Septal-lateral annnular cinching perturbs basal left ventricular transmural strains.

OBJECTIVE: Septal-lateral annular cinching ('SLAC') corrects both acute and chronic ischemic mitral regurgitation in animal experiments, which has led to the development of therapeutic surgical and interventional strategies incorporating this concept (e.g., Edwards GeoForm ring, Myocor Coapsys, Ample Medical PS3). Changes in left ventricular (LV) transmural cardiac and fiber-sheet strains after SLAC, however, remain unknown. METHODS: Eight normal sheep hearts had two triads of transmural radiopaque bead columns inserted adjacent to (anterobasal) and remote from (midlateral equatorial) the mitral annulus. Under acute, open chest conditions, 4D bead coordinates were obtained using videofluoroscopy before and after SLAC. Transmural systolic strains were calculated from bead displacements relative to local circumferential, longitudinal, and radial cardiac axes. Transmural cardiac strains were transformed into fiber-sheet coordinates (X(f), X(s), X(n)) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (alpha) and sheet (beta) angle measurements. Results: SLAC markedly reduced (approximately 60%) septal-lateral annular diameter at both end-diastole (ED) (2.5+/-0.3 to 1.0+/-0.3 cm, p=0.001) and end-systole (ES) (2.4+/-0.4 to 1.0+/-0.3 cm, p=0.001). In the LV wall remote from the mitral annulus, transmural systolic strains did not change. In the anterobasal region adjacent to the mitral annulus, ED wall thickness increased (p=0.01) and systolic wall thickening was less in the epicardial (0.28+/-0.12 vs 0.20+/-0.06, p=0.05) and midwall (0.36+/-0.24 vs 0.19+/-0.11, p=0.04) LV layers. This impaired wall thickening was due to decreased systolic sheet thickening (0.20+/-0.8 to 0.12+/-0.07, p=0.01) and sheet shear (-0.15+/-0.07 to -0.11+/-0.04, p=0.02) in the epicardium and sheet extension (0.21+/-0.11 to 0.10+/-0.04, p=0.03) in the midwall. Transmural systolic and remodeling strains in the lateral midwall (remote from the annulus) were unaffected. CONCLUSIONS: Although SLAC is an alluring concept to correct ischemic mitral regurgitation, these data suggest that extreme SLAC adversely effects systolic wall thickening adjacent to the mitral annulus by inhibiting systolic sheet thickening, sheet shear, and sheet extension. Such alterations in LV strains could result in unanticipated deleterious remodeling and warrant further investigation.     

Recurrent mitral regurgitation after annuloplasty for functional ischemic mitral regurgitation

OBJECTIVES: We sought to characterize the temporal return of mitral regurgitation after annuloplasty for functional ischemic mitral regurgitation; to identify its predictors, particularly with respect to annuloplasty type; and to determine whether annuloplasty type influences survival. METHODS: From April 1985 through November 2002, 585 patients underwent annuloplasty alone for repair of functional ischemic mitral regurgitation, generally with concomitant coronary revascularization (95%). A flexible band (Cosgrove) was used in 68%, a rigid ring (Carpentier) in 21%, and bovine pericardial annuloplasty (Peri-Guard) in 11%. Six hundred seventy-eight postoperative echocardiograms were available in 422 patients to assess the time course of postoperative mitral regurgitation and its correlates. Most echocardiograms were performed early after the operation (median, 8 days); 17% were performed at 1 year or beyond. RESULTS: During the first 6 months after repair, the proportion of patients with 0 or 1+ mitral regurgitation decreased from 71% to 41%, whereas the proportion with 3+ or 4+ regurgitation increased from 13% to 28% ( P < .0001); the regurgitation grade was stable thereafter. The temporal pattern of development of 3+ or 4+ regurgitation was similar for Cosgrove bands and Carpentier rings (25%) but substantially worse for Peri-Guard annuloplasties (66%). Small annuloplasty size did not influence postoperative regurgitation grade ( P = .2), although Cosgrove bands were used in most patients receiving 26- and 28-mm annuloplasties. Freedom from reoperation was 97% at 5 years. Annuloplasty type was not associated with survival. CONCLUSIONS: Although initial mitral valve replacement would eliminate the risk of postoperative mitral regurgitation, this strategy has been associated with reduced survival. Therefore the development of additional techniques is necessary to achieve more secure repair of functional ischemic mitral regurgitation.     

Effects of acute ischemic mitral regurgitation on three-dimensional mitral leaflet edge geometry.

BACKGROUND: Improved quantitative understanding of in vivo leaflet geometry in ischemic mitral regurgitation (IMR) is needed to improve reparative techniques, yet few data are available due to current imaging limitations. Using marker technology we tested the hypotheses that IMR (1) occurs chiefly during early systole; (2) affects primarily the valve region contiguous with the myocardial ischemic insult; and (3) results in systolic leaflet edge restriction. METHODS: Eleven sheep had radiopaque markers sutured as five opposing pairs along the anterior (A(1)-E(1)) and posterior (A(2)-E(2)) mitral leaflet free edges from the anterior commissure (A(1)-A(2)) to the posterior commissure (E(1)-E(2)). Immediately postoperatively, biplane videofluoroscopy was used to obtain 4D marker coordinates before and during acute proximal left circumflex artery occlusion. Regional mitral orifice area (MOA) was calculated in the anterior (Ant-MOA), middle (Mid-MOA), and posterior (Post-MOA) mitral orifice segments during early systole (EarlyS), mid systole (MidS), and end systole (EndS). MOA was normalized to zero (minimum orifice opening) at baseline EndS. Tenting height was the distance of the midpoint of paired markers to the mitral annular plane at EndS. RESULTS: Acute ischemia increased echocardiographic MR grade (0.5+/-0.3 vs 2.3+/-0.7, p<0.01) and MOA in all regions at EarlyS, MidS, and EndS: Ant-MOA (7+/-10 vs 22+/-19 mm(2), 1+/-2 vs 18+/-16 mm(2), 0 vs 17+/-15 mm(2)); Mid-MOA (9+/-13 vs 25+/-17 mm(2), 3+/-6 vs 21+/-19 mm(2), 0 vs 25+/-17 mm(2)); and Post-MOA (8+/-10 vs 25+/-16, 2+/-4 vs 22+/-13 mm(2), 0 vs 23+/-13 mm(2)), all p<0.05. There was no change in MOA throughout systole (EarlyS vs MidS vs EndS) during baseline conditions or ischemia. Tenting height increased with ischemia near the central and the anterior commissure leaflet edges (B(1)-B(2): 7.1+/-1.8mm vs 7.9+/-1.7 mm, C(1)-C(2): 6.9+/-1.3mm vs 8.0+/-1.5mm, both p<0.05). CONCLUSIONS: MOA during ischemia was larger throughout systole, indicating that acute IMR in this setting is a holosystolic phenomenon. Despite discrete postero-lateral myocardial ischemia, Post-MOA was not disproportionately larger. Acute ovine IMR was associated with leaflet restriction near the central and the anterior commissure leaflet edges. This entire constellation of annular, valvular, and subvalvular ischemic alterations should be considered in the approach to mitral repair for IMR.     

缺血性二尖瓣关闭不全的外科治疗

目的　探讨缺血性二尖瓣关闭不全的外科治疗方法 ,分析影响手术疗效的因素。方法　1998年 4月至 2 0 0 3年 11月 ,外科治疗 4 4例冠心病缺血性二尖瓣关闭不全 ,其中轻～中度 7例 ,中度 2 4例 ,重度 13例。行二尖瓣成形术 30例 ,其中交界区瓣环成形术 12例 ,用人工瓣环行瓣环成形术 17例 ,1例行双孔二尖瓣成形 ;4例同时行后瓣叶楔形切除 ,1例作腱索转移。瓣膜置换术 14例 ,置入双叶机械瓣 12例 ,生物瓣 2例。结果　全组手术死亡 7例 ,其中低心排出量综合征或心衰死亡 4例 ,心律失常 2例 ,脑栓塞 1例。 33例术后平均随访 2 0个月 ,远期死亡 2例 ,生存者远期心功能I～II级 2 9例 ,III级 2例。术后超声复查左心室内径较术前明显缩小 [(6 2 3± 6 3)mm对 (5 4 3± 7 1)mm]。行瓣膜成形术者远期复查超声显示无反流或轻微反流 12例 ,轻度反流 5例 ,中度反流 2例。瓣膜置换术者 12例出现瓣周漏 ,其余病例瓣膜功能良好。统计分析显示 ,左心室功能、临床心功能级别与手术风险相关。结论　冠心病合并二尖瓣关闭不全应积极处理 ,手术矫治方式应根据瓣膜病理改变及心功能决定 ,尽量施行瓣膜成形术。     

冠心病合并缺血性二尖瓣关闭不全的处理方法

目的　探讨冠心病合并缺血性二尖瓣关闭不全 (IMR)病例 ,在行冠状动脉旁路移植术(CABG)时是否要对二尖瓣进行处理及最合适的处理方法。方法　回顾分析 2 0 0 0年 1月至 2 0 0 3年 1 0月期间连续行CABG者中 37例合并IMR者在不同手术处理前后的变化。结果　术前合并有轻 -重度IMR者中 2 4例仅行CABG ,无手术死亡 ,术后 1周左室舒张直径由 5 2 95mm降至 4 8 1 8mm(P =0 0 0 1 ) ,左室射血分数从 0 46上升到 0 5 5 (P <0 0 0 1 ) ,二尖瓣反流面积 (MR)由 3 93cm2 下降至 1 48cm2 (P <0 0 0 1 ) ;1 3例同期行CABG和二尖瓣成形或置换 ,手术死亡 1例。结论　缺血性心脏病合并无二尖瓣明显病理结构改变的IMR ,单纯行再血管化后左心室收缩功能改善、IMR短期内明显减轻或消失。中度以上IMR并有二尖瓣发生病理结构改变时 ,需同期对二尖瓣进行干预 ,但是手术死亡率较高。     

Surgical treatment of ischemic mitral regurgitation

Ischemic mitral regurgitation (IMR) is a serious problem, which conveys adverse prognosis, doubling mortality after myocardial infarction. It is common and increases mortality even when mild. IMR is often associated with the occlusion of left circumflex coronary artery, such as second or third obtuse marginal branches by experimental model. However, cause of IMR still remains unclear in many respects. Several study using echocardiography and magnetic resonance imaging show some probable reasons left ventricular structure and deformity of left ventricle may cause mitral leaflet restriction and mitral annulus deformity, lead to tethering. The aim of surgical treatment of IMR is to reduce the grade of mitral regurgitation and left ventricular remodeling. Recent study clarified the advantage of valve repair in IMR opposed to valve replacement that may affect the patient poor quality of life. Some new technique of saddle shaped ring repair, second chordal cutting, edge-to-edge repair are available but these long-term outcome remain unclear. It may be effective combined left ventricular revascularization and mitral valve repair. Understanding mechanism of IMR will improve therapies for targeted primary causes with new therapeutic options provided a more flexible approach for surgical repair of IMR.     

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.     

Surgical repair of ischemic mitral regurgitation]

We studied surgical results of 14 cases of ischemic mitral regurgitation. There was no surgical death in 10 cases with left ventricular aneurysm, and their clinical symptoms improved except 3 with the combined operation of left ventricular aneurysmectomy, mitral annuloplasty and bypass grafting. The range of the abnormal contracting segment significantly decreased after surgery except in 3 cases in whom clinical status was not improved. Three of 4 cases which underwent bypass grafting and mitral annulo-valvuloplasty survived, but one of them died of graft-versus-host disease. In the three survived cases, severe mitral regurgitation disappeared. We have concluded as follows: In cases of left ventricular aneurysm, a sufficient aneurysmal resection is very important to control the mitral regurgitation, and the additional procedures of mitral annuloplasty and bypass grafting are essential. The mitral valve replacement is recommended in case of the complete disruption of the papillary muscle. Mitral valvuloplasty combined with annuloplasty is suitable to control the regurgitation in the regional mitral prolapse due to the torn chordae.     

Anterior leaflet augmentation for ischemic mitral regurgitation

Background

Mitral valve repair improves survival and quality of life in patients with ischemic mitral regurgitation (MR). Although many repair methods exist for this condition, the ideal approach remains unknown. The purpose of this study is to describe a simple technique for repair of ischemic MR that addresses the pathophysiology of tethered leaflets and to report its early results.

Methods

The technique consists of pericardial patch enlargement of the anterior mitral leaflet and placement of a flexible annuloplasty band. Candidates for the repair had ischemic cardiomyopathy and echocardiographic evidence of moderate or severe Carpentier type IIIb MR. Patients were followed with serial echocardiography.

Results

Between January 2002 and November 2003, 25 adult patients underwent anterior leaflet augmentation for ischemic MR. Mean age was 64.8 ± 10.6 years, and mean left ventricular ejection fraction was 0.36 ± 0.14. Preoperative MR by transesophageal echocardiography was severe in 84% of patients and moderate in 16%. Annuloplasty band sizes were 27 mm to 31 mm (mean, 28.4 ± 1.1 mm). Concomitant coronary artery bypass grafting was performed in all patients. Transesophageal echocardiography immediately after repair revealed MR to be none or trace in 80% of patients and mild in 20%. No intraoperative conversion to valve replacement was performed. In follow-up, 2 patients have experienced moderate MR and are being treated medically, and no patients have mitral stenosis. At 2 years, actuarial freedom from moderate or greater MR is 81%.

Conclusions

For patients with ischemic MR, anterior leaflet augmentation is a simple and reproducible method of valve repair that addresses the pathophysiology of tethered leaflets. Early results in a small number of patients have been encouraging.     

Another multidisciplinary look at ischemic mitral regurgitation

Ischemic mitral regurgitation (IMR) continues to challenge surgeons and scientists alike. This vexing clinical entity frequently complicates myocardial infarction and carries a poor prognosis both in the setting of coronary disease and idiopathic dilated cardiomyopathy. Ischemic mitral regurgitation encompasses a difficult patient population that is characterized by high operative mortality, poor long term outcomes, and frequent recurrent insufficiency after standard surgical repair. Yet optimal surgical repair and improved clinical outcomes can only be achieved with better knowledge of the pathophysiology of IMR which is still incompletely understood. The causative mechanism of IMR appears to lie in the annular and subvalvular frame of the valve rather than leaflet or chordal structure leading to such labels as "ischemic," "functional," "non-organic," and "cardiomyopathy associated" being applied in the clinical literature. Although ischemic mitral regurgitation is a prevailing clinical entity, it has not been consistently defined in the literature, contributing to considerable confusion and contradictory results of clinical studies. As the mechanisms of pathophysiology have been better elucidated, novel surgical and interventional strategies have been developed recently to provide better treatment for this difficult patient population. In this review, we undertake a multidisciplinary update of the pathophysiology, classification, and surgical and interventional treatment of ischemic mitral regurgitation in today's clinical practice.