in those with recurrent MR versus 47.3 ± 23.0 ml/m² in those without recurrent MR (P < 0.001) suggesting that if a durable repair can be achieved, there likely remains an advantage to repair over replacement.

In order to further investigate the question of whether failure of mitral valve repair can be predicted by certain preoperative characteristics, the CTSN investigators have performed a recent posthoc analysis of the 116 patients who were randomized to and received mitral valve repair in the Severe MR trial with 2-year follow-up [12]. Logistic regression was used to determine baseline echocardiographic and clinical characteristics that predict failure of repair or death and a predictive model based on 10 factors (age; gender; race; body mass index; NYHA class; effective regurgitant orifice; basal aneurysm/dyskinesia; and history of coronary artery bypass grafting, percutaneous coronary intervention, or ventricular arrhythmias) was developed with a favorable area under the receiver operating characteristic curve of 0.82. Those patients who suffered from recurrent moderate/severe MR or who died were older, had a lower frequency of NYHA class III or IV, and had a higher frequency of basal aneurysm/dyskinesis. Of the ten variables, the standout predictor of recurrent moderate or severe MR, or death, was basal aneurysm/dyskinesia; reflecting a severe form of preoperative LV ischemic remodeling with the abnormalities of papillary muscle displacement, leaflet tethering, and annular dilation. It stands to reason that in these patients with preoperative basal aneurysm/dyskinesia, mitral repair with a downsized annuloplasty ring alone is insufficient and that either upfront replacement or additional subvalvular repair techniques are necessary for a durable result.