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Essentially, all degenerative mitral valves are repairable. By matching echocardiographic findings to the appropriate surgical skill level required to consistently deliver a repair, valve replacement for degenerative mitral valve disease should be infrequent.

Most patients with mitral regurgitation remain asymptomatic for long periods of time. The most common presenting signs and symptoms include fatigue, decreased exercise capacity, shortness of breath, and palpitations or supra-ventricular arrhythmias such as atrial fibrillation. Auscultatory examination usually reveals a high-pitched systolic murmur radiating from the apex to the axilla. A holosytolic murmur suggests prolapse simultaneous with ejection typical of chordal rupture, whereas a murmur beginning in mid- or late systole favors billowing or chordal elongation. Radiographic findings may include left atrial and ventricular dilatation and prominent pulmonary vasculature in patients with long standing severe mitral regurgitation. The electrocardiogram may be normal, or show evidence of left atrial enlargement or atrial fibrillation.

Two dimensional echocardiography with doppler is essential to determine the mechanism (dysfunction) and severity of mitral regurgitation. Semi-quantitative assessment of regurgitant flow using maximal jet length, area, and ratio of jet to left atrial area is recommended to assess the severity of mitral regurgitation¹. Regurgitant jet geometry and area are assessed in multiple views and mitral regurgitation severity is graded typically as a rank order variable (e.g. 1+ trace, 2+ mild, 3+ moderate and 4+ severe mitral regurgitation). The direction of the jet provides evidence of segmental involvement as it is typically opposite to the prolapsing segment. Quantitative doppler grading of mitral regurgitation is gaining in popularity and is based on the calculation of regurgitant volume (the difference between the mitral and aortic stroke volumes) and effective regurgitant orifice (ratio of regurgitant volume to regurgitant time velocity integral). Table 1 shows the correlation between the semi-quantitative and quantitative grading of mitral regurgitation in degenerative mitral disease. Transesophageal echocardiography (TEE) is a useful adjunct to confirm the diagnosis and understand the mechanism of degenerative valve disease in the case of a non-definitive transthoracic examination. Experience is also gaining with three dimensional echocardiography in the assessment of annular geometry and leaflet dysfunction in the setting of mitral regurgitation, and can be predicted to have a more significant role in planning reparative procedures in the future.

(1)  Zoghbi WA, Enriquez-Sarano M, Foster E et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003 July;16(7):777-802.
(2)  Dujardin KS, Enriquez-Sarano M, Bailey KR, et al: Grading of mitral regurgitation by quantitative Doppler echocardiography: calibration by left ventricular angiography in routine clinical practice. Circulation 96(10):3409-15 1997.

The syndrome of mid-systolic click accompanying a systolic murmur was first described in the late 1800s, but it was in the early 1960s that its association with mitral regurgitation was demonstrated by Barlow and colleagues using cine-ventriculography¹. Criley et al.² correctly identified the mechanism of the regurgitation as posterior leaflet prolapse due to excess leaflet motion, coining the phrase ‘mitral valve prolapse’. Carpentier and co-workers later characterized the surgical lesions resulting from the myxoid degeneration present in Barlow’s disease, which included leaflet thickening, large redundant leaflets, chordal elongation or rupture, and annular dilatation. As the myxoid degenerative process often affects the entire valve, patients with Barlow’s disease generally have complex valve pathology and dysfunction, which is most often multisegmental (i.e. involves more than one segment of the posterior or anterior leaflet).

Clinical Presentation

Patients with Barlow mitral-valve disease are generally adults around the age of 50 years who have known for a long period of time, often decades, that they ‘have a murmur’. Often asymptomatic, patients may have been followed by an internist for years, and referral to a cardiologist and subsequently to a cardiac surgeon is usually triggered by the development of symptoms or signs such as atrial fibrillation, shortness of breath and fatigue, or echocardiographic documentation of ventricular or atrial enlargement, or a decline in ventricular function, often accompanied by varying degrees of pulmonary hypertension. Physical examination most often reveals the presence of a mid-systolic click and a mid to late systolic murmur, which reflects the timing of prolapse in the setting of excess tissue and chordal elongation without chordal rupture (i.e. flail leaflet)².

Echocardiographic Findings

Echocardiography is a sensitive tool in the differentiation of degenerative mitral valve disease. A striking feature of the patient with Barlow’s disease is the size of the valve apparatus – the leaflets are usually thick, bulky, elongated, and distended; the chords thickened and elongated, often mesh-like in nature; and the annulus dilated and enlarged, often times greater than 36mm in the intercommissural distance (Figure 1). The prolapse is often multisegmental, and involves both leaflets in up to 40% of patients³. The insertion of the posterior leaflet is often displaced toward the left atrium away from its normal insertion in the atrio-ventricular groove, creating a cul-de-sac at the base of the leaflet. The bodies of distended leaflet segments often billow above the plane of the annulus, and the margin of the leaflet segments prolapse in mid-systole in the setting of chordal elongation, or in early systole if chordal rupture has occurred. Calcification of the annulus and papillary muscles may be present. Real time three-dimensional echocardiography is allowing additional clarity of the segmental nature of the billowing, as well as prolapse, in Barlow’s disease^4,5,6 and may play a critical role in the preoperative work up of these patients in the future.

Surgical Considerations

The complexity of surgical lesions in Barlow mitral-valve disease is consistent with the echocardiographic findings (Figure 1). Lesions include excessively thick and billowing leaflet segments, chordal elongation and chordal rupture, calcification of the papillary muscles and/or annulus with chordae restriction, and severe annular dilatation with giant valve size. It is important that the cardiologist as well as the surgeon has an appreciation for these lesions, as the complexity of techniques required to achieve a successful repair then becomes obvious in this subset of degenerative mitral-disease patients. Dealing with excess tissue height is an important consideration to reduce the likelihood of postoperative systolic anterior motion. Repair of Barlow valves is thus more complicated and, in our experience, often requires multiple different techniques and 2–3 hours to remove all of the diseased tissue, and reconstruct the leaflets to a normal configuration³.

To achieve a Barlow repair, the surgeon therefore needs to be well versed with various advanced mitral repair techniques, such as extensive leaflet resection, sliding leaflet plasty, chordal transfer, neochordoplasty, commissuroplasty, annular decalcification and use of large annuloplasty rings. Patients with advanced forms of Barlow’s disease will therefore likely have a high probability of successful valve repair only if done in reference centers by mitral subspecialists (Table 1).

Excerpted, with permission, Adams DH, Anyanwu AC. The cardiologist’s role in increasing the rate of mitral valve repair in degenerative disease. Current Opinion in Cardiology 2008, 23:105–110.
(1)  Barlow JB, Pocock WA, Marchand P, Denny M. The significance of late systolic murmurs. Am Heart J 1963; 66:443–452.
(2)  Criley JM, Lewis KB, Humphries JO, Ross RS. Prolapse of the mitral valve: clinical and cine-angiocardiographic findings. Br Heart J 1966; 28:488–496.
(3)  Adams DH, Anyanwu AC, Rahmanian PB, et al. Large annuloplasty rings facilitate mitral valve repair in Barlow’s disease. Ann Thorac Surg 2006; 82:2096–2100.
(4)  Sharma R, Mann J, Drummond L, et al. The evaluation of real-time 3-dimensional transthoracic echocardiography for the preoperative functional assessment of patients with mitral valve prolapse: a comparison with 2-dimensional transesophageal echocardiography. J Am Soc Echocardiogr 2007; 20:934– 940.
(5)  Patel V, Hsiung MC, Nanda NC, et al. Usefulness of live/real time threedimensional transthoracic echocardiography in the identification of individual segment/scallop prolapse of the mitral valve. Echocardiography2006; 23:513–518. (6)  Muller S, Muller L, Laufer G, et al. Comparison of three-dimensional imaging to transesophageal echocardiography for preoperative evaluation in mitral valve prolapse. Am J Cardiol 2006; 98:243–248.

In contrast to Barlow’s disease, patients with mitral regurgitation due to fibroelastic deficiency have a lack of connective tissue as the pathological mechanism that triggers leaflet and chordal thinning and eventual chordal rupture¹. Carpentier’s group characterized the typical findings in fibroelastic deficiency, noting that the chordal rupture resulting in mitral valve prolapse was often isolated, usually leading to prolapse of a single leaflet segment².

Clinical Presentation

The typical patient with fibroelastic deficiency is over the age of 60 years, and does not have a long history of a heart murmur. Often asymptomatic until the time of chordal rupture, the patient often presents with palpitations or shortness of breath of limited duration. Patients may remain asymptomatic after chordal rupture, and present as a new-onset murmur or abnormal echocardiogram, but this is less frequent than in the setting of Barlow’s disease. Physical examination is remarkable for a holosystolic murmur, often harsh in nature.

Echocardiographic Findings

In contrast to Barlow’s disease, echocardiographic signatures of fibroelastic deficiency include normal or near-normal valve size, thin leaflets and chordae, and typically single segment prolapse, most commonly of the middle scallop of the posterior leaflet (P2) (Figure 1). The prolapsing segment may appear to be distended, thickened, and elongated, while the adjacent segments appear normal in height and consistency. Billowing of nonprolapsing segments is not observed, and bi-leaflet dysfunction is uncommon.

Surgical Considerations

In contradistinction to Barlow’s disease, patients with fibroelastic deficiency often present with minimal, as opposed to excess, tissue (Figure 1), so extensive leaflet resection or complex leaflet remodeling procedures are rarely indicated. In general, a limited quadrangular or triangular resection, or simple leaflet resuspension with a chordal transfer or artificial chord, is all that is required to correct leaflet prolapse. For posterior leaflet prolapse, although the prolapsing segment may look very abnormal, the remainder of the valve is relatively unaffected, so that the surgeon does not usually require advanced techniques to achieve a successful mitral valve reconstruction.

It should, however, be noted that ‘complex’ prolapse can occur in fibroelastic deficiency, usually involving an anterior leaflet segment or a commissural segment, and in this setting more advanced techniques and surgical skill are generally required to perform a successful reconstruction. Otherwise, simple fibroelastic deficiency with P2 prolapse is a condition associated with high repair rates in most experienced surgeons’ hands, and a virtually 100% repair rate within a reference center setting with a mitral repair subspecialist (Table 1).

Excerpted, with permission, Adams DH, Anyanwu AC. The cardiologist’s role in increasing the rate of mitral valve repair in degenerative disease. Current Opinion in Cardiology 2008, 23:105–110.
(1)  Anyanwu AC, Adams DH. Etiologic Classification of Degenerative Mitral Valve Disease: Barlow’s Disease and Fibroelastic Deficiency. Semin Thorac Cardiovasc Surg 2007; 19:90–96.
(2)  Carpentier A, Chauvaud S, Fabiani JN, et al. Reconstructive surgery of mitral valve incompetence: ten-year appraisal. J Thorac Cardiovasc Surg 1980; 79:338–348.

Numerous studies that have compared long term-survival of patients undergoing mitral valve repair or replacement have consistently shown a survival benefit with mitral valve repair. The ‘repair rate’ is thus an important variable. The ideal repair technique should be applicable to over 90% of cases. Repair rate statistics are not integral to the technique and vary from surgeon to surgeon. Unfortunately, most series do not include repair rates and prospective databases generally do not differentiate etiologies of mitral disease, such that it is not possible to accurately define repair rates for degenerative disease. We believe that the overall replacement rate in degenerative disease may be as high as 50%. In a review of United States practice in 1999 and 2000, 42.4% of patients having isolated mitral valve surgery for valve regurgitation had a valve repair (all etiologies of mitral disease)¹. Similarly, in the United Kingdom, 35% of mitral procedures were repairs in 2000-2001². In the United Kingdom, more mechanical mitral valve replacements were performed than mitral repairs (ratio 6:5). We believe that as degenerative disease often occurs in young patients (who are the usual candidates for mechanical valves), and as the incidence of rheumatic disease has declined substantially in western countries, a considerable number of these mechanical mitral valve replacements are likely performed for degenerative disease. Indeed a review of contemporary mitral valve replacement literature shows substantial proportions of replacements for degenerative disease. For example, Bouchard and associates³ in a series examining outcomes of mitral valve replacement, include 213 replacements for degenerative disease over a ten-year period. In another recent study, Yun et al⁴ randomized 47 patients over two years to two forms of chordal sparing valve replacement; 31 of these patients had degenerative disease. Finally in a series of 154 bioprosthetic implants reported by Rizzoli et al, 34 were performed for degenerative disease⁵. Repair rates in large published series generally range from 85% to 90%, although most include historical patients from the 1980s. Our philosophy is that repair should be attempted in all degenerative valves. Using this approach we have achieved a 99.5% repair rate over a 4 year period. For mitral valve repair to be the standard of care for degenerative disease, it should be available and applicable to all patients. Certainly any surgeon performing surgery for asymptomatic degenerative disease should have > 95% repair rate for the lesion present, as mitral repair is the only therapy currently advisable in this group⁶. Current national repair rates, however, suggest that there remains a considerable body of surgical practice that has not embraced systematic repair of degenerative valves.

(1)  Savage EB, Ferguson TB, Jr., DiSesa VJ. Use of mitral valve repair: analysis of contemporary United States experience reported to the Society of Thoracic Surgeons National Cardiac Database. Ann Thorac Surg 2003 March;75(3):820-5.
(2)  Keogh BE, Kinsman R. Fifth National Adult Cardiac Surgical Database Report 2003. Henley-on-Thames: Dendrite; 2004.
(3)  Bouchard D, Pellerin M, Carrier M et al. Results following valve replacement for ischemic mitral regurgitation.Can J Cardiol 2001 April;17(4):427-31.
(4)  Yun KL, Sintek CF, Miller DC et al. Randomized trial comparing partial versus complete chordal-sparing mitral valve replacement: effects on left ventricular volume and function. J Thorac Cardiovasc Surg 2002 April;123(4):707-14.
(5)  Rizzoli G, Bottio T, Vida V et al. Intermediate results of isolated mitral valve replacement with a Biocor porcine valve. J Thorac Cardiovasc Surg 2005 February;129(2):322-9.
(6)  Hayek E, Gring CN, Griffin BP. Mitral valve prolapse. Lancet 2005 February 5;365(9458):507-18.

When interpreting data on long-term survival, it should be appreciated that available data refer to the outcomes of mitral repair and cardiac surgery as practiced 10 to 20 years previously¹. Cardiac surgery has, however, since improved in several ways; for example, the widespread adoption of blood cardioplegia has likely reduced the ventricular damage during surgery which in turn will impact long-term survival (as left ventricular function is a major determinant of long-term survival). There is therefore no way of knowing the long-term survival outcomes of mitral valve surgery as currently practiced. Based on existing data, it appears that if surgery is undertaken before onset of symptoms and where left ventricular function is preserved, the life expectancy should be similar to that of the general population^{2, 3, 4}. When significant symptoms of heart failure have developed (NYHA III – IV) before mitral valve surgery is undertaken, the long term survival is significantly reduced (Figure 1), regardless of the left ventricular function⁵. Similarly, patients with an impaired left ventricular ejection fraction at time of surgery have a reduced long-term survival (Figure 2).

Figure 1: Comparison of observed and expected survival after mitral valve surgery in patients in NYHA classes I-II (left) and classes III-IV (right). Numbers underneath indicate percentage of expected survival achieved.*

Figure 2: Survival after mitral valve surgery according to preoperative echocardiographic ejection fraction (EF). Numbers at bottom indicate patients at risk.**

(1)  Adams DH, Anyanwu A. Pitfalls and limitations in measuring and interpreting the outcomes of mitral valve repair. J Thorac Cardiovasc Surg 2006 March;131(3):523-9.
(2)  Enriquez-Sarano M. Timing of mitral valve surgery. Heart 2002 January;87(1):79-85.
(3)  Mohty D, Orszulak TA, Schaff HV, Avierinos JF, Tajik JA, Enriquez-Sarano M. Very long-term survival and durability of mitral valve repair for mitral valve prolapse. Circulation 2001 September 18;104(12 Suppl 1):I1-I7.
(4)  Braunberger E, Deloche A, Berrebi A et al. Very long-term results (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circulation 2001 September 18;104(12 Suppl 1):I8-11.
(5)  Tribouilloy CM, Enriquez-Sarano M, Schaff HV et al. Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications. Circulation 1999 January 26;99(3):400-5.
(*)  Modified from Tribouilloy CM, Enriquez-Sarano M, Schaff HV, et al: Impact of preoperative symptoms on survival after surgical correction of organic mitral regurgitation: rationale for optimizing surgical indications.Circulation 99 (3):400-5, 1999. Lippincott Williams & Wilkins
(**)  Modified from Enriquez-Sarano M, Tajik AJ, Schaff HV, et al: Echocardiographic prediction of survival after surgical correction of organic mitral regurgitation. Circulation; 90(2):830-7, 1994. Lippincott Williams & Wilkins

Figure 1: Outcome after mitral valve repair. A,freedom from reoperation in patients with posterior, anterior and bileaflet prolapse. B,freedom from recurrent moderate (3+) or severe (4+) MR according to prolapsing leaflet. AL, anterior leaflet, PL, posterior leaflet, BL, bileaflet prolapse.*

Failure of repair, defined by recurrence of moderate or severe mitral regurgitation, or re-operation for mitral regurgitation are principal endpoints to evaluate the long-term outcomes of mitral valve repair. Failure rates of mitral valve repair are determined principally by the original dysfunction (posterior leaflet, anterior leaflet and bi leaflet) and by repair technique. The longest term follow-up available is for conventional ‘Carpentier’ techniques. Braunberger and colleagues¹reported in 2001 on the long term outcomes of 162 non-rheumatic patients (of whom 90% were degenerative) who underwent a Carpentier repair between 1970 and 1984. They observed that 97% of patients with posterior leaflet, 86% with anterior leaflet and 83% of patients with bileaflet prolapse were free of re-operation at 20 years (Figure 1a). They also found 74% were free from cardiac events at 20 years. The difference between freedom from reoperation and freedom from cardiac event rates, however highlights the limitations of re-operation rate as an outcome measure for mitral repair. Because the decision to undergo reoperation is physician and patient dependent, at least some of those patients with cardiac symptoms had recurrent mitral regurgitation, but never underwent reoperation. In the absence of echocardiographic follow-up, there is no way of quantifying the true long-term failure rate. David and colleagues² also presented 20 year follow-up for patients (operated between 1981 and 2001) using a variety of repair techniques, including conventional Carpentier techniques and gortex neochordoplasty, and found 96%, 88% and 94% freedom from re-operation rates at 12 years for posterior, anterior and bileaflet prolapse respectively. They also reported on freedom from moderate or severe mitral regurgitation – 80%, 65% and 67% respectively at 12 years (Figure 1b) – however, follow-up echocardiographic data was available for only half of the patients. The lack of systematic echocardiographic follow-up is the major limiting factor in determining the true durability of all mitral repair techniques³; most series have focused on survival and re-operation rates which may not necessarily be reflective of the durability of repair.

Figure 2: Freedom from recurrent mitral regurgitation after mitral valve repair. Kaplan-Meier estimates of freedom from non-trivial MR (MR>1/4) and failing repair (MR>2/4). A linearized recurrence rate per year of 8.3% is found for MR grade >1/4. The rate grade >2/4 is 3.4%.**

The most complete and elaborate follow-up for mitral repair in contemporary literature is probably the series of Flameng and associates⁴ who report a series of 242 consecutive mitral repairs with serial follow-up echocardiography done at 6 month intervals. They found a freedom from moderate or severe mitral regurgitation of 71% at 7 years and found that new recurrent mitral regurgitation appeared at a rate of 3.7% per year (Figure 2). The data of Flameng and colleagues⁴ suggest that durability of many mitral repairs is limited; the linear recurrence rate implies that recurrent mitral regurgitation is likely a reflection of progression of underlying valve disease. This hypothesis is supported by data from mitral re-operations after previous repair, as the previous repairs are found to be intact in two-thirds of patients, with recurrent regurgitation usually due to new valve lesions (chordal rupture, fibrosis, calcification, leaflet perforation)⁵. Technical failure can be a major cause of recurrence, particularly with early failures⁶, but should be minimal in experienced hands. Some surgical factors that predispose to recurrence of mitral regurgitation include the non-use of an annuloplasty ring, and the technique of chordal shortening.

The edge-to-edge technique is a relatively new repair strategy with limited follow-up compared to Carpentier techniques. One large published series from De Bonis and colleagues⁷ included 133 patients, followed for a median of 3 years, in whom anterior leaflet prolapse was treated with the edge-to-edge technique; they estimated a 10 year freedom from re-operation of 96.5%, but do not include data that allow computation of the freedom from mitral regurgitation rate.

(1)  Braunberger E, Deloche A, Berrebi A et al. Very long-term results (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circulation 2001 September 18;104(12 Suppl 1):I8-11.
(2)  David TE, Ivanov J, Armstrong S, Christie D, Rakowski H. A comparison of outcomes of mitral valve repair for degenerative disease with posterior, anterior, and bileaflet prolapse. J Thorac Cardiovasc Surg 2005 November;130(5):1242-9.
(3)  Adams DH, Anyanwu A. Pitfalls and limitations in measuring and interpreting the outcomes of mitral valve repair. J Thorac Cardiovasc Surg 2006 March;131(3):523-9.
(4)  Flameng W, Herijgers P, Bogaerts K. Recurrence of mitral valve regurgitation after mitral valve repair in degenerative valve disease. Circulation 2003 April 1;107(12):1609-13.
(5)  Cerfolio RJ, Orzulak TA, Pluth JR, Harmsen WS, Schaff HV. Reoperation after valve repair for mitral regurgitation: early and intermediate results. J Thorac Cardiovasc Surg 1996 June;111(6):1177-83.
(6)  Shekar PS, Couper GS, Cohn LH. Mitral valve re-repair. J Heart Valve Dis 2005 September;14(5):583-7.
(7)  De BM, Lorusso R, Lapenna E et al. Similar long-term results of mitral valve repair for anterior compared with posterior leaflet prolapse. J Thorac Cardiovasc Surg 2006 February;131(2):364-70.
(*)  Modified from A, Braunberger E, Deloche A, Berrebi A, et al: Very long-term results (more than 20 years) of valve repair with carpentier’s techniques in nonrheumatic mitral valve insufficiency. Circulation 104(12 Suppl 1):I8-11 2001 Lippincott Williams & Wilkins and B, Reprinted from J Thorac Cardiovasc Surg 130(5), David TE, Ivanov J, Armstrong S, et al, A comparison of outcomes of mitral valve repair for degenerative disease with posterior, anterior, and bileaflet prolapse, 1242-9, Copyright 2005, with permission from the American Association for Thoracic Surgery.
(**)  Modified from Flameng W, Herijgers P, Bogaerts K: Recurrence of mitral valve regurgitation after mitral valve repair in degenerative valve disease. Circulation 107(12):1609-13 2003. Lippincott Williams & Wilkins

Most complex mitral valve repair surgery can be performed through a 4 inch sternotomy.

Our Minimally Invasive Heart Surgery Center offers minimally invasive heart valve surgery to selected patients. Not all patients are suitable for minimally invasive surgery. Patients who require additional cardiac procedures like coronary artery bypass surgery, elderly patients, patients with very diseased arteries, and patients with a very weakly contracting heart will not be suitable for this approach. Our paramount objective is to ensure a good valve repair, with no residual leakage, at a low operative risk.Our surgeons will only perform a repair through a small incision when they believe they can do a good quality valve repair at a low risk to the patient; if the valve disease is complicated (as assessed by the echocardiogram) then we recommend a full incision as we believe a larger scar is preferable to an imperfect repair.

Ask the surgeon if this is an option for you.

Different Approaches to Minimally Invasive Heart Surgery

Dr. David Adams and Dr. Ani Anyanwu use special instruments to perform minimally invasive heart valve surgery.

The term “minimally invasive surgery” covers a spectrum of approaches. The goal is to perform surgery through a smaller incision without compromising the safety and long-term results of conventional mitral valve repair. The advantage of a small incision is mainly cosmetic (the scars are smaller and less visible). In some patients, the pain after surgery may be reduced and recovery from surgery is faster when surgery is done through a smaller incision. Operating through small incisions is however more technically demanding and in some cases could reduce the safety of the procedure. This page describes the various incisions, and you can read more about the associated benefits and disadvantages of each.

Lower Sternotomy

Dr. David Adams with Mary D., five weeks after surgery, whose minimally invasive valve repair was performed with a sternotomy.

In this approach the surgeon makes a 4 inch incision over the lower aspect of the midline of the chest and divides only the lower portion of the breast bone to gain access to the valve. This limits the actual amount of opening, and thus chest wall trauma. Through this incision we can easily access the heart and all the major vessels and can perform most complex mitral valve repairs along with aortic valve replacement or coronary artery bypass grafting. This incision has the advantage that if the surgeon encounters problems, he or she can easily extend the incision and divide the remaining breast-bone and convert to the standard approach. When fully healed the lower sternotomy scar is concealed by clothing, even when the patient wears low-necked clothing. In some women the scar is well concealed by their brassiere. It is the most flexible approach to the heart, and it is the approach we use in most patients.

Mini-Thoracotomy

Mitral valve surgery can be carried out through a 2-3 inch incision, usually under the right breast, which allows the surgical team to see and work on the mitral valve directly. The patient is placed on the heart-lung machine either through the same chest incision or through the vessels in the groin via a 1 inch incision. Durable, simple and more complex mitral repairs can be performed, eliminating mitral regurgitation in a wide range of patients.

Thoracotomy

Dr. David Adams shows a thoracotomy incision from a minimally invasive heart valve repair, eight days after surgery.

In this approach the surgeon makes a 4 to 6 inch incision in the right side (instead of middle) of the chest and gains access to the heart by going through the ribs. Some women prefer this incision because the scar may be placed underneath the breast crease and is therefore largely concealed. Access to the heart may be difficult in some cases making it more difficult to achieve a perfect repair.

Low Skin Incisions

Patients who are concerned about cosmesis, but who are not suitable for minimally invasive surgery, can request a low incision. The surgeon can make the standard skin incision start an inch lower and yet perform full division of the breastbone. The scar will therefore not be visible when wearing normal clothing. Patients who cannot have a minimally invasive operation, but who are concerned about the scar, can also request the services of our plastic surgeon to cosmetically close the incision.

Robotic Surgery and Endoscopic Surgery

In these approaches the surgeon performs the operation through several mini-incisions or “port sites”, the largest being about 2 inches. Robotic mitral valve repair is performed using the assistance of a ‘robot’ and specially designed instruments to perform the operation. The surgeon sits at a console and controls the instruments which are mounted on the arms of a robot by another surgeon. Endoscopic mitral valve repair is performed using long instruments placed through the port sites. The patient is placed on the heart-lung machine via blood vessels in the groin. In both cases, the surgeon uses video cameras to see inside the chest cavity.

Although cosmetically superior, these approaches limit the complexity of repair that can be undertaken by the surgeon, and in some cases may compromise on the quality of repair. For this reason, we do not offer these two approaches at Mount Sinai as we cannot guarantee the same high standards of mitral valve repair as we can with other approaches.

Figure 1: Cardiac events among patients with asymptomatic mitral regurgitation and medical management according to the effective regurgitant orifice (ERO). Kaplan-Meier estimates of means ± standard deviation. Cardiac events were defined as death due cardiac causes, congestive heart failure, or new onset of atrial fibrillation.*

As current existing guidelines do not recommend surgery for asymptomatic or mildy symptomatic patients¹, there is a large cohort of patients with significant mitral regurgitation that do not undergo surgery, thus allowing for observational studies of outcomes in non-surgically treated cohorts. Additionally, before expanded application of mitral valve repair in the 1990s, cohorts of symptomatic patients with mitral valve prolapse were followed on medical therapy allowing determination of natural history of mitral regurgitation. Mitral valve prolapse with severe regurgitation reduces long-term survival irrespective of medical therapy. It appears that the prolapse itself is not the cause of mortality or morbidity (cardiac event rates are extremely low for the entire population with prolapse), but it is severe regurgitation and consequent left ventricular dilatation that results in morbidity^{2, 3}. Heart failure, arrhythmia, endocarditis and stroke are the leading causes of death. Enriquez-Sarano and colleagues have performed analyses to define which group of patients with mitral regurgitation are at greatest risk of cardiac events^{4, 5, 6}. Notably, when considering asymptomatic patients, the greater the severity of mitral regurgitation (preferably determined by quantitative echocardiography), the higher the frequency of cardiac events irrespective of a normal ventricular function (Figure 1). Other risk factors for cardiovascular morbidity include atrial fibrillation, left atrial enlargement, age > 50 years and thickening of mitral leaflets⁷ – presence of these factors implies a reduced life expectancy if mitral regurgitation is uncorrected. Current evidence from surgical cohorts, suggests that mitral valve repair (assuming an operative mortality below 1%) yields a better outcome (survival and freedom from cardiac events) compared to the outcomes observed in non-surgically treated patients with severe regurgitation. For example mitral valve repair in patients with good ventricular function has a long term survival similar to expected survival in age matched cohorts^{5, 8, 9}, whereas long term follow-up of patients with mitral valve prolapse treated medically shows a reduced survival compared to expected survival¹⁰ (Figure 2).

Figure 2: Long-term survival with medical treatment compared with expected durations of survival for patients with mitral regurgitation due to flailing leaflets. Kaplan-Meier curve of survival.**

It should be emphasized that the alternative to surgical therapy is, strictly speaking, not medical therapy, but observation, as there are no pharmacological options for treatment of severe mitral regurgitation. Data supporting the role of any medical treatment – particularly vasodilators – in the management of severe regurgitation due to degenerative mitral valve disease is scant¹¹. Indeed it has been suggested that vasodilator therapy can lead to paradoxical worsening in mitral regurgitation by shifting the prolapse earlier in the cardiac cycle¹². Vasodilator therapy can also mask left ventricular dysfunction and result in (potentially deleterious) delay to mitral valve surgery. According to current guidelines, there is little role for pharmacological treatment in the management of severe mitral regurgitation¹.

(1)  Bonow RO, Carabello B, de Leon AC et al. ACC/AHA Guidelines for the Management of Patients With Valvular Heart Disease. Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Patients With Valvular Heart Disease). J Heart Valve Dis 1998 November;7(6):672-707.
(2)  St John SM, Weyman AE. Mitral valve prolapse prevalence and complications: an ongoing dialogue.Circulation 2002 September 10;106(11):1305-7.
(3)  Enriquez-Sarano M, Tajik AJ. Natural history of mitral regurgitation due to flail leaflets. Eur Heart J 1997 May;18(5):705-7.
(4)  Zoghbi WA, Enriquez-Sarano M, Foster E et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr 2003 July;16(7):777-802.
(5)  Enriquez-Sarano M. Timing of mitral valve surgery. Heart 2002 January;87(1):79-85.
(6)  Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D et al. Quantitative determinants of the outcome of asymptomatic mitral regurgitation. N Engl J Med 2005 March 3;352(9):875-83.
(7)  Avierinos JF, Gersh BJ, Melton LJ, III et al. Natural history of asymptomatic mitral valve prolapse in the community. Circulation 2002 September 10;106(11):1355-61.
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(*)  Modified from Enriquez-Sarano M, Avierinos JF, Messika-Zeitoun D, et al: Quantitative determinants of the outcome of asymptomatic mitral regurgitation. New Engl J Med 352(9):875-83 2005. Copyright © 2005 Massachusetts Medical Society. All rights reserved.
(**)  Modified from Ling LH, Enriquez-Sarano M.M, Long-term outcomes of patients with flail mitral valve leaflets. Coron Artery Dis. 2000 Feb;11(1):3-9. Review. Lippincott Williams & Wilkins