Atlas of Mitral Valve Repair, 1st Edition

12

Complications and Assessing the Quality of Repair

INTRAOPERATIVE ASSESSMENT OF VALVE COMPETENCE

The simplest and most reliable method to assess valve competence is to rapidly and forcibly inject saline through the valve to fill and distend the left ventricle and aortic root. This can be done with a 20 Fr. red rubber catheter attached to a bulb syringe. The catheter is inserted through the valve and rapidly withdrawn after the injection. Multiple injections may be necessary to ensure adequate ventricular distension to pull the leaflets down below the annular plane; a competent valve may leak if ventricular filling is not adequate to allow valvular coaptation. When evaluating the valve leaflets the entire line of closure should be parallel to the mural part of the annulus (1). Approximately 0.5 cm or more of tissue apposition along the entire line of closure is important. Focal areas of inadequate apposition should be evaluated closely as they may be sites of potential early failure (Figs. 12.1,12.2,12.3,12.5,12.5). Any residual leaflet prolapse, even in the absence of a leak, should be addressed to prevent early failure.

 

Figure 12.1 Testing the valve after ring placement. (Clip 5, Case 2) 

 

Figure 12.2 Intraoperative evaluation of a posterior leaflet cleft after a posterior sliding plasty. (Clip 6, Case 1) 

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Figure 12.3 Testing after ring placement. (Clip 6, Case 5) 

 

Figure 12.4 Testing the valve after medial commissuroplasty. (Clip 7, Case 4) 

 

Figure 12.5 Final test after band placement. (Clip 11, Case 1) 

 

Figure 12.6 Postoperative echocardiogram showing reduced annular diameter. (Clip 6, Case 2) 

Once the heart is beating and the patient has been weaned from cardiopulmonary bypass, the valve should be evaluated using transesophageal echocardiography as described in Chapter 4. Intraoperative echocardiography identified early failures (8%) that were immediately addressed (2). Any leak more than trace or 1+ should be evaluated closely because the long-term rate of failure will be higher with 2+ or more regurgitation (3). As a rule-of-thumb, any degree of regurgitation noted intraoperatively will increase by 1 in the awake patient. If regurgitation is noted the systolic blood pressure should be raised with vasoconstrictor agents to between 150 and 160 mmHg to assure the degree of regurgitation remains unchanged (Figs. 12.6,12.7,12.8).

Another method of assessment is to infuse blood into the aortic root, allowing the heart to beat with the aortic cross-clamp in place to assess dynamic function (Fig. 12.9). This can be used before repair to assess the site of leak and after repair to assess the adequacy of repair (4). Alternatively, an additional cannula can be placed through the ventricular apex to pressurize the ventricle simultaneous with aortic root perfusion (Fig. 12.10) (5). In most scenarios these techniques are unnecessary and more useful in the assessment of excessive regurgitation noted on echocardiography after competency was noted with saline infusion through the valve.

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Figure 12.7 Postoperative echocardiogram dilated cardiomyopathy. (Clip 7, Case 5) 

 

Figure 12.8 Postoperative echocardiogram. (Clip 9, Case 4) 

If combined aortic and mitral procedures are performed, the mitral repair should be completed and tested before opening the aorta. If the aorta must be opened prior to repair (e.g., to administer cardioplegia in the presence of aortic insufficiency) the aorta can be clamped below the aortotomy. Alternatively, a foley catheter can be passed through the annulus, the balloon inflated, and the catheter wedged in the outflow tract; fluid for distension can then be infused through the lumen of the catheter to distend the ventricle and test the valve (6) (Fig. 12.11).

SYSTOLIC ANTERIOR MOTION (SAM)

Systolic anterior motion (SAM) occurs when the anterior leaflet is caught in the stream of ejecting blood and pulled anteriorly toward the septum rather than closing by moving posteriorly, causing left ventricular outflow tract obstruction and mitral regurgitation (Fig. 12.12).

 

Figure 12.9 Aortic root perfusion for assessment of the mitral valve in the beating heart. (From Marshall Jr. WG. Technique for visualization of the functioning mitral valve. Ann Thorac Surg. 1990;49:1013.)

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Figure 12.10 Setup for controlled root and ventricular perfusion to assess the mitral valve in the beating heart. (From Sundt 3rd TM, Khaghani A, Yacoub MH. Alternative technique for assessment and repair of the mitral valve. Ann Thorac Surg. 1996;61:1552-1554.)

 

Figure 12.11 Occlusion of the left ventricular outflow tract with a foley catheter to test the mitral repair with an open aorta. (From Ferguson Jr. TB, Wechsler AS. Testing of mitral valve competence following combined mitral valve repair and aortic valve replacement. Ann Thorac Surg. 1985;40,631-633.)

Originally reported to occur in between 4.5% and 10% of patients (7), the incidence is much lower with newer repair techniques (8,9). SAM is more common in patients with smaller ventricles and taller posterior leaflets (10). SAM was noted when the ratio of the length of the anterior to the posterior leaflet was small (0.99 with SAM, 1.95 without SAM) (11). The general consensus is that SAM is caused by anterior displacement of the site of coaptation of the leaflets secondary to excessive height or redundant tissue in the posterior leaflet (12,13,14). Anterior displacement was attributed to annular plication of the annulus after extensive (>3 cm) quadrangular resection and leaflet prolapse (15). This can be avoided by alternative posterior leaflet techniques, such as posterior leaflet sliding plasty (see Chapter 9), when large portions of the posterior leaflet are resected and avoiding an annuloplasty ring that is too small (10). SAM has been reported to be associated with the use of a rigid annuloplasty ring (15), but can occur with a flexible ring (16) or in the absence of a ring (17).

SAM is most commonly noted intraoperatively, and is usually associated with hypotension, hypovolemia, a small ventricular cavity, ventricular hypertrophy, and a hyperdynamic

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state induced by catecholamine use. In most cases, it will resolve with withdrawal of inotropic stimuli, volume loading, slowing heart rate to increase ventricular filling, and increasing afterload to reduce ventricular emptying. Raney et al. used the “Pomeroy Procedure” or anterior leaflet shortening (Chapter 8) described above to correct SAM in one patient (18). If persistent after above measures an alternative to repair revision is transaortic septal myectomy, used in two patients by Rescigno et al. (19) and five patients by Civelek et al. (20).

 

Figure 12.12 Systolic anterior motion (SAM); A: Before repair; B: SAM after repair; C: elimination of SAM after re-repair. (From Lee KS, Stewart WJ, Lever HM, Underwood PL, Cosgrove DM. Mechanism of outflow obstruction following failed valve repair: anterior displacement of leaflet coaptation. Circulation. 1993;88 (Suppl II):II-24-9.)

HEMOLYTIC ANEMIA

Hemolytic anemia secondary to the repair usually presents within the first few months, and has been attributed to a high velocity jet directed at the cloth-covered annuloplasty ring (21). However, it can be associated with high shear stress due to the regurgitant jet (22,23). It can occur in the presence of mild regurgitation (24). The diagnosis of hemolytic anemia is suggested by increased serum haptoglobin, elevation of serum lactate dehydrogenase (LDH), and schistocytosis. This may improve over time if the ring heals in (though the regurgitant jet may prevent this) (25). Beta-blockers have been used to reduce the velocity of the regurgitant jet. Reoperation is often necessary and re-repair is possible.

STENOSIS

Early stenosis is unusual and late stenosis is rare. Reviewing 478 patients with regurgitation secondary to nonrheumatic etiology repaired with various rings and bands, 4 patients developed late stenosis secondary to pannus overgrowth on the annuloplasty ring, extending onto the leaflets (26). This occurred in a subgroup of 138 patients repaired with a Duran ring.

MISCELLANEOUS RESULTS

A number of groups have reported long-term results that have been summarized in Table 12.1. Valve repair has also been performed with good success in the presence of endocarditis (27,28). Causes of reoperation were discussed for 49 patients by Cerfolio et al. Reasons for reoperation included recurrent severe regurgitation (70%), hemolytic anemia (14%), mixed regurgitation and stenosis (14%), and mitral stenosis (2%). In 65% the initial repairs were intact. Regurgitation was due to fibrosis and calcification, ruptured chordae, or leaflet perforations. Causes of regurgitation when the repair had failed included dehiscence of commissural repairs or the ring annuloplasty, or breakdown of chordal or leaflet repair. Operative mortality for the second procedure was 4%; most were replaced but 16% were re-repaired (29). Gillinov et al. reviewed 86 reoperations in 81 patients. They categorized failures as procedure related, valve related, or of unknown cause. Fifty of the failures (58%) were procedure related and included suture dehiscence, 21; rupture of previously shortened chordae, 19; or incomplete correction, 10. Valve-related failures (33, 38%) included progressive disease, 27; endocarditis, 5; or leaflet retraction, 1. In the remaining failures (3, 3%) no cause could be identified. Seventy percent of failures were procedure related with valves affected by degenerative disease; whereas most failures with rheumatic disease valves were related to progression of disease. Re-repair was performed in 21%. They concluded that chordal shortening should not be used (30).

WHEN TO GIVE UP

One lasting concern for surgeons is the effect of immediate failure, requiring subsequent replacement on operative modality. Northrup et al. investigated this, comparing morbidity and mortality among patients who underwent repair with those whose repair failed and required replacement during the same operation (31). No increase in morbidity or mortality was conferred by the failed attempt despite longer cross clamp, perfusion, and operative times.

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TABLE 12.1 RESULTS OF MITRAL VALVE REPAIR

Author

Date of Publication

Number of Patients (Hospital Survivors)

Freedom from Reoperation Years/%

Note

Fernandez (32)

1992

313

5y/90%, 8y/80%*

5y/80%, 10y/72%**

Pure MR or MS*

Mixed MS/MR**

Less durability with rheumatic etiology and greater with ischemic etiology

Thourani (33)

2003

625

5y/94%, 10y/78%

+ 10 years freedom from reoperation with replacement was 66%

Fucci (34)

1995

299

7y/86%

At 7 years freedom from reoperation for anterior triangular resection was 61%; anterior chordal shortening, 56%; ischemic etiology, 51%

Gillinov (35,36)

1998

1072

10y/93%

Degenerative disease only

Durability reduced with chordal shortening, annuloplasty alone, leaflet resection without annuloplasty

For posterior quadrangular resection with annuloplasty 98% (36)

The quality of the repair at the time of surgery is the best guide for indicator of long-term success or failure. The greater the amount of residual mitral regurgitation, the greater the risk of recurrence. The disease process also dictates failure rates, rheumatic higher for others. The complexity of the repair may contribute to long-term failures. Finally, the amount of experience the surgeon has with repair will impact long-term results. The threshold for abandoning the repair and replacing the valve is an individual decision and should be based on all of these contributing factors.

FOLLOW-UP

An echocardiogram to assess the repair is recommended prior to hospital discharge. Technical failures will occur early and are easiest to address in the early postoperative period. Anticoagulation is surgeon dependent with no agreed upon strategies. Some surgeons treat only with aspirin, others use warfarin for 2 to 3 months until the ring or band becomes incorporated. An alternative might be a selective strategy, treating simple annuloplasty with aspirin and using warfarin for more complex repairs. Hypertension control is important. Many of these patients are on afterload-reducing medications, which should be continued in the early postoperative period. Activities that increase blood pressure, such as weightlifting, should be restricted until healing is complete.

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REFERENCES

  1. Carpentier A. Cardiac valve surgery: the “French Correction.” J Thorac Cardiovasc Surg.1986;86:323.
  2. Marwick TH, Stewart WJ, Currie PJ, Cosgrove DM. Mechanisms of failure of mitral valve repair: an echocardiographic study. Am Heart J.1991;122:149-156.
  3. Fix J, Isada L, Cosgrove DM, et al. Do patients with less than “echo-perfect” results from mitral valve repair by intraoperative echocardiography have a different outcome?Circulation.1993;88:39.
  4. Marshall Jr. WG. Technique for visualization of the functioning mitral valve. Ann Thorac Surg.1990;49:1013.
  5. Sundt TM 3rd, Khaghani A, Yacoub MH. Alternative technique for assessment and repair of the mitral valve. Ann Thorac Surg.1996;61:1552-1554.
  6. Ferguson Jr. TB, Wechsler AS. Testing of mitral valve competence following combined mitral valve repair and aortic valve replacement. Ann Thorac Surg.1985;40:631-633.
  7. Kreindel MS, Schiavone WA, Lever HM, Cosgrove DM. Systolic anterior motion of the mitral valve after Carpentier ring valvuloplasty for mitral valve prolapse. Am J Cardiol.1986;57:408.
  8. Jebara VA, Mihaileanu S, Acar C, et al. Left ventricular outflow obstruction after mitral valve repair: results of the sliding leaflet technique. Circulation.1993;88 (Part 2):30.
  9. Perier P, Clausnizer B, Mistarz K. Carpentier “sliding leaflet” technique for repair of the mitral valve: early results. Ann Thorac Surg.1994;57:383.
  10. Sanders JH Jr, Scott ML. Pitfalls in surgical decision-making during mitral valve repair. Curr Opin Cardiol.2001;16:140-145.
  11. Maslow AD, Regan MM, Haering JM, Johnson RG, Levine RA. Echocardiographic predictors of left ventricular outflow tract obstruction and systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol. 1999:34:2096-2104.
  12. He S, Hopmeyer J, Lefebvre XP, et al. Importance of leaflet elongation in causing systolic anterior motion of the mitral valve. J Heart Valve Dis. 1997;6:149-159.
  13. Lee KS, Stewart WJ, Lever HM, Underwood PL, Cosgrove DM. Mechanism of outflow obstruction following failed valve repair: anterior displacement of leaflet coaptation.Circulation.1993;88 (Suppl II): II-24-9.
  14. Mihaileanu S, Marino JP, Chauvaud S, et al. Left ventricular outflow obstruction after mitral repair (Carpentier's technique): proposed mechanism of disease. Circulation.1988;78 (Suppl I):78-84.
  15. Grossi EA, Galloway AC, Parish MA, et al. Experience with twenty-eight cases of systolic motion after mitral valve construction by Carpentier technique. J Thorac Cardiovasc Surg.1992;103:466-470.
  16. Lopez JA, Schnee M, Gaos CM, Wilansky S. Left ventricular outflow tract obstruction and hemolytic anemia after mitral valve repair with a Duran ring. Ann Thorac Surg.1994;58:876-867.
  17. Kupferschmid JP, Carr T, Connelly GP, Shemin RJ. Systolic anterior motion of the mitral valve after valve repair without an annular ring. Ann Thorac Surg.1994;57:484-486.
  18. Raney AA, Shah PM, Joyo CI. The “Pomeroy procedure”: a new method to correct post-mitral valve repair systolic anterior motion. J Heart Valve Dis.2001;10:307-311.
  19. Rescigno G, Matteucci MLS, Iacovoni A, et al. Systolic anterior motion after mitral valve repair: myectomy as an alternative solution. J Thorac Cardiovasc Surg.2003;126:1196-1197.
  20. Civelek A, Szalay Z, Roth M, et al. Post-mitral valve repair systolic anterior motion produced by non-obstructive septal bulge. Eur J Cardiothorac Surg.2003;24:857-861.
  21. Wilson JH, Rath R, Glaser R, Panke T. Severe hemolysis after incomplete mitral valve repair. Ann Thorac Surg.1990;50:136-137.
  22. Garcia MJ, Vandervoort P, Stewart WJ, et al. Mechanisms of hemolysis with mitral prosthetic regurgitation. Study using transesophageal echocardiography and fluid dynamic simulation. J Am Coll Cardiol.1996;27:399-406.
  23. Yeo TC, Freeman WK, Schaff HV, Orszulak TA. Mechanisms of hemolysis after mitral valve repair: assessment by serial echocardiography. J Am Coll Cardiol.1998;32:717-723.
  24. Cerfolio RJ, Orszulak TA, Daly RC, Schaff HV. Reoperation for hemolytic anaemia complicating mitral valve repair. Eur J Cardiothorac Surg.1997;11:479-484.
  25. Inoue M, Kaku B, Kanaya H, et al. Reduction of hemolysis without reoperation following mitral valve repair. Circ J.2003;67:799-801.
  26. Ibrahim MF, David TE. Mitral stenosis after mitral valve repair for non-rheumatic mitral regurgitation. Ann Thorac Surg.2002;73:34-36.
  27. Dreyfus G, Serraf A, Jebara VA, et al. Valve repair in acute endocarditis. Ann Thorac Surg.1990;49:706-711.
  28. Hendren WG, Morris AS, Rosenkranz ER, et al. Mitral valve repair for bacterial endocarditis. J Thorac Cardiovasc Surg.1992;103:124-128.
  29. 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;111:1177-1183.
  30. Gillinov AM, Cosgrove DM, Lytle BW, et al. Reoperation for failure of mitral valve repair. J Thorac Cardiovasc Surg.1997;113:467-473.
  31. Northrup 3rd WF, DuBois KA, Kshettry VR. Morbidity and mortality of a failed attempt at mitral valve repair converted to replacement at the same operation. J Heart Valve Dis.2003;12:700-706.
  32. Fernandez J, Joyce DH, Hirschfeld K, et al. Factors affecting mitral valve reoperation in 317 survivors after mitral valve reconstruction. Ann Thorac Surg.1992;54:440-447.
  33. Thourani VH, Weintraub WS, Guyton RA, et al. Outcomes and long-term survival for patients undergoing mitral valve repair versus replacement: effect of age and concomitant coronary artery bypass grafting. Circulation.2003;108:298-304.
  34. Fucci C, Sandrelli L, Pardini A, et al. Improved results with mitral valve repair using new surgical techniques. Eur J Cardiothorac Surg.1995;9:621-626.
  35. Gillinov AM, Cosgrove DM, Blackstone EH, et al. Durability of mitral valve repair for degenerative disease. J Thorac Cardiovasc Surg.1998;116:734-743.
  36. Gillinov AM, Cosgrove DM. Mitral valve repair for degenerative disease. J Heart Valve Dis.2002;11 Suppl 1:S15-20.

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