59. Ischemic Mitral Regurgitation- Review of CT Surgery

Alexander A. Brescia, Habib Jabagi, and Steven F. Bolling

This chapter is a revision and update of that included in the previous editions of the TSRA Review written by Alexander Iribarne (2^nd edition) and Tom C. Nguyen (1^st edition). 

Anatomy

The components of the mitral valve apparatus include: the mitral annulus, anterior and posterior leaflets, chordae tendineae, papillary muscles (anterolateral and posteromedial), and the lateral wall of the left ventricle. The surgical anatomy of the mitral valve is discussed in Chapter 45 and should be reviewed with particular attention to the spatial relationship between the mitral annulus, circumflex coronary artery and coronary sinus, AV node, and the left and non-coronary cusps of the aortic valve, which make up the aortomitral curtain. 

Epidemiology and pathophysiology

Mitral regurgitation (MR), or mitral insufficiency, is classified into primary and secondary MR. Non-ischemic MR, including all forms of primary MR, will be covered in Chapter 55, while this chapter focuses on ischemic MR (IMR). Secondary MR, also known as functional MR (FMR), occurs when coaptation of structurally normal mitral valve leaflets is impaired due to dilatation and/or dysfunction of the left ventricle (LV). The two leading causes of FMR are dilated cardiomyopathy and ischemic MR (IMR). IMR accounts for 20% of the total cases of MR and occurs as a result of ischemic cardiomyopathy (ICM), which results in LV dysfunction and subsequent congestive heart failure.

MR is defined as leakage of blood from the LV to the left atrium (LA) during systole, and exists over a spectrum including acute MR, chronic compensated MR, and chronic decompensated MR. Acute MR can be a consequence of chordal rupture/flail, papillary muscle rupture, acute MI, or even trauma, and presents as acute, symptomatic, severe heart failure that often requires surgical intervention. In less severe forms that are not acute in nature, the LV will have time to undergo remodeling (LV hypertrophy) to preserve stroke volume in the presence of increased preload and LV dilation from the MR, resulting in chronic compensated MR. Eventually the LV will no longer be able to compensate for continued LV dilatation, and stroke volume will decrease resulting in decreased cardiac output and CHF – a state known as chronic decompensated MR.

Under normal conditions, the papillary muscles contract as the LV shortens to maintain the distance between papillary muscle ends and the mitral annulus, preventing prolapse of the mitral leaflets into the LA. In IMR, the papillary muscles become displaced apically and laterally, resulting in stretched chordae with tethered leaflets, which restrict or inhibit normal closing during systole. An understanding of coronary anatomy in IMR is important in post-MI papillary muscle rupture, as supply to each papillary muscle is different. The anterolateral papillary muscle has dual blood supply from the LAD (via diagonal branches) as well as the left circumflex (via marginal branches), while the posteromedial papillary muscle is supplied solely by the PDA; thus, inferior or posterior MIs are more likely to result in papillary muscle rupture and IMR. Consequently, MV leaflet tethering predominantly occurs on the posteromedial scallop of the posterior leaflet in IMR. MR can be further exacerbated in IMR by annular dilatation secondary to LV dilation as the annulus adopts a circular or asymmetric geometry rather than the normal saddle, resulting in loss of leaflet coaptation and central MR. Similarly, DCM results in incomplete leaflet coaptation due to LV dilatation and correlates to the degree of LV dysfunction, rather than isolated papillary muscle dysfunction.

Diagnosis

Symptoms associated with MR can vary and depend on both the severity and chronicity of the disease. Common symptoms include shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea, fatigue, palpitations (atrial fibrillation), as well as symptoms of a low output state. On physical exam, the murmur of MR is best heard at the apex with the patient in the left lateral decubitus position. With severe MR, the murmur is holosystolic and radiates to the axilla. The murmur of MR can be accentuated by squatting, handgrip, and during exhalation, while it is decreased by standing or the valsalva maneuver. CXR may demonstrate cardiomegaly and/or LA enlargement. On EKG, LA enlargement (bifid P wave with >40ms between the two peaks) is usually present and/or atrial fibrillation may be seen.

Echocardiography is the gold standard for diagnosing MR, providing information on the mechanisms and severity of MR, LV function and size, LA size, degree of pulmonary hypertension, presence of associated valvular disease, as well as suitability for repair.  Both TTE and TEE are effective in evaluating MR, with TEE being more accurate secondary to the probe’s proximity to the MV. Echocardiographic assessment of MR is divided into quantitative and qualitative measures. Qualitative measures include vena contracta (VC) width (narrowest diameter of the jet flow) and jet area (% of LA), while quantitative measures include regurgitant volume (RV) and fraction (RF) as well as effective regurgitant orifice area (EROA). Severe MR is characterized by a VC ≥0.7 cm, EROA ≥0.4 cm², RV ≥60 mL/beat, RF ≥50%, and a jet area >40% of LA area. Other important makers of severe MR include enlarged LA and LV size, as well as systolic reversal in pulmonary vein flow rate.  A diagnosis of severe MR in FMR/IMR only needs a RV >30 mL/beat or RF ≥50% or EROA >0.2 cm².

It is important to note the LVEF assessment by ECHO in patients with MR can overestimate LV function, as it cannot discern between blood volume ejected into the aorta versus that ejected into the low resistance LA trough the noncompetent MV. Thus, significant myocardial dysfunction may exist despite a normal EF on report. This is important, as LVEF has been shown to predict success rate following MV surgery, with outcomes worse in patients with a preoperative EF <60%.

Classification

Carpentier’s classification classifies MR according to the movements of the mitral leaflet and is used to help guide surgical approach.

• Type I. Normal leaflet motion. MR secondary to annular dilation (DCM, ICM ± significant LV dysfunction) or leaflet perforation (infective endocarditis).
• Type II. Increased leaflet motion (leaflet prolapse or flail). MR secondary to chordal elongation or more commonly rupture (myxomatous or degenerative disease) or papillary muscle rupture (ICM).
• Type IIIa. Restricted leaflet motion/opening in systole and diastole. MR secondary to leaflet calcification (degenerative) or chordal thickening, shortening, or fusion/commissural fusion (rheumatic heart disease).
• Type IIIb. Restricted leaflet motion/closing in systole. MR secondary to papillary muscle displacement or leaflet tethering (IMR) or LV dilatation (DCM)

Surgical indications

The 2020 ACC/AHA Guidelines are summarized below for chronic secondary (functional) MR. Prompt mitral valve surgery (preferably mitral repair, if possible) is indicated for the symptomatic patients with acute severe MR. 

Chronic severe secondary MR

Class I recommendations: 

• Patients with chronic severe secondary MR (Stages C and D) and heart failure with reduced EF should receive standard guideline-directed medical therapy for heart failure, including ACE inhibitors, ARBs, beta blockers, aldosterone antagonists, and/or sacubitril/valsartan, and biventricular pacing as indicated. – Level of Evidence A
• In those with chronic severe secondary MR and heart failure with reduced EF, a cardiologist expert in the management of patients with heart failure and LV systolic dysfunction should be the primary multidisciplinary member responsible for implementing and monitoring optimal GDMT. – Level of Evidence C-EO

Class IIa recommendations: 

• In patients with chronic severe secondary MR related to LV systolic dysfunction (EF <50%) who have persistent symptoms (NYHA class II, III, or IV) while on optimal GDMT for heart failure (Stage D), transcatheter edge-to-edge repair is reasonable in patients with appropriate anatomy as defined on TEE and with EF between 20% and 50%, LVESD ≤70mm, and systolic PAP ≤70mmHg. – Level of Evidence B-R
• In patients with severe secondary MR (Stages C: asymptomatic and D: symptomatic), mitral valve surgery is reasonable when CABG is undertaken for the treatment of myocardial ischemia. – Level of Evidence B-NR

Class IIb recommendations: 

• In patients with chronic severe secondary MR from atrial annular dilation with preserved LV systolic function (EF ≥50%) who have severe persistent symptoms (NYHA class III or IV) despite therapy for associated atrial fibrillation or other comorbidities (Stage D), mitral valve surgery may be considered. – Level of Evidence B-NR 
• In patients with chronic severe secondary MR related to LV systolic dysfunction (EF <50%) who have persistent severe symptoms (NYHA class III or IV) while on optimal GDMT for heart failure (Stage D), mitral valve surgery may be considered. – Level of Evidence B-R
• In patients with CAD and chronic severe secondary MR related to LV systolic dysfunction (EF <50%) (Stage D) who are undergoing mitral valve surgery because of severe symptoms (NYHA class III or IV) that persistent despite GDMT for HF, chordal-sparing mitral valve replacement may be reasonable to choose over downsized annuloplasty repair. – Level of Evidence B-R

Treatment

Medical Therapy

The standard of care for IMR is GDMT, with goals to improve symptoms, optimize cardiac performance, and maximize survival. GDMT includes achieving and maintaining euvolemia and unloading the LV with diuretics, angiotensin converting enzyme inhibitors or angiotensin receptor antagonists, and ß-blockers. It is a class I indication in the United States and Europe for all patients with IMR to undergo GDMT, with consideration for cardiac resynchronization therapy (CRT) for those with a QRS wavelength greater than 150 milliseconds. Dyssynchrony is presumed to exacerbate the underlying cause of IMR, while uncoordinated LV contraction worsens papillary muscle displacement and leaflet tethering. CRT reduces IMR by decreasing leaflet tenting and increased closing forces. Surgical treatment for chronic secondary MR is only considered after appropriate medical and device therapy have been instituted as above. 

Mitral Valve Surgery

To date, neither surgical MV repair or replacement has been shown to improve survival in patients with severe FMR. 

Historically, the surgical approach to IMR was non-chordal-sparing mitral valve replacement.  Previously, little was understood of the interdependence between ventricular function and annular-papillary muscle continuity. Consequently, patients with low LVEF undergoing MVR with removal of the subvalvular apparatus had extremely high mortality rates. While patient selection in the context of IMR remains controversial, consensus now exists on performing a total valve-sparing mitral valve replacement when replacing the valve. One randomized trial comparing partial versus complete chordal-sparing mitral valve replacement found that LV volume and function were better preserved with complete leaflet sparing. Mitral repair is preferred by some for IMR, although some doubt persists about its benefit in this population, especially after the randomized CTSN trial by Acker and colleagues showed no difference in primary outcome of LV end systolic volume index or survival, but a rate of 2+ or worse recurrent MR at 2 years in 59% after repair, compared to only 4% after replacement.

Several randomized trials for surgical mitral repair in addition to CABG for IMR have been performed but are not definitive. One analysis found no significant benefit to adding mitral valve repair to CABG alone but with a single-center, underpowered trial of 102 patients. A subset analysis of the STITCH trial concluded CABG with mitral valve repair had superior survival to CABG alone, but the decision to perform mitral repair was left to surgeon discretion rather than randomized. The randomized RIME trial evaluating 73 patients found improved MR severity, LV remodeling, and NYHA heart failure class with CABG plus mitral repair compared to CABG alone; however, this trial was not powered for survival as an outcome. A CTSN randomized study of 301 patients by Michler and colleagues concluded that adding mitral repair to CABG did not promote reverse LV remodeling or improve survival and was associated with more adverse events, though mitral repair did reduce the prevalence of moderate or severe MR at one year.

As shown through these studies, IMR can have a wide range of outcomes depending on the quality of mitral repair. Since dilatation occurs not only along the insertion of the posterior leaflet but also the anterior portion, the intertrigonal distance is not consistent in IMR and thus is not a reliable method for sizing. We feel that performing an undersized, “restrictive” annuloplasty by downsizing one to two sizes smaller than measured by intertrigonal length is essential to a favorable outcome in the setting of mitral repair for IMR.

There are several structures at risk during MV repair/replacement that a surgeon must be cognizant about and include injury to the circumflex artery (6:00-8:00 position, A1/P1), coronary sinus, (4:00-6:00 position, P2/P3), as well as the AV node, conduction bundles, and membranous septum. The most morbid complication, however, is atrioventricular (AV) disruption/dehiscence, and is divided into three types. Type 1 is the most common type and occurs at the AV groove. Type 2 is rupture of the LV posterior wall at the base of the papillary muscle, while type 3 is rupture of the LV wall between the base of the papillary muscle and the AV groove. 

Type 1 AV ruptures usually occur following injury to the MV annulus, as a result of excessive decalcification in patients with severe MAC, placement of an oversized prosthesis, deep sutures entering the myocardium or during cardiac massage. Type 2 ruptures tend to occur following excessive posterior valvular (PMVL) and sub-valvular apparatus (posteromedial papillary muscle) resection with local hemorrhage and rupture. Management of AV ruptures requires immediate reinstitution of cardiopulmonary bypass, removal of the prosthetic valve and repair AV the groove with a pericardial patch, followed by implantation of a smaller/lower profile prosthesis. Strategies to avoid this complication include avoiding excessive MV annular decalcification and lifting the heart post MV prosthesis implantation, performing CABG distals first in patients with concomitant CAD, and preserving the PMVL during MV repair/replacement.

Systolic anterior motion (SAM) is another important complication that may occur after mitral valve surgery. With SAM, the anterior mitral leaflet obstructs the LVOT during systole due to anterior displacement of the leaflet coaptation point, resulting in mitral regurgitation with a posteriorly directed jet. SAM is a feature of degenerative MV disease, where there is excessive leaflet redundancy (usually of the AMVL) compared to the annulus and LVOT. Therefore, SAM is rarely a feature of IMR, where leaflet tissue is usually deficient and tethered or post MV replacement, where the AMVL is usually removed. Anatomic features which increase the risk of SAM include excessive anterior or posterior leaflet tissue (P1-P3 length >2 cm or A2 >3 cm), absolute height of the posterior leaflet (>1.5 cm), anterior to posterior leaflet height ratio (<1.4), anterior papillary muscle displacement, minimum distance from the coaptation point to the septum (C-Sept, <2.5 cm), aortomitral angle <120°, and annular undersizing in mitral valve repair (annuloplasty rings). SAM can also occur in patients with hypertrophic obstructive cardiomyopathy (HOCM) but is not discussed here.

Intraoperative management of SAM following MV intervention begins with conservative management directed at increasing LVOT diameter. This can be achieved by stopping/decreasing inotropes, volume loading, increasing afterload, decreasing heart rate and achieving AV synchrony. Mild/moderate SAM normally resolves with conservative management; however, if medical therapy is not adequate and severe SAM/LVOT obstruction persists on echocardiographic assessment, surgical reintervention is indicated. Depending on the mechanism of SAM, surgical reintervention may include implantation of a larger ring or banding removal and subsequent MV replacement (with low profile prosthesis), reduction of the PMVL height to ≤1.5 cm (quadrangular resection and sliding annuloplasty), neochord placement to move the MV coaptation point posteriorly, or via anterior to posterior papillary muscle attachment.

Transcatheter Techniques

Recently, percutaneous and minimal incision transcatheter MV (TMV) techniques have been developed for both MV replacement and repair for IMR, with acceptable clinical outcomes and avoidance of the morbidity associated with open surgery. Newly developed devices target leaflet repair, modification of LV geometry, chordal replacement, and complete valve replacement.

The MitraClip device (Abbott Vascular, Santa Clara, California) was first used in 2003 and was approved for commercial use in 2013 to treat severe symptomatic degenerative MR based on European data and the EVEREST II trial and in March 2019 added an expanded indication for secondary MR based on the COAPT trial. Several other transcatheter repair devices for MV repair are delivered either minimal-incision surgical transapical or percutaneous transseptal approaches. Each of these have undergone observational studies to demonstrate feasibility and improvement in heart failure symptoms but require further evaluation.

Please see Chapter 63 for more details on transcatheter mitral valve procedures.

Suggested Readings

1. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients with Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143(5):e72-e227.
2. Brescia AA,Watt TMF, Bolling SF. Ischemic Mitral Regurgitation: Current Understanding and Surgical Options. Indian J Thorac Cardiovasc Surg. 2020;36:27-33.
3. Goldstein D, Moskowitz AJ, Gelijns AC, et al. Two-year outcomes of surgical treatment of severe ischemic mitral regurgitation. N Engl J Med. 2016;374:344-53.
4. Michler RE, Smith PK, Parides MK, et al. Two-year outcomes of surgical treatment of moderate ischemic mitral regurgitation. N Engl J Med. 2016;374:1932-41.