应用Carpentier-Edwards生理环治疗退行性二尖瓣反流的二尖瓣成形术后的二尖瓣狭窄

Repair durability for degenerative mitral regurgitation is excellent. Although the main reason for reoperation is residual or recurrent regurgitation, Postoperative mitral stenosis is extremely rare.     

Mechanism of Mitral Regurgitation in Dilated Cardiomyopathy

Dilated cardiomyopathy is a condition characterized by chamber dilatation and impaired systolic function, resulting in the clinical manifestations of congestive heart failure. Mitral regurgitation occurs with varying frequency in dilated cardiomyopathy, and its detection depends on the diagnostic modality utilized. The presence of mitral regurgitation imposes an additional burden on the failing ventricle, and appears to be an independent prognostic indicator of mortality. The mechanism of mitral regurgitation in dilated cardiomyopathy is complex, controversial, and incompletely understood. The mitral apparatus consists of the left atrial wall, mitral annulus, mitral leaflets, chordae tendineae, papillary muscles, and left ventricular wall, and each of these components and the intimate interrelationship between these structures may contribute to the development of mitral regurgitation. Left atrial enlargement, reduced left atrial contractility, mitral leaflet retraction, abnormal vector of chordal tendineae pull, papillary muscle dysfunction (either asynergic contraction or malalignment), mitral annular dilatation, and changes in the size, shape, and function of the left ventricle have been suggested as possible mechanisms for the development of mitral regurgitation in dilated cardiomyopathy. The primary event in the development of mitral regurgitation appears to be left ventricular dilatation and dysfunction. Controversy persists as to whether the associated mechanism is annular dilatation, papillary muscle or free left ventricular wall dysfunction, or a combination of all, but recent echo-Doppler studies reviewed in this article support the notion that annular dilatation is the predominant mechanism. Improved understanding of the mechanism of mitral regurgitation in dilated cardiomyopathy may lead to a more aggressive approach with regard to pharmacological therapy, thus impacting on survival in this group of patients. (ECHOCARDIOGRAPHY, Volume 8, March 1991)     

Exacerbation of mitral regurgitation after tricuspid valve replacement for isolated tricuspid regurgitation

A 74-year-old woman, with a history of aortic valve replacement and open mitral commissurotomy due to rheumatic aortic and mitral stenosis, presented with dyspnea. She developed severe tricuspid regurgitation (TR), requiring tricuspid valve replacement (TVR). Despite an uneventful postoperative course, she was readmitted for dyspnea 2 months later. Trans-thoracic echocardiogram revealed severe mitral regurgitation (MR), despite mild MR at the time of TVR, which has not been previously reported. The main MR mechanism was increased left ventricular preload due to improved TR. Increased diuresis has controlled her congestive heart failure, but her MR remained moderate.     

Mitral valve hemodynamic effects of percutaneous edge-to-edge repair with the MitraClip device for mitral regurgitation.

INTRODUCTION: The Endovascular Valve Edge-to-Edge REpair STudies (EVEREST) are investigating a percutaneous technique for edge-to-edge mitral valve repair with a repositionable clip. The effects on the mitral valve gradient (MVG) and mitral valve area (MVA) are not known. METHODS: Twenty seven patients with moderate to severe or severe mitral regurgitation (MR) were enrolled. Echocardiography was performed preprocedure, at discharge, and at 1, 6, and 12 months. Mean MVG was measured by Doppler and MVA by planimetry and pressure half-time, and evaluated in a central core laboratory. Pre- and postclip deployment, simultaneous left atrial/pulmonary capillary wedge and left ventricular pressures were obtained in eight patients. RESULTS: Three patients did not receive a clip, six patients had their clip(s) explanted by 6 months (none for mitral stenosis), and four were repaired with two clips. Results are notable for a slight increase in mean MVG by Doppler postclip deployment (1.79 +/- 0.89 to 3.31 +/- 2.09 mm Hg, P < 0.01) and an expected decrease in MVA by planimetry (6.49 +/- 1.61 to 4.46 +/- 2.14 cm(2), P < 0.001) and by pressure half time (4.35 +/- 0.98 to 3.01 +/- 1.42 cm(2), P < 0.05). There were no significant changes in hemodynamic parameters postclip deployment by direct pressure measurements. There was no change in MVA by planimetry from discharge to 12 months (3.90 +/- 1.90 to 3.79 +/- 1.54 cm(2), P = 0.78). CONCLUSIONS: Echocardiographic and hemodynamic measurements after percutaneous mitral valve repair with the MitraClip show an expected decrease in mitral valve area with no evidence of clinically significant mitral stenosis either immediately after clip deployment or after 12 months of follow-up.     

Mitral regurgitation and cardiac resynchronization therapy

Secondary mitral regurgitation (MR) is frequent in patients with severely depressed left ventricular function. It increases mortality, and decreases exercise capacity. Its main mechanisms are multifactorial, related to apical and outward displacement of the papillary muscles, secondary to an enlarged and a more spherical left ventricle, causing increased subvalvar traction; mitral annular dilatation; and poor contraction of the left ventricle, with a slowed rate of rise of intraventricular pressure and slow closure of the leaflets. Since mechanical dyssynchrony is a major contributor factor to secondary MR, cardiac resynchronization therapy (CRT) could be considered as an alternative therapeutic option for MR, alone or in combination with surgical correction. Effects of CRT on secondary MR are acute and long-term, due to the reverse remodeling of the left ventricle. CRT reduces systolic MR by 30-40%, both at rest and during exercise, and abolishes diastolic MR, by increase of the closing forces and decrease of the tethering forces, acting on the mitral valve; decrease of the mitral annular dilatation represents a minor mechanism. Patients more likely to benefit should have moderate-to-severe MR (but not too severe), of nonischemic etiology, and high interpapillary muscles dyssynchrony. Effects are similar in patients with sinus rhythm and in patients with atrial fibrillation, and in patients with broad and narrow QRS complexes, provided that they have similar extent of dyssynchrony. Biventricular mode is the pacing modality of choice.     

Left ventricular mechanics following restrictive mitral annuloplasty for functional mitral regurgitation: two-dimensional speckle tracking echocardiographic study

Background: Restrictive mitral annuloplasty (RMA) is widely employed for patients with functional mitral regurgitation (MR). Its improvement of left ventricular (LV) function has been demonstrated by only a gradual increase in LV ejection fraction (EF) in the chronic phase. However, the detailed evaluation of changes in LV function has not been fully elucidated in functional MR patients before and after RMA. Therefore, we performed two‐dimensional speckle tracking echocardiography (2D‐STE), which enables accurate evaluation of myocardial deformation and rotation that are undetectable by conventional echocardiography. Methods: We studied 13 patients (mean age 61 ± 10 years) with functional MR associated with cardiomyopathy undergoing RMA. In addition to conventional echocardiographic measurements, 2D‐STE was performed to measure peak systolic radial (RS), circumferential (CS), and longitudinal (LS) strains and twist before and 4 ± 2 weeks after surgery. LV twist was defined as the difference between the apical and basal rotations. Results: After RMA, EF and LS remained unchanged, but RS and CS were significantly improved at the mid‐LV (RS, 20.6 ± 10.8 vs 24.5 ± 11.6%; CS, ?9.6 ± 5.2 vs ?12.8 ± 5.6%) and at the apex (RS, 15.0 ± 12.2 vs 18.7 ± 8.6%; CS, ?4.4 ± 3.0 vs ?7.8 ± 4.8%). RS and CS were unchanged at the base. The apical and basal rotations changed significantly, from 3.5°± 0.7° to 9.2°± 2.1°, and ?2.1°± 0.7° to ?3.8°± 1.0°, respectively. Consequently, the LV twist increased significantly, from 5.6°± 1.0° to 13.0°± 1.9°. Conclusions: Radial and circumferential strains and LV twist increased significantly in the early postoperative period in functional MR patients after RMA and concomitant procedures. (Echocardiography 2012;29:445‐450)     

Hypertrophic Cardiomyopathy with Intermittent Free Mitral Regurgitation–A Surgical Dilemma

We describe the case of a 52‐year‐old woman presenting with non‐ST elevation myocardial infarction, atrial fibrillation, and a new diagnosis of hypertrophic cardiomyopathy. Transesophageal echocardiography following hemodynamic deterioration revealed completely restricted mitral leaflet motion with free mitral regurgitation, and severe left ventricular outflow tract (LVOT) obstruction. Surgical intervention was considered; however, repeat imaging following a period of clinical stability revealed resolution of the findings suggesting a transient ischemic etiology. The case is supported by clinical and echocardiographic images with movie clips, and a discussion of the likely pathology in the context of the underlying condition.     

The mechanism of mitral regurgitation in dilated left ventricle

To assess the mechanism of mitral regurgitation in ventricular dilatation, 24 patients with dilated cardiomyopathy (13 with and 11 without mitral regurgitation) and 10 normal individuals were studied by two-dimensional echocardiography. Left ventricular dimensions and mitral ring diameters in systole and diastole were measured in the long-axis section, and systolic interpapillary muscle distance in the short-axis section. The results showed: (1) Mitral ring diameter is increased in most patients with dilated cardiomyopathy. (2) Neither increased ring diameter, reduced ring contraction, nor decreased interpapillary muscle distance determine the presence of mitral regurgitation. (3) The only difference between those patients with and without mitral regurgitation was the degree of left ventricular dilatation (p<0.05).     

Severe Mitral Regurgitation after Radiotherapy

We present the case of a 69‐year‐old patient with a history of gynecological neoplasia and a pulmonary metastasis, who in 1996 underwent chemotherapy and mediastinal radiotherapy followed by cancer remission. Ten years later she presented with heart failure and her Doppler echocardiogram showed severe mitral regurgitation with pulmonary hypertension. In 2011, she underwent a mitral valve replacement with a biological prosthesis and the pathology exam revealed valve damage consistent with radiotherapy‐induced changes. This unusual mechanism of mitral regurgitation can be demonstrated clearly by echocardiography and should be disseminated among cardiology physicians and in patients who have survived for long periods after radiotherapy, it is important to remember that cardiac complications may indeed occur, and the treating physician is responsible for detecting them.     

Development of mitral stenosis after single mitraclip insertion for severe mitral regurgitation

We report the first case of mitral stenosis following Mitra‐Clip insertion in a patient with symptomatic NYHA IV heart failure, secondary to severe mitral regurgitation (MR). A 79‐year‐old female with a history of prior aortic valve replacement underwent percutaneous mitral valve (MV) repair. A single clip was advanced coaxially down onto the MV under TOE guidance, with the anterior and posterior leaflets clipped together between A2 and P2. TOE confirmed a significant reduction in MR (grade 4 to grade 1). Despite initial symptomatic relief, she represented 3 months later with similar symptoms. Repeat TOE confirmed a well positioned Mitra‐Clip with mild residual MR. However, the possibility of significant mitral stenosis was raised due to the presence of significant turbulence through the bi‐orifice valve, with a peak gradient of 25 mm Hg. In addition there was evidence of severe functional tricuspid valve (TV) regurgitation with elevated pulmonary artery pressures (PAP 90 mm Hg), confirmed on subsequent right heart catheterization. After repeated heart team discussions and a failure of optimal medical therapy, and despite a logistic EuroScore of 35.5, minimally invasive surgical replacement of the MV and simultaneous TV repair was undertaken via a right thoracotomy. Despite procedural success and initial good postoperative response, the patient died subsequently from a combination of hospital‐acquired pneumonia and significant gastrointestinal bleeding (post operative day 35). Mitra‐Clip is a promising novel approach to MV repair. The establishment of further clinical and echocardiographic based selection criteria will help identify the correct patients for this treatment. © 2013 Wiley Periodicals, Inc.     

Percutaneous mitral valve repair: A new treatment for mitral regurgitation

Mitral valve disease affects more than 4 million people in the United States. The gold standard of treatment in these patients is surgical repair or replacement of the valve with a prosthesis. The MitraClip (Abbott Vascular, Menlo Park, CA) is a new technology, which offers an alternative to open surgical repair or replacement via a minimally invasive route. We present an evidence-based clinical update that provides an overview of this technology as it relates to managing patients with significant mitral regurgitation. This review article is particularly useful to noninterventional cardiologists and interventional cardiologists who will be managing patients with this novel technology in increased volumes over the next decade but who do not perform this procedure.     

Values for Mitral Valve Annulus Dimensions in Normals and Patients with Mitral Regurgitation

Objectives. The present study was designed to investigate the dimensions of mitral valve annulus in the presence of mitral regurgitation. Method. Fifty-four patients were examined. On transthoracic echocardiographic images, we performed linear measurements in the parasternal plane in order to define the size of the left ventricle, left atrium, and mitral valve annulus. We compared these findings with those obtained in 16 control subjects. Results. Twenty-one patients with mild or moderate mitral regurgitation demonstrated no significant change of the mitral valve annulus compared with the control group (P > 0.05). Seventeen patients with severe mitral regurgitation (grade of 4) had a significant increase of the dimensions of the mitral valve annulus, left ventricle, and left atrium (P < 0.05). The etiology of mitral regurgitation was degenerative in 32 patients, rheumatic in 2 patients, and mitral valve prolapse in 4 patients. All patients had normal left ventricular systolic function. Thirty-one patients were in normal sinus rhythm, and seven were in atrial fibrillation. Conclusions. The measurement of the diameter of the mitral valve annulus is feasible with transthoracic echo-cardiography. In addition to the evaluation of mitral valve leaflets and subvalvular apparatus, the measurement of the mitral valve annulus is important in the evaluation of mitral regurgitation, as its enlargement is indicative for severe mitral regurgitation .     

Impact of concomitant tricuspid regurgitation on outcome after edge-to-edge mitral valve repair

Aims

To evaluate the impact of tricuspid regurgitation (TR) on echocardiographic and functional outcome after mitral valve transcatheter edge-to-edge-repair (M-TEER).

Methods and Results

A total of 740 patients underwent M-TEER at our center from 2010 to 2021. Patients were analyzed according to severity of concomitant TR at the time of M-TEER procedure: low-grade TR (grade ≤I [trace–mild], 279 patients [37.7%]), moderate TR (grade II, 170 patients [23.0%]) and high-grade TR (grade III-V [severe–torrential], 291 patients [39.3%]). Patients with moderate to high-grade TR had higher morbidity. Procedural success of M-TEER was achieved similarly in all groups (98.2% vs. 97.6% vs. 95.9%, p = 0.22). TR severity decreased rapidly and consistently after M-TEER to only 48.0% of high-grade TR patients after 3 months (p < 0.001) and to 46.8% after 12 months (p = 0.99). High-grade TR patients had significantly higher mortality (21.5% vs. 18.2% vs. 11.1%, p = 0.003) up to 12 months after M-TEER. However, high-grade TR did not independently predict mortality (HR 1.302, 95% CI 0.937–1.810; p = 0.116). Echocardiographic and functional outcome was similar in both secondary and primary MR patients.

Conclusions

High-grade concomitant TR did not independently predict adverse outcome following M-TEER. A wait-and-observe approach for these patients is reasonable.     

心交感神经阻滞对扩张型心肌病二尖瓣和三尖瓣返流的影响

目的:观察心交感神经阻滞对扩张型心肌病二、三尖瓣返流的影响。方法:选取扩张型心肌病患者32名,随机分为对照组（n=14）和治疗组（n=18）。对照组给予常规治疗,治疗组在常规治疗的同时给予心区交感神经阻滞（胸15）,5 g/L利多卡因每2h经胸段硬膜外导管推注一次（夜间睡眠除外）。于治疗前和1个月后进行常规经胸心脏彩超检查,测量左室舒张末期内径（LVEDD）,左房收缩末期内径（LAD s）,左室射血分数（LVEF）,左室短轴缩短率（FS）,二尖瓣（MRA）和三尖瓣（TRA）最大的返流面积,计算返流面积占各自心房面积的百分数（二尖瓣MRAP,三尖瓣TRAP）来衡量返流的严重程度。并测量三尖瓣返流速度,计算肺动脉压（PAP）,比较治疗组与对照组上述指标的差异。结果:治疗组LAD s和LVEDD均较治疗前明显缩小,LVEF和FS较治疗前显著增加。治疗组MRA、TRA、MRAP和TRAP均较治疗前明显减少（MRA 13±4vs7±3 mm2,P<0.01;TRA 7.68±3.55vs1.75±0.21 mm2,P<0.01）,PAP也明显降低（34±17vs15±7 mmHg,1 mmHg=0.133 kPa,P<0.01）。而对照组上述指标治疗前后无明显变化。结论:心交感神经阻滞在明显缩小扩张型心肌病的心腔大小,增强左心室收缩功能的基础上能显著减少二尖瓣和三尖瓣的返流,这为改善扩张型心肌病的预后提供了依据。     

Mitral regurgitation: comprehensive assessment by echocardiography

Two-dimensional and Doppler echocardiography have become the major modalities for the assessment of mitral regurgitation. The combined use of these techniques provides information regarding the morphology of the valvular apparatus as well as the severity of regurgitation. Transesophageal and three-dimensional echocardiography provide a more-detailed evaluation of valve morphology, which can be valuable in determining suitability for valve repair. In patients with severe mitral regurgitation, echocardiographic assessment of ventricular size and function plays a critical role in determining the optimal timing of surgery.     

Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.     

Early results after mitral valvuloplasty for pure mitral regurgitation

In this study we present the results of 105 consecutive patientswith pure mitral regurgitation who underwent surgical treatment.In all patients mitral regurgitation was associated with mitralvalve prolapse: 54 patients underwent mitral valvuloplasty and51 patients mitral valve replacement. Clinical assessment and echocardiography were used as follow-upcriteria at one year after surgery. After mitral valvuloplasty,NYH A decreased from 2.7±0.8 to 1.1±0.7 (P<0.01)and workload capacity increased from 65±28% to 96±25%(P<0.001); left endsystolic atrial dimension and enddiastolicdimension decreased from 6.2±0.8 to 4.8±1.2 cm(P<0.001) and from 7.2±1.3 to 5.9±0.8 cm (P<0.01);ventricular contraction fraction did not change significantly. After mitral valve replacement, clinical and echocardiographicimprovement was significant but less remarkable than after valvuloplasty;ventricular contraction fraction fell from 39±7% to 29±8%in contrast to patients undergoing mitral valvuloplasty in whomno significant change occurred. Complications were rare in both groups though only a minorityof patients undergoing mitral valvuloplasty received anticoagulants.We conclude that mitral valvuloplasty in patients with puremitral regurgitation associated with mitral valve prolapse givesexcellent results, particularly regarding left ventricular functionwhen compared with the patients after mitral valve replacement.