The effects of mitral annuloplasty rings on mitral valve complex 3-D geometry during acute left ventricular ischemia.

OBJECTIVE: Annuloplasty rings are used to treat ischemic mitral regurgitation (IMR), but their exact effects on 3-D geometry of the overall mitral valve complex during acute left ventricular (LV) ischemia remain unknown. METHODS: Radiopaque markers were sutured to the mitral leaflet edges, annulus, papillary muscle tips, and ventricle in three groups of sheep. One group served as control (n = 5), and the others underwent Duran (n = 6) or Physio (n = 5) ring annuloplasty. One week later, 3-D marker coordinates at end-systole were obtained before and during balloon occlusion of the circumflex artery. RESULTS: In all control animals, acute LV ischemia was associated with: (i) septal-lateral separation of the leaflet edges, which was predicted by lateral displacement of the lateral annulus during septal-lateral mitral annular dilatation; (ii) apical restriction of the posterior leaflet edge, which was predicted by displacement of the lateral annulus away from the non-ischemic anterior papillary muscle; (iii) displacement of the posterior papillary muscle, which was not predictive of either septal-lateral leaflet separation or leaflet restriction; and (iv) mitral regurgitation. In the Duran group during ischemia, the posterior leaflet edge shifted posteriorly due to posterior movement of the lateral annulus, but no IMR occurred. In the Physio group during ischemia, neither the posterior leaflet edge nor the lateral annulus changed positions, and there was no IMR. In both the Duran and Physio groups, displacement of the posterior papillary muscle did not lead to IMR. CONCLUSIONS: Either annuloplasty ring prevented the perturbations of mitral leaflet and annular--but not papillary muscle tip--3-D geometry during acute LV ischemia. By fixing the septal-lateral annular dimension and preventing lateral displacement of the lateral annulus, annuloplasty rings prevented systolic septal-lateral leaflet separation and posterior leaflet restriction, and no acute IMR occurred. The flexible ring allowed posterior displacement of the posterior leaflet edge and the lateral annulus, which was not observed with a semi-rigid ring.     

Surgical repair for ischemic mitral regurgitation: a method of mitral valve plasty with evaluation of morphological changes of mitral valve]

We evaluated a method of mitral valve plasty (MVP) for ischemic mitral regurgitation (IMR) by examining the morphological changes of the mitral valve. From November 1992 to May 1998, 8 patients (M : F = 4/4, age 44-79 years, mean age 65.1 years) with IMR underwent surgical repair. Preoperative mitral regurgitation (MR) was grade III of Sellers classification in 7 patients and grade IV in 1 patient. The cause of MR was mitral valve annular dilatation in 4 patients, mitral valve prolapse due to papillary muscle elongation in 2 patients, and partial papillary muscle rupture (PMR) in 2 patients. Cardiac surgery consisted of CABG + MVP in 7 patients and MVP in 1 patient. Mitral valve repair was separated into three types. Repair for annular dilatation consisted of commissuroplasty in 3 patients (2 patients Kay method, 1 patient Reed method) and ring annuloplasty using a Carpentier-Edwards ring (C-E ring) in 1 patient. Repair for papillary muscle elongation consisted of papillary muscle shortening and ring annuloplasty using a C-E ring. Repair for partial PMR consisted of papillary muscle implantation and ring annuloplasty for anterior leaflet prolapse in 1 patient, and quadrangular resection, posterior leaflet plasty (McGoon method) and ring annuloplasty in 1 patient. There was no hospital death. Postoperative outcome was 6 patients with no MR and 2 patients with grade II MR, but they were well-controlled with medication. Based on the morphological changes of the mitral valve, it is considered that MVP for IMR is an effective and recommended procedure.     

Surgical correction of posterior leaflet tethering in ischemic mitral regurgitation

Ischemic mitral regurgitation is a common complication in ischemic heart disease. It is generally accepted that intervention for the mitral valve is required if there is moderate to severe regurgitation. Generally, this would involve the placement of an annuloplasty ring or band to cinch down the dilated posterior annulus. More recently, attention has been drawn to the common problem of posterior leaflet tethering in these ischemic patients and the need to specifically address this pathology. A novel method has recently been described whereby the posteromedial papillary muscle is hitched up toward the annulus by a suture and then supported with a partially flexible annuloplasty ring. The purpose of this report is to show that this technique is easily performed and reproducible in other centres, and that it produces good short to medium term results. The report details the results achieved in six consecutive patients with at least moderate mitral regurgitation and posterior leaflet tethering.     

Annuloplasty ring selection for chronic ischemic mitral regurgitation: lessons from the ovine model

BACKGROUND: Chronic ischemic mitral regurgitation (CIMR) is poorly understood and repair operations are often unsatisfactory. This study elucidates the mechanism of CIMR in an ovine model. METHODS: Sonomicrometry array localization measured the three-dimensional geometry of the mitral annulus and subvalvular apparatus in five sheep before and 8 weeks after a posterior infarction of the left ventricle that produced progressive severe CIMR. RESULTS: End systolic annular area increased from 647 +/- 44 mm(2) to 1,094 +/- 173 mm(2) (p = 0.01). Annular dilatation occurred equally along the anterior (47.0 +/- 5.6 mm to 60.2 +/- 4.9 mm, p = 0.001) and posterior (53.8 +/- 3.1 mm to 68.5 +/- 8.4 mm, p = 0.005) portions of the annulus. The tip of the anterior papillary muscle moved away from both the anterior and posterior commissures by 5.2 +/- 3.2 mm (p = 0.021) and 7.3 +/- 2.2 mm (p = 0.002), respectively. The distance from the tip of the posterior papillary muscle to the anterior commissure increased by 11.0 +/- 5.7 mm (p = 0.032) while the distance from the tip of the posterior papillary muscle to the posterior commissure remained constant. CONCLUSIONS: Progressive dilatation of both the anterior and posterior mitral annuli, increased annular area, and asymmetric ventricular dilatation combine to cause CIMR by distortion of mitral valve geometry and tethering of leaflet coaptation. Therefore complete ring annuloplasty may be superior to partial annuloplasty in the treatment of CIMR.     

Posterior mitral valve restoration for ischemic regurgitation

Chronic ischemic mitral regurgitation is traditionally a complex lesion to repair. Only restrictive annuloplasty has become an accepted strategy to avoid valve replacement, but results are unsatisfactory in some subgroups of patients. We describe an original technique that addresses the pathophysiologic mechanisms responsible for one of the most common subtypes of ischemic mitral regurgitation, ie, asymmetric tethering of the mitral leaflets after inferior myocardial infarction. The technique includes partial detachment of the posterior leaflet from the mitral annulus, annular plication, and posterior cusp plasty.     

Potential mechanism of left ventricular outflow tract obstruction after mitral ring annuloplasty

OBJECTIVES: The purpose of this study was to explore whether geometric changes that predispose to left ventricular outflow tract obstruction after mitral ring annuloplasty are coupled to subvalvular apparatus disturbances. METHODS: Radiopaque markers were implanted in sheep: 9 in the ventricle, 1 in the high interventricular septum, 1 on each papillary muscle tip, 8 around the mitral anulus, 4 on the anterior mitral leaflet, and 2 on the posterior leaflet. One group served as control (n = 5); the others were randomized to undergo annuloplasty with the Duran ring (n = 6; Medtronic, Inc, Minneapolis, Minn) or Carpentier-Edwards Physio ring (n = 6; Baxter Healthcare Corp, Irvine, Calif). After a 7- to 10-day recovery period, 3-dimensional marker coordinates were measured with biplane videofluoroscopy. RESULTS: At the beginning of ejection, (1) the anterior leaflet was displaced toward the left ventricular outflow tract; (2) the normal atrially flexed anterior anulus was flattened into the left ventricular outflow tract; (3) the posterior anulus was displaced toward the left ventricular outflow tract; (4) the anterior papillary muscle was displaced septally; and (5) the posterior papillary muscle was dislocated inwardly toward the anterior papillary muscle in the Physio ring group compared with the control group. During ejection, all these structures moved septally, encroaching further on the left ventricular outflow tract. In the Duran ring group, only the posterior anulus was displaced toward the left ventricular outflow tract; the anterior leaflet was not displaced toward the left ventricular outflow tract, and it did not move septally during ejection. CONCLUSIONS: The semirigid Physio ring was associated with perturbations in annular dynamics that caused changes in papillary muscle geometry. We propose an integrated valvular-subvalvular mechanism to explain displacement of the anterior leaflet into the left ventricular outflow tract after mitral ring annuloplasty.     

Annular or subvalvular approach to chronic ischemic mitral regurgitation?

OBJECTIVE: We sought to investigate whether annular or subvalvular interventions corrected chronic ischemic mitral regurgitation differently. METHODS: Sheep underwent placement of markers on the left ventricle, mitral annulus, papillary muscles (anterior and posterior), and both leaflet edges. A transannular suture (septal-lateral annular cinching) was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. Another suture (papillary muscle repositioning) from the posterior papillary muscle was passed through the mitral annulus near the posterior commissure and externalized. After 7 days, 3-dimensional marker data were obtained before inducing posterolateral myocardial infarction. After 7 weeks, animals in whom chronic ischemic mitral regurgitation developed (n = 10) were restudied before and after pulling septal-lateral annular cinching or papillary muscle repositioning sutures. End-systolic septal-lateral annular diameter and 3-dimensional displacement of the papillary muscles and leaflet edges were computed. RESULTS: Infarction increased mitral regurgitation (0.6 +/- 0.5 to 2.3 +/- 1.1); mitral annular septal-lateral dilation (4 +/- 1 mm); posterior papillary muscle displacement laterally (4 +/- 2 mm), posteriorly (9 +/- 3 mm), and toward the annulus (2 +/- 1 mm); posterior mitral leaflet apical tethering (3 +/- 1 mm); and interleaflet separation (+3 +/- 1 mm, P < .05 baseline vs chronic ischemic mitral regurgitation). Septal-lateral annular cinching reduced septal-lateral dimension (-9 +/- 3 mm), corrected lateral posterior papillary muscle displacement (4 +/- 1 mm) and septal-lateral interleaflet separation (-4 +/- 2 mm), and decreased mitral regurgitation (0.6 +/- 0.6, P < .05 septal-lateral annular cinching vs chronic ischemic mitral regurgitation) without affecting posterior leaflet restriction. Papillary muscle repositioning reduced septal-lateral diameter (-4 +/- 1 mm), moved the anterior papillary muscle closer to the annulus (2 +/- 1 mm), and relieved posterior leaflet apical restriction (2 +/- 1 mm, P < .05 papillary muscle repositioning vs chronic ischemic mitral regurgitation) but did not change lateral posterior papillary muscle displacement or decrease mitral regurgitation (1.9 +/- 1.2). CONCLUSIONS: Septal-lateral annular cinching moved the lateral annulus and the posterior papillary muscle closer to the septum and reduced mitral regurgitation unlike posterior papillary muscle repositioning, and thus the key mitral subvalvular repair component must correct posterior papillary muscle lateral displacement.     

Reconstruction of mitral valve chordae and leaflets with one piece of autologous pericardium in extensively destructed mitral valve due to active infective endocarditis

A 20-year-old female patient underwent urgent surgery for extensive mitral valve endocarditis. All marginal chordae and rough zone of A3 leaflet, posterior commissure leaflet, and P3 leaflet down to the annulus became defective after complete debridement of infected tissues. After annular plication, defective leaflets and chordae were reconstructed with a piece of triangular shaped autologous pericardium. Top of the pericardium was directly attached to the posterior papillary muscle, side edges to remnant leaflets, and the base to the annulus, thus substituting for chordae and leaflets at once. No mitral regurgitation was observed during 3 years of follow-up after the operation.     

Surgical relocation of the posterior papillary muscle in chronic ischemic mitral regurgitation

Mitral annuloplasty is the preferred surgical treatment for chronic ischemic mitral regurgitation. Although this is usually successful, leaflet restriction by apical displacement of the posterior papillary muscle tip may cause residual mitral regurgitation. Ventricular remodeling surgery is an effective procedure for surgical relocation of the posterior papillary muscle tip in the setting of a severely dilated left ventricle. Direct relocation of the posterior papillary muscle may be useful for patients with a minimally dilated left ventricle or regional left ventricular geometric changes causing mitral regurgitation. Such a surgical procedure is described.     

The effects of ring annuloplasty on mitral leaflet geometry during acute left ventricular ischemia

BACKGROUND: The perturbed mitral leaflet geometry that leads to acute ischemic mitral regurgitation during acute left ventricular ischemia has not been quantified, nor is it known whether annuloplasty rings affect these detrimental changes in leaflet geometry. METHODS: Radiopaque markers were implanted on both mitral leaflets and around the anulus in 3 groups of sheep: one group without rings served as the control group (n = 7); the others underwent Duran (n = 6; Medtronic Heart Valve Division, Minneapolis, Minn) or Carpentier-Edwards Physio (n = 5; Baxter Cardiovascular Division, Santa Ana, Calif) ring annuloplasty. After recovery, 3-dimensional marker coordinates were obtained by means of biplane videofluoroscopy before and during acute posterolateral left ventricular ischemia. Leaflet geometry was defined by measuring distances between annular and leaflet markers and perpendicular distances to the leaflet markers from a best-fit annular plane. RESULTS: In all control animals, left ventricular ischemia was associated with acute ischemic mitral regurgitation and apical displacement (away from the annular plane) of the posterior leaflet edge and base markers by 0.6 +/- 0.4 mm (P =.01) and 0.7 +/- 0.2 mm (P <.001), respectively. The distance between the posterior leaflet markers and the mid-posterior anulus did not change significantly during ischemia. The anterior leaflet edge marker extended 1.0 +/- 0. 5 mm (P =.01) away from the mid-anterior anulus during ischemia, but compared with its nonischemic position, the anterior leaflet was not displaced apically away from the annular plane. In all animals in the Duran and Physio groups, leaflet geometry was unchanged during ischemia, and acute ischemic mitral regurgitation was not detected. CONCLUSION: Acute ischemic mitral regurgitation was associated with restricted motion of the posterior leaflet and extension of the anterior leaflet. Annuloplasty rings prevented these geometric perturbations of the mitral leaflets during acute left ventricular ischemia and preserved valvular competence.     

Mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior myocardial infarction: quantitative analysis of left ventricular and mitral valve geometry in 103 patients with prior myocardial infarction

OBJECTIVE: The mechanism of higher incidence of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction despite less global left ventricular remodeling and dysfunction is controversial. We hypothesized that inferior myocardial infarction causes left ventricular remodeling, which displaces posterior papillary muscle away from its normal position, leading to ischemic mitral regurgitation. METHODS: In 103 patients with prior myocardial infarction (61 anterior and 42 inferior) and 20 normal control subjects, we evaluated the grade of ischemic mitral regurgitation on the basis of the percentage of Doppler jet area, left ventricular end-diastolic and end-systolic volumes, midsystolic mitral annular area, and midsystolic leaflet-tethering distance between papillary muscle tips and the contralateral anterior mitral annulus, which were determined by means of quantitative echocardiography. RESULTS: Global left ventricular dilatation and dysfunction were significantly less pronounced in patients with inferior myocardial infarction (left ventricular end-systolic volume: 52 +/- 18 vs 60 +/- 24 mL, inferior vs anterior infarction, P<.05; left ventricular ejection fraction: 51% +/- 9% vs 42% +/- 7%, P <.0001). However, the percentage of mitral regurgitation jet area and the incidence of significant regurgitation (percentage of jet area of 10% or greater) was greater in inferior infarction (percentage of jet area: 10.1% +/- 7.5% vs 4.4% +/- 7.0%, P =.0002; incidence: 16/42 (38%) vs 6/61 (10%), P <.0001). The mitral annulus (area = 8.2 +/- 1.2 cm2 in control subjects) was similarly dilated in both inferior and anterior myocardial infarction (9.7 +/- 1.7 vs. 9.5 +/- 2.3 cm2, no significant difference), and the anterior papillary muscle-tethering distance (33.8 +/- 2.6 mm in control subjects) was also similarly and mildly increased in both groups (35.2 +/- 2.4 vs 35.2 +/- 2.8 mm, no significant difference). However, the posterior papillary muscle-tethering distance (33.3 +/- 2.3 mm in control subjects) was significantly greater in inferior compared with anterior myocardial infarction (38.3 +/- 4.1 vs 34.7 +/- 2.9 mm, P =.0001). Multiple stepwise regression analysis identified the increase in posterior papillary muscle-tethering distance divided by body surface area as an independent contributing factor to the percentage of mitral regurgitation jet area (r2 = 0.70, P <.0001). CONCLUSIONS: It is suggested that the higher incidence and greater severity of ischemic mitral regurgitation in patients with inferior compared with anterior myocardial infarction can be related to more severe geometric changes in the mitral valve apparatus with greater displacement of posterior papillary muscle caused by localized inferior basal left ventricular remodeling, which results in therapeutic implications for potential benefit of procedures, such as infarct plication and leaflet or chordal elongation, to reduce leaflet tethering.     

Valve reconstruction in the Heart Institute of São Paulo,Brazil

In the Heart Institute of University of S?o Paulo Medical School, between 1980 and 2000, were performed 712 mitral valve repair procedures, 39 aortic valve repairs and 469 tricuspid valve repairs. In our experience with mitral valve repair, the most performed techniques were quadrangular resection of the posterior leaflet, posterior annuloplasty with bovine pericardial sling and Carpentier ring annuloplasty. Quadrangular resection of the posterior leaflet is the technique of choice in mitral regurgitation due to degenerative disease, and repair is possible in 90% of the cases. Since 1994, we perform the quadrangular resection without ring annuloplasty, a modification in the technique called "Double Teflon" technique, with good results. Aortic valve repair is performed in specific situations. In congenital aortic insufficiency, we perform the suspention of the prolapsed leaflets in the comissures. In rheumatic aortic insufficiency, when we found leaflet retraction, we elongate the leaflets with bovine pericardial patchs. Our experience of aortic valve repair, between 1980 and 2000, consists of a small group of 39 patients. The results are satisfactory, but these techniques are feasible only in selected cases. Tricuspid insufficiency is generally a consequence of annular enlargement in patients with mitral valve disease and we prefer the De Vega annuloplasty in these cases. In cases with large annulus dilatation, we prefer to use the "Revuelta" or the "bicuspidization" techniques. In patients with previous tricuspid repair and annulus distortion, we prefer to use bovine pericardial sling or Carpentier ring annuloplasty.     

Mitral Valve Re‐Repair in an Adolescent Patient with Prosthetic Ring Endocarditis: Posterior Leaflet Augmentation and Posterior Strip Annuloplasty

Abstract Endocarditis after mitral valve (MV) annuloplasty is uncommon. The ring used in MV annuloplasty is often inadequate because it opposes the growth of the MV leaflets and annulus. We report a 15‐year‐old male that required redo surgery for prosthetic ring endocarditis 40 months after a previous MV annuloplasty. After the previous ring was removed, the undergrown posterior leaflet was repaired with pericardial augmentation and the posterior annulus was stabilized with a Mitra‐Lift® supra‐annular strip to preserve a flexible valve orifice and allow the anterior MV annulus and the commissures to grow in relation to body size. (J Card Surg 2012;27:560‐562)     

Redefinition of tricuspid valve structures for successful ring annuloplasty

Background

Although numerous reports have described suturing techniques for tricuspid annuloplasty, most studies were not based on a detailed anatomy of the tricuspid annulus. Thus, the definition of the tricuspid commissures remains unclear. This study aimed to clearly define the commissures and leaflets of the tricuspid valve and subvalvular structures, and to define a standard method for tricuspid annuloplasty.

Ischemia in three left ventricular regions: Insights into the pathogenesis of acute ischemic mitral regurgitation

BACKGROUND: Acute posterolateral left ventricular ischemia in sheep results in ischemic mitral regurgitation, but the effects of ischemia in other left ventricular regions on ischemic mitral regurgitation is unknown. METHODS: Six adult sheep had radiopaque markers placed on the left ventricle, mitral annulus, and anterior and posterior mitral leaflets at the valve center and near the anterior and posterior commissures. After 6 to 8 days, animals were studied with biplane videofluoroscopy and transesophageal echocardiography before and during sequential balloon occlusion of the left anterior descending, distal left circumflex, and proximal left circumflex coronary arteries. Time of valve closure was defined as the time when the distance between leaflet edge markers reached its minimum plateau, and systolic leaflet edge separation distance was calculated on the basis of left ventricular ejection. RESULTS: Only proximal left circumflex coronary artery occlusion resulted in ischemic mitral regurgitation, which was central and holosystolic. Delayed valve closure (anterior commissure, 58 +/- 29 vs 92 +/- 24 ms; valve center, 52 +/- 26 vs 92 +/- 23 ms; posterior commissure, 60 +/- 30 vs 94 +/- 14 ms; all P <.05) and increased leaflet edge separation distance during ejection (mean increase, 2.2 +/- 1.5 mm, 2.1 +/- 1.9 mm, and 2.1 +/- 1.5 mm at the anterior commissure, valve center, and posterior commissure, respectively; P <.05 for all) was seen during proximal left circumflex coronary artery occlusion but not during left anterior descending or distal left circumflex coronary artery occlusion. Ischemic mitral regurgitation was associated with a 19% +/- 10% increase in mitral annular area, and displacement of both papillary muscle tips away from the septal annulus at end systole. CONCLUSIONS: Acute ischemic mitral regurgitation in sheep occurred only after proximal left circumflex coronary artery occlusion along with delayed valve closure in early systole and increased leaflet edge separation throughout ejection in all 3 leaflet coaptation sites. The degree of left ventricular systolic dysfunction induced did not correlate with ischemic mitral regurgitation, but both altered valvular and subvalvular 3-dimensional geometry were necessary to produce ischemic mitral regurgitation during acute left ventricular ischemia.     

Restoring papillary muscle dimensions during restoration in dilated hearts

Left ventricular papillary muscle geometry is distorted in dilated non-ischemic hearts, and following anterior infarction caused by a wrap around left anterior descending artery occlusion. Loss of the apex creates a spherical left ventricular (LV) chamber, and subsequent dilation causes secondary mitral insufficiency by stretching the annulus, altering tethering of the chords and widening the dimension between the bases of papillary muscles to impair leaflet coaptation. This report will describe an intraventricular way to narrow the widened inter papillary muscle distance toward normal.     

Artificial chordae

Expanded polytetrafluoroethylene sutures have been used for replacement of chordae tendineae since 1985. They have been used for correction of prolapse of mitral and tricuspid valve leaflets as well as for resuspension of the papillary muscles during mitral valve replacement when the native chordae cannot be preserved to maintain continuity between the mitral annulus and papillary muscles. The sutures used were 5CV Gore-Tex for replacement of the chordae tendineae of the anterior leaflet and 6CV for the posterior leaflet and commissural areas of the mitral valve. Initially one suture was used to create two artificial chordae, but as experience increased, the technique was modified and multiple pairs of artificial chordae were created with a single suture by passing successively through the fibrous portions of the a papillary muscle and the free margin of the prolapsing segment of leaflet, and tying the tends together on the papillary muscle head. This technique creates artificial chordae that are interdependent and their lengths are self-adjusting when pressure is exerted on the leaflets. From 1985 to 1998, 288 patients had artificial chordae used during mitral valve repair for degenerative disease of the mitral valve. Prolapse of both leaflets was present in 51% of patients, isolated prolapse of the anterior leaflet in 28%, and posterior leaflet in 21%. The mean follow-up was 4.8 +/- 3.0 years and was complete. At 10 years, the freedom from mitral regurgitation >2+ was 88 +/- 6% and the freedom from reoperation was 92 +/- 2%. Failures of repair were unrelated to the artificial chordae. Gore-Tex sutures are an excellent material to replace chordae tendineae, appear to be free of adverse effects, and have become a valuable adjunct to the surgical armamentarium to treat mitral and tricuspid valve disease.     

Partial hammock valve: surgical repair in adulthood

We describe a forme frustrée of hammock valve involving only the posterior mitral leaflet. Three adult patients were referred to surgery with the diagnosis of severe mitral regurgitation due to fibrosis of the posterior mitral leaflet. The final diagnosis was done intraoperatively. In all of them the posterior leaflet was attached to some accessory papillary muscles arranged en palisade, with three to four fused muscle heads producing restrictive leaflet motion in systole. Repair consisted in division of the papillary muscles, patch augmentation, and ring annuloplasty. This previously unreported lesion is congenital but manifests itself in adulthood.     

Mitral valve replacement for extensive calcification: half and half technique

A 50-year-old woman who had been undergoing hemodialysis for 18 years underwent mitral valve replacement because of mitral valve stenosis. Her mitral valve leaflet and annulus were highly calcified, and it was impossible to remove the posterior leaflet from the ventricular wall. At the time of surgery, noneverted horizontal mattress sutures were placed from the left ventricle to the left atrium on the anterior half of the mitral annulus and everted horizontal mattress sutures on the left atrial wall close to the calcified posterior annulus. A 25-mm St. Jude valve was seated successfully at a supra-annular position. The St. Jude valve is suitable for this technique because its leaflets protrude less into the left ventricle.     

Does septal-lateral annular cinching work for chronic ischemic mitral regurgitation?

OBJECTIVES: Ring annuloplasty, the current treatment of choice for chronic ischemic mitral regurgitation, abolishes dynamic annular motion and immobilizes the posterior leaflet. In a model of chronic ischemic mitral regurgitation, we tested septal-lateral annular cinching aimed at maintaining normal annular and leaflet dynamics. METHODS: Twenty-five sheep had radiopaque markers placed on the mitral annulus and anterior and posterior mitral leaflets. A transannular suture was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. After 7 days, biplane cinefluoroscopy provided 3-dimensional marker data (baseline) prior to creating inferior myocardial infarction by snare occlusion of obtuse marginal branches. After 7 weeks, the 9 animals that developed chronic ischemic mitral regurgitation were restudied before and after septal-lateral annular cinching. Anterior and posterior mitral leaflet angular excursion and annular septal-lateral and commissure-commissure dimensions and percent shortening were computed. RESULTS: Septal-lateral annular cinching reduced septal-lateral dimension (baseline: 3.0 +/- 0.2; chronic ischemic mitral regurgitation: 3.5 +/- 0.4 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 2.4 +/- 0.3 cm; maximum dimension) and eliminated chronic ischemic mitral regurgitation (baseline: 0.6 +/- 0.5; chronic ischemic mitral regurgitation: 2.3 +/- 1.0 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 0.6 +/- 0.6; mitral regurgitation grade [0 to 4+]) but did not alter dynamic annular shortening (baseline: 7 +/- 3; chronic ischemic mitral regurgitation: 10 +/- 5; septal-lateral annular cinching: 6 +/- 2, percent septal-lateral shortening) or posterior mitral leaflet excursion (baseline: 46 degrees +/- 8 degrees; chronic ischemic mitral regurgitation: 41 degrees +/- 13 degrees; septal-lateral annular cinching: 46 degrees +/- 8 degrees ). CONCLUSIONS: In this model, septal-lateral annular cinching decreased chronic ischemic mitral regurgitation, reduced annular septal-lateral diameter (but not commissure-commissure diameter), and maintained normal annular and leaflet dynamics. These findings provide additional insight into the treatment of chronic ischemic mitral regurgitation.