60. Degenerative Mitral Regurgitation- Review of CT Surgery

Anthony B. Mozer and Patrick M. McCarthy

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

Anatomy

The surgical anatomy of the mitral valve discussed in Chapter 45 should be reviewed in the “surgeon’s view,” with special attention given to the relationships of the annulus to the circumflex coronary artery, AV node and His bundle, coronary sinus, and aorto-mitral curtain. In addition to careful stitch placement to avoid injury to these structures, it is critical to delineate the hinge point of the valve such that annuloplasty sutures are passed correctly into the annulus and above the base of the leaflets.

Epidemiology

Mitral regurgitation (MR) has a prevalence of 1.7% of the population in the United States, which increases to 9.3% in adults over the age of 75. Degenerative mitral valve disease (DMR) is the most common cause of mitral regurgitation (MR) in developed countries, comprising 60-70% of cases. Degeneration may be hastened by fibroelastic deficiency, Barlow’s disease, or more rarely, connective tissue disorders such as Marfan’s syndrome.

Pathophysiology

MR is defined as the retrograde flow of blood from the LV to the LA during systole, and classified as degenerative (primary, organic) when due to abnormal valve leaflet morphology. Therefore, DMR is typically categorized as Type II valvular pathology in Carpentier’s functional classification. The most frequent cause is myxomatous disease inducing posterior leaflet pathology, followed by bileaflet failure as seen in younger patients with Barlow’s syndrome, and, rarely, isolated anterior leaflet failure. The saddle shape configuration, mechanics of the mitral valve during the cardiac cycle, and bulging leaflet tissue between two scallops of the middle of the posterior leaflet (P2) is the reason why P2 flail is the most common etiology.

Patients with DMR infrequently present acutely in severe, symptomatic heart failure due to the absence of adequate compensatory changes to the cardiac chambers as a result of perforation from endocarditis, or from acute chord rupture secondary to myxomatous disease. In progressive MR, gradual LV remodeling occurs from increased preload resulting in LV and LA dilation and hypertrophy. This remodeling process increases total stroke volume and allows for a chronic compensated state. Many patients maybe asymptomatic or mildly symptomatic at this stage. Decompensated MR occurs when systolic dysfunction inhibits normal ventricular contraction, resulting in a decreased cardiac output and stroke volume.

Diagnosis

While some patients develop overt valvular symptoms including fatigue, shortness of breath, and/or decrease in exercise tolerance, others are asymptomatic at presentation, referred for surgical evaluation due to the presence of a murmur. Not infrequently, patients self-report as asymptomatic but subtle, compensatory changes in lifestyle and a decline in activity level are observed by their family members. Many asymptomatic patients have a sometimes decades-long history of a heart murmur not previously investigated, and new presentation indicates low levels of MR and prolapse with recent worsening from rupture of the chordae tendinae. On physical exam, the murmur of MR is usually heard best at the apex with the patient in the left lateral decubitus position. With severe degenerative MR, the murmur is holosystolic radiating to the axilla. CXR may demonstrate cardiomegaly and/or LA enlargement and axis deviation suggesting LA enlargement and atrial fibrillation may be seen on EKG.

Echocardiography is the most valuable study in MR, yielding insight into valvular morphology and resultant change in the size of the cardiac chambers, as well as observed systolic flow reversal in the pulmonary veins. Although final determination of severity includes both qualitative and quantitative assessments, the following constellation of measured values are recommended and highly specific for severe MR:

• RVol ≥60 mL
• Regurgitant fraction ≥50%
• EROA ≥0.4 cm²

Vena contracta (narrowest diameter of the jet flow) width ≥0.7 cm and LV dilation to end systolic diameter >40 mm should also be measured. It should be noted that EF may be a misleading assessment of LV function, as the measured EF in compensated MR may be greater than normal due to the increase in preload and the afterload reducing effect of regurgitation into a low-resistance, enlarged LA. When parameters are discordant, heart catheterization with invasive pressure measurement and LV angiogram may be useful.

Surgical indications

In general, Class I indications for repair in DMR include valve-associated symptoms, reduced ejection fraction ≤60%, and enlarged LV end systolic diameter ≥40mm. The 2020 ACC/AHA Guidelinesfor DMR are summarized below.

Class I (Level of Evidence, LoE) recommendations:

• Symptomatic patients with chronic severe primary MR and LVEF >30% (LoE B)
• Asymptomatic with chronic severe primary MR and LV dysfunction (LVEF 30-60% and/or LV end-systolic diameter [LVESD] ≥40 mm) (LoE B)
• MV repair recommended over replacement when surgical treatment is indicated for patients with chronic severe primary MR limited to the posterior leaflet (LoE B)
• MV repair recommended over replacement when surgical treatment is indicated for patients with chronic severe primary MR involving the anterior leaflet or both leaflets when a successful and durable repair can be accomplished (LoE B)
• Concomitant MV repair or replacement is indicated in patients with chronic severe primary MR undergoing cardiac surgery for other indications (LoE B)

Class IIa recommendations: 

• MV repair is reasonable in asymptomatic patients with chronic severe primary MR with preserved LV function (LVEF ≥60% and LVESD ≤40 mm) in whom the likelihood of a successful and durable repair without residual MR is >95% with an expected mortality <1% when performed at a Heart Valve Center of Excellence (LoE B)
• MV surgery is reasonable for asymptomatic patients with chronic severe primary MR and preserved LV function with a progressive increase in LV size or decrease in EF on serial imaging studies (LoE C)
• MV repair is reasonable for asymptomatic patients with chronic severe nonrheumatic primary MR and preserved LV function where there is a high likelihood of a successful and durable repair with 1) new onset of AF or 2) resting pulmonary hypertension (PA systolic arterial pressure >50 mmHg) (LoE B)
• Concomitant MV repair is reasonable in patients with chronic moderate primary MR undergoing cardiac surgery for other indications (LoE C)
• In pregnant women with severe MR and NHYA class IV symptoms refractory to medical therapy, intervention during pregnancy is reasonable (LoE C).

Class IIb recommendations: 

• MV surgery may be considered in symptomatic patients with chronic severe primary MR and LVEF ≤30% (LoE C)
• Transcatheter MV repair may be considered for severely symptomatic patients (NYHA class III/IV) chronic severe primary MR with favorable anatomy for the procedure and reasonable life expectancy, but remain a prohibitive surgical risk because of severe comorbidities with severe symptoms despite optimal Guideline-Directed Medical Therapy (GDMT) for Heart Failure (HF) (LoE B)

Class III (Harm) recommendations:

• MVR should not be performed for the treatment of isolated severe primary MR limited to less than one half of the posterior leaflet unless mitral valve repair has been attempted and was unsuccessful (LoE B)

Surgical Approach

Repair is preferred over replacement for severe MR with high rates of successful, durable repair and improved 10-year survival well-published in high-volume centers of excellence. Although not yet widely practiced, early repair in patients with asymptomatic DMR is equally safe and durable with a 99% repair rate, 100% 10-year freedom from reoperation and 99.4% freedom from recurrent or greater MR.

In general, the goals of repair are to:

• Preserve leaflet mobility
• Restore leaflet coaptation length (CL) of 5-10mm without systolic anterior motion (SAM)
• Stabilize the annulus to protect the resultant repair

Anterior leaflet repair techniques include the use of artificial chords (neochords), chord transfer, chord advancement, edge-to-edge approximation (Alfieri repair), commissuroplasty, limited anterior leaflet resection, and free edge remodeling. Posterior and bileaflet approaches include but are not limited to the use of neochords, leaflet resection, sliding annuloplasty, cleft closure, folding plasty, and free edge remodeling. These techniques are frequently used in combination. Ring annuloplasty should be the standard of care in all repairs. A standardized approach and algorithm using the length of the A2 segment (measured by intraoperative TEE and/or direct measurement), and the distance from the coaptation point to the septum (c-sept) in systole (measured by TEE), allows highly reproducible results with the proper coaptation length without systolic anterior motion.

Transcatheter Repair

Transcatheter edge-to-edge repair (MitraClip or Pascal devices) for DMR are a part of the treatment algorithm for some patients, typically those of prohibitive surgical risk. While beyond the scope of this chapter, ideal transcatheter repair relies on favorable anatomic features including:

• Grasping zone ≥10 mm and without calcification
• Flail width <15 mm
• Flail gap <10 mm
• Single middle segment prolapse

Pitfalls and Postoperative Management

There are several potential complications after mitral valve surgery, including injury to the circumflex artery and conduction system. The most morbid complication, however, is AV groove disruption, which involves separation between the LA and LV. This complication is rare after repair but may occur following mitral replacement and is more common if the mitral annulus is calcified, such as seen in older patients. If this occurs, the most successful approach is reinstitution of CPB, cardioplegic arrest, explant of the prosthesis, and internal repair using a pericardial patch followed by implantation of a new prosthesis.

Systolic anterior motion (SAM) is an important but avoidable pitfall in mitral valve repair, wherein the anterior mitral leaflet obstructs the LVOT. Factors that reliably predict SAM are a narrowed aorto-mitral angle <100°, septal hypertrophy (HOCM), and a displaced coaptation point with c-sept distance <25 mm. Post-repair SAM is mitigated by careful attention to ensure no residual “tall” posterior leaflet is left and by avoiding the use of an inappropriately undersized annuloplasty ring. In patients with SAM after repair, the tenets of medical management are:

• Avoidance of inotropes
• Filling pressure optimization by volume expansion of the LV to minimize LVOT obstruction (transfuse the remaining volume in the cardiopulmonary bypass circuit)
• ß-blockade infusion to augment diastolic filling time by avoiding tachyarrhythmias

Suggested Readings

1. Bonow RO, O’Gara PT, Adams DH, et al. 2020 focused update of the 2017 ACC expert consensus decision pathway on the management of mitral regurgitation. J Am Coll Cardiol. 2020;75:2236–70.
2. Desai A, Thomas JD, Bonow RO, et al. Asymptomatic degenerative mitral regurgitation repair: Validating guidelines for early intervention. J Thorac Cardiovasc Surg. 2021;161(3):981-994.e5.
3. McCarthy PM, Herborn J, Kruse J, et al. A multiparameter algorithm to guide repair of degenerative mitral regurgitation. J Thorac Cardiovasc Surg. 2020;S0022-5223(20)32811-7.
4. 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.