Papillary Muscle Displacement Research Articles

Influence of Chronic Tethering of the Mitral Valve on Mitral Leaflet Size and Coaptation in Functional Mitral Regurgitation

The purposes of this study were to examine whether tethering of the mitral leaflets affects coaptation in patients with functional mitral regurgitation (FMR) and to assess the interaction between the mitral coaptation and mitral regurgitation severity. Functional mitral regurgitation causes restriction of leaflet closure as a result of enhanced tethering of the mitral leaflets and papillary muscle (PM) displacement. Three-dimensional transesophageal echocardiography was performed in 44 patients with FMR related to the bilateral PM displacement and in 56 controls. The distance between the tip of the anterior or posterior PM and the intervalvular fibrosa were measured as the lateral or medial tethering length (TL) in midsystole. To evaluate the degree of coaptation, coaptation length (CL) at medial, middle, and lateral sites of mitral valve and an estimate of coaptation area (CA) were measured. The FMR group showed the significantly decreased CA (1.3 ± 0.4 cm(2) vs. 1.6 ± 0.4 cm(2), p = 0.005) and CL (medial 3.2 ± 0.9 mm vs. 4.8 ± 0.6 mm, middle 3.8 ± 1.3 mm vs. 5.8 ± 0.7 mm, lateral 3.3 ± 0.9 mm vs. 4.8 ± 0.6 mm; all p < 0.0001) compared with the controls. Each CL correlated negatively and significantly with both medial and lateral TL (all p < 0.0001). Annular area (p = 0.004) was significantly smaller and leaflet-to-annular area ratio (p < 0.0001) was significantly larger in patients with nonsignificant FMR than in the patients with significant (moderate to severe) FMR. Significant correlations were found between effective regurgitant orifice area and CA or each CL (all p < 0.0001). Coaptation decreased significantly in patients with FMR. The CL at each region was related to PM displacement and the indexes of coaptation were associated with mitral regurgitation severity.

Measurement of strut chordal forces of the tricuspid valve using miniature C ring transducers

Tricuspid valve (TV) leaflets, papillary muscles (PM), and tendinous chords must work together to ensure proper coaptation. Alterations in valvular mechanics, including chordal forces, may lead to improper coaptation resulting in tricuspid regurgitation. Little is known about TV mechanics as right-sided heart diseases have been overlooked. We sought to fill this gap by understanding the role of TV strut chords with the objective to understand how strut chordal force varies depending on papillary muscle (PM) origin and leaflet attachment in the normal state. Additionally we investigated how these forces are altered with abnormal geometry. Porcine TVs (n=18) were studied in a right-heart simulator capable of reproducing physiological and pathological conditions. Miniature force transducers were placed on strut chords to measure forces throughout the cardiac cycle. In the normal state, chordal force depended upon PM attachment in which chords branching from the septal PM (SPM) carried significantly less force compared to those branching from the anterior PM (APM) (p≤0.05). Annular dilatation resulted in significant increase in chordal force (p≤0.05) on all strut chords. Severe PM displacement led to increased chordal force in chords attaching the APM to the posterior leaflet as well as chords attaching the PPM to the septal leaflet. Elevated chordal force due to isolated annular dilatation was further increased only with addition of apical displacement of the APM. These results provide initial knowledge of TV chordal force mechanics and may be applied to future studies on TV repair techniques.

Different Influences of Left Ventricular Remodeling on Anterior and Posterior Mitral Leaflet Tethering

Different influences of left ventricular (LV) remodeling on anterior and posterior mitral leaflet (AML and PML) tethering in ischemic mitral regurgitation (MR) has not been fully investigated. We hypothesized that progressive outward displacement of papillary muscles, including posterior vector, may cause greater tethering to PML compared to AML. In 79 patients with LV ejection fraction <50% and 20 controls, LV sphericity, AML and PML tethering angles, apical and posterior displacement of coaptation, mitral annular area, and severity of MR (vena contracta width) were measured using 3-D echocardiography. To examine different influences of LV remodeling on AML and PML tethering, interaction between AML/PML and LV sphericity was tested using multiple regression analysis. Both AML and PML tethering significantly increased with increased LV sphericity (r=0.59 and 0.65, P<0.001). Multiple regression yielded a significant interaction term between AML vs. LV sphericity and PML vs. LV sphericity (t=3.69, P<0.001), indicating greater influence from LV remodeling on PML compared to that for the AML. Multivariate analysis demonstrated independent contributions to MR severity from PML tethering primarily along with posterior and apical displacement of coaptation. LV remodeling augments tethering of both AML and PML, with greater influence on PML.

The Effects of a Three-Dimensional, Saddle-Shaped Annulus on Anterior and Posterior Leaflet Stretch and Regurgitation of the Tricuspid Valve

Tricuspid regurgitation (TR) is present in trace amounts or more in 82-86% of the population and is greater than mild in 14% of the population. In severe cases, it can contribute to right heart failure and adversely affect mitral valve repair durability. One major cause of TR is the dilation of the tricuspid annulus, which alters the geometry of the annulus from a saddle-shape to a more planar profile. Another cause of TR is the displacement of the papillary muscles (PMs), which results from right ventricular dilation. The objective of this study was to identify the effect of a saddle-shaped annulus on native tricuspid leaflet stretch mechanics and TR. In addition, the effects of geometric alterations, including annular dilatation and PM displacement, on leaflet stretch was investigated. Fresh porcine tricuspid valves (TVs) (n = 8) were excised and sutured to an adjustable three-dimensional annulus plate (allowing for dilatation and saddle-shape) and three PM attachment rods. The valve was then placed in the in vitro Georgia Tech right heart simulator. Dual-camera photogrammetry, was used to quantify the stretch ratio experienced by the valve leaflets at peak systole for the following conditions: physiologically normal, 100% annular dilatation, displaced PMs, and a combination of annular dilatation and PM displacement. In addition, a saddle and flat annulus were implemented for each of the four conditions. PM displacement was simulated by displacing all PMs by 10 mm in all directions (laterally, apically, posteriorly/anteriorly). The physiologically normal condition-normal annulus area, saddle-shaped annulus with PMs in a normal position, was used as a control. The results showed that the posterior leaflet exhibited significantly (p ≤ 0.05) higher major and areal stretch ratios as compared to the anterior leaflet at peak systole for all conditions tested. No significant difference was seen in stretch when a flat annulus was compared to saddle for the anterior or posterior leaflet for normal or disease conditions. Investigation of the impact of disease found a significant increase (p ≤ 0.10) in stretch in the posterior leaflet with a combination of annular dilatation and PM displacement (2.01 ± 0.68) as compared to the normal condition with a saddle annulus (1.43 ± 0.20). In addition displacement of the PMs resulted in a significant (p ≤ 0.01) reduction in TR, although the actual volume reduced was minimal (1.2 mL). Stretch values were measured for the anterior and posterior leaflet under both physiologic and pathologic conditions for the first time. Further, these results provide an understanding of the effects of geometric parameters on valve mechanics and function, which may lead to improved TV repairs.

Correlates of Tricuspid Regurgitation as Determined by 3D Echocardiography: Pulmonary Arterial Pressure, Ventricle Geometry, Annular Dilatation, and Papillary Muscle Displacement

While it is understood that annular dilatation contributes to tricuspid regurgitation (TR), other factors are less clear. The geometry of the right ventricle (RV) and left ventricle (LV) may alter tricuspid annulus size and papillary muscle (PM) positions leading to TR. Three-dimensional echocardiographic images were obtained at Emory University Hospital using a GE Vivid 7 ultrasound system. End-diastolic area was used to classify ventricle geometry: control (n=21), isolated RV dilatation (n=17), isolated LV dilatation (n=13), and both RV and LV dilatation (n=13). GE EchoPAC was used to measure annulus area and position of the PM tips. Patients with RV dilatation had significant (P≤ 0.05) displacement of all PMs apically and the septal PM and posterior PM away from the center of the RV toward the LV. Patients with LV dilatation had significant (P≤0.05) apical displacement of the anterior PM. Pulmonary arterial pressure (r=0.66), annulus area (r=0.51), apical displacement of the anterior PM (r=0.26), posterior PM (r=0.49), and septal PM (r=0.40), lateral displacement of the septal PM (r=0.37) and posterior PM (r=0.40), and tenting area and height (r=0.54, 0.49), were significantly (P≤0.05) correlated to the grade of TR. Ventricle classification (r=0.46) and RV end-diastolic area (r=0.48) also were correlated with the grade of TR. A regression analysis found ventricle classification (P=0.001), pulmonary arterial pressure (P≤0.001) annulus area (P=0.027), and apical displacement of the anterior PM (P=0.061) to be associated with the grade of TR. Alterations in ventricular geometry can lead to TR by altering both tricuspid annulus size and PM position. Understanding these geometric interactions with the aim of correcting pathological alterations of the tricuspid valve apparatus may lead to more robust repairs.

Abstract 9177: Mitral Valve Adaptation in Chronic Aortic Regurgitation with Preserved Systolic Function: A Three-Dimensional Echocardiographic Study

Introduction: Chronic aortic regurgitation (AR) causes left ventricular (LV) remodeling and ultimately heart failure. This creates the potential for functional mitral regurgitation (MR) caused by papillary muscle displacement and mitral valve tethering. However, MR is typically absent during the compensated stage of AR despite substantial LV dilatation. Increased mitral leaflet area has been identified in ischemic and non-ischemic heart failure. It is unknown whether increased mitral valve size could represent a compensatory mechanism capable of preventing MR in patients with LV dilatation due to chronic AR. Hypothesis: Chronic AR is associated with mitral valve enlargement and this can prevent functional MR in patients with LV dilatation. Our objective is to compare mitral valve leaflet area in patients with chronic AR and preserved systolic function to that of normal patients using 3D-echocardiography. Methods: From January to April 2011, we prospectively enrolled 44 patients (22 with at least moderate aortic regurgitation and 22 controls). 3D echocardiograms were performed to assess mitral valve geometry including total diastolic leaflet area measured by a previously validated method. Results: Both groups had normal ejection fraction (60 ± 7 % in AR vs 63 ± 7 % in normals, p=0.17). Only 1 AR patient had significant (more than mild) functional MR. LV volume by 3D echocardiography was significantly larger in the AR group (LV end-diastolic volume index: 80 ± 23 cm3/m2 vs 49 ± 12 cm3/m2, p&lt;0.01). The mitral valve leaflet area indexed for body surface area was significantly increased in the AR group (8.9 ± 1.7 cm2/m2 vs 7.4 ± 1.2 cm2/m2, p&lt;0.01). Patients with AR also had increased mitral leaflet thickness (2.3 ± 0.3 mm vs 2.0 ± 0.3 mm, p&lt;0.01) regardless of AR jet impact on the valve. Mitral valve leaflet area significantly correlated with LV end-diastolic LV volume (p&lt;0.01). Conclusion: Mitral valve leaflet area and thickness are significantly increased in patients with chronic AR and preserved ejection fraction. Area enlargement is proportional to LV volume, and can potentially explain why functional MR is uncommon in this population. Understanding the mechanisms underlying this adaptation could lead to new therapeutic interventions for functional MR.

Abstract 18059: Papillary Muscle Abnormalities in Apical Hypertrophic Cardiomyopathy and Their Association with Mid-Ventricular Obstruction: Insignt from Cardiac Magnetic Resonance Imaging

Background Abnormal papillary muscles(PM) are often found in hypertrophic cardiomyopathy(HCM) and the significance relating left ventricular(LV) outflow obstruction has been identified. Mid-ventricular obstruction(MVO) can be found in apical HCM and accompanied by apical aneurysm and ventricular tachycardia. We sought to investigate PM structures including numbers, thickness, insertion site and their association with MVO in apical HCM. Methods In 44 patients(30 men, age 57±8 yrs) with apical HCM, cardiac magnetic resonsnce was performed to characterize PM morphology. PM numbers, maximal PM thickness in diastole, and their insertion site on LV were evaluated. Patients with isolated asymmetric apical hypertrophy were classified as a pure type, and those with coexistent hypertrophy of the interventricular septum as a mixed type. MVO were examined using Doppler echocardiography and diagnosed when the systolic peak flow velocity at the mid-ventricle was≥2.5 m/s. Subjects were divided into 2 groups according to the presence of MVO; Group I(n=28): MVO(-), Group II(n=15): MVO(+). Results The mixed type was more prevalent(54 vs 93%, p=0.014) and posterior wall thickness at mid LV was higher(10.2±1.8 vs 12.9±2.1, p&lt;0.001) in group II compared with group I. Apical aneurysm was found in 3 patients in group II. Group II showed higher PM numbers(2.7±0.8 vs 3.3±0.8, p=0.070) and maximal thickness(8.7±0.9 vs 10.8±1.5, p=0.045). PMs were displaced closer to the LV apex(displaced apically: 68 vs 93%, p=0.042) in almost of group II patients. There was no significant difference in heart rate between two groups. Conclusion In apical HCM, patients with MVO showed different PM structures and displacement than those without MVO. Increased number of PMs and their apical displacement can be one of contributors of MVO. Combined with the LV morphologic type, the assessement of PM morphology would be important to predict the development of MVO and its subsequent outcomes in apical HCM.

In Vitro Characterization of the Mechanisms Responsible for Functional Tricuspid Regurgitation

Functional tricuspid regurgitation (TR) is increasingly recognized as a source of morbidity. Current repair strategies focus on annular remodeling because annular dilatation is common in patients with TR. Although papillary muscle (PM) displacement is recognized in functional mitral regurgitation, its role in TR is less well characterized. The objective of this in vitro study was to further clarify the mechanisms by which TR occurs as an effect of annular dilatation and PM displacement. Porcine tricuspid valves (n=16) were studied in an in vitro right heart simulator. The valve dynamics were quantified with isolated annular dilatation starting with a normal annular size (6 cm(2)) and incrementally dilated up to 100%, isolated PM displacement, and a combination of the 2. All valves lost competence at 40% dilatation, resulting in a TR of 7.9 ± 3.4 mL (P ≤ 0.05) compared with baseline and central residual leaflet length of 0.5 ± 0.2 cm. Multidirectional displacement of the anterior and posterior/septal PMs and all PMs significantly (P ≤ 0.05) increased TR, with normal annular area. Malcoaptation was observed where the 3 leaflets joined with all significant levels of TR. The anterior leaflet had the greatest percent change in residual leaflet length, whereas PM displacement caused a reduction in residual leaflet length for the septal leaflet for all conditions. This study shows that although annular dilatation alone leads to TR, isolated PM displacement can also cause TR; annular remodeling strategies should be tailored in the setting of severe PM displacement.

Ischemic mitral regurgitation

Secondary or 'functional' mitral regurgitation (MR) is often due to ischemic heart disease that results in disordered left ventricle and mitral valve geometry. In patients with coronary disease, concomitant MR results in worse morbidity and mortality. Coronary artery disease may result in annular dilation due to left ventricle cavity dilation, excessive leaflet motion, impaired leaflet motion due to leaflet tethering and papillary muscle displacement, and/or decreased mitral valve closing forces due to systolic dysfunction. Although transthoracic echocardiography is the first step in the diagnosis of ischemic MR, transesophageal and three-dimensional echocardiography are often useful adjuncts to better understand the mechanism(s) of disease and planning repair. Furthermore, noninvasive evaluation of ischemia and viability may provide important prognostic information. Medical therapy for ischemic MR is directed at the underlying ischemic substrate and concomitant systolic dysfunction, and consists of β-blockers and vasodilators. Percutaneous strategies for repair are currently under investigation, and have shown promising results. Surgical repair is favored over replacement, and is generally recommended for patients with moderate or severe MR undergoing coronary artery bypass. Unfortunately, long-term freedom from MR is elusive even with surgical repair, and trials are currently underway to determine the best approach to treatment in patients with moderate disease.

The Mitral Valve in Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) has evoked both fascination and controversy since its first modern description >50 years ago.1 Originally described as “functional aortic subvalvar stenosis” by Brock, the majority of articles about HCM in the ensuing first decade emanated from observations made in the operating room or in the cardiac catheterization laboratory.1 The actual cause of left ventricular outflow tract (LVOT) obstruction in patients with this condition had not yet been clarified. Ironically, the mechanisms of LVOT obstruction in HCM were only elucidated several years after surgery was first performed in these patients. In fact, an early report by Morrow described the septal myotomy procedure as surgical treatment for HCM and proposed that the myotomy interfered with the sphincter-like muscular contraction ring in the LVOT.1 Article see p 40 Noninvasive cardiovascular imaging studies have greatly advanced our knowledge about HCM.2 Hypertrophic cardiomyopathy is now felt to have tremendous genetic,3 clinical, morphological, and hemodynamic heterogeneity.1 Nevertheless, the presence of LVOT obstruction in patients with HCM has continued to inspire interest. The often contentious debates surrounding LVOT obstruction have centered on its very existence, its causes, its clinical impact and prognosis, and its optimal management.1 These issues have inextricably included the mitral valve, which has long been felt to play a pivotal role in the pathophysiology of LVOT obstruction in patients with HCM. In the present issue of Circulation , Maron et al use cardiovascular magnetic resonance (CMR) imaging to characterize mitral valve leaflets in patients with HCM.4 This study assessed the lengths of the anterior mitral leaflet (AML) and posterior mitral leaflet in 172 consecutive patients with HCM. Their findings were compared with 172 normal control subjects matched for age, sex, and body surface area. In addition, the study included a small cohort of …

Mitral-Valve Surgery in the Elderly: Comparative Results of Mitral Repair and Replacement

Evaluation of: Chikwe J, Goldstone AB, Passage J et al.: A propensity score-adjusted retrospective comparison of early- and mid-term results of mitral-valve repair versus replacement in octogenarians. Eur. Heart J. 32(5), 618–626 (2011). Mitral regurgitation (MR) is common in the elderly, increasing in prevalence with age. Common causes of MR include: degenerative disease of the valve and subvalvular apparatus; ischemic MR due to annular dilatation, papillary muscle displacement and left ventricular remodeling; rheumatic mitral valve disease and infectious endocarditis. The optimal treatment of severe mitral insufficiency in the elderly remains unknown. Mitral-valve repair or replacement have historically been considered high risk in older patients and, for this reason, many elderly patients are not offered surgery. Yet with recent advances in surgical techniques and outcomes, mitral-valve surgery is being increasingly utilized in elderly patients. A recent study by Chikwe et al. in the European Heart Journal examines overall and comparative outcomes of mitral-valve repair and mitral-valve replacement in an elderly cohort. This study finds that mitral-valve repair confers a survival benefit relative to mitral-valve replacement in octogenarians, particularly in patients undergoing surgery for degenerative disease.

A Pulsatile Simulator for the in Vitro Analysis of the Mitral Valve with Tri-Axial Papillary Muscle Displacement

We developed a new pulsatile hydrodynamic simulator for the in vitro testing of mitral valve (MV) samples. The required specifications included a 3D positioning system for the papillary muscles (PMs) that is accurate and simple to manage; measurement of the force exerted by the chordae tendineae on the PMs; and the possibility to visually inspect the MV for kinematic analysis. An atrial/ventricular chamber system was developed. The ventricular chamber housed a tri-axial actuator system that was aligned to a morphometric Cartesian frame, allowing for PM positioning even while tests are running. Each PM holder had an embedded load cell for force measurement. The atrial chamber was designed so as to permit MV visual inspection, maintaining a non-disturbed flow at the sample inlet. The setup was subjected to trials with fresh porcine MVs. Flow and pressure difference across the MVs and PM forces were measured in different MV configurations, with different PM spatial dislocations. High speed video recordings were acquired. The positioning accuracy was assessed. Tests with MVs showed good usability, even by the non-engineering personnel. The effects of PM displacement on valve function (valve competence and PM forces) was consistent with previously published data, thus confirming the general soundness of the design principles. The developed simulator is a promising instrument for performing MV in vitro tests in a precise, well-repeatable manner. The ability to completely adjust the PM position while a test is running boosts the simulator's potential for detailed investigations of the pathological and surgically treated MV.

The Role of Mecahnical Dyssynchrony on Functional Mitral Regurgitation in Patients with Dilated Cardiomyopathy

REFER TO THE PAGE 69-75 Functional mitral regurgitation (FMR) occurs despite a structurally normal mitral valve (MV) as a consequence of global or regional left ventricular (LV) dysfunction. It is a common complication and predicts poor outcome in patients with dilated cardiomyopathy.1) The pathophysiology of FMR is closely related to several factors such as systolic MV tenting as a result of LV geometric changes, a reduced closing force, dilatation of the mitral annulus and LV dyssynchrony.2) Of these, mechanical dyssynchrony of the LV may play a potential role in determining the degree of FMR as a result of uncoordinated contraction of the papillary muscles and reduced closing force.3) This hypothesis support the ability of cardiac resynchronization therapy (CRT) to decrease the severity of FMR due to improved coordinated timing of the papillary muscles and reverse remodeling of the LV, which tends to recur when CRT is withdrawn.4) However, a mechanistic study has suggested that mechanical dyssynchrony is less important than LV remodeling and MV tethering.5) The role of mechanical dissynchrony in the pathophysiology of FMR remains unclear. In this issue of the journal, Choi et al.6) reported the role of mechanical dyssynchrony on FMR in patients with dilated cardiomyopathy using real time 3D echocardiography. The dyssynchrony index was significant higher in the patients with FMR than that in the patients with non-FMR and the dyssynchrony index was well correlated with the effective regurgitation orifice area (ERO) of the FMR. However, the dyssynchrony index was not a significant determinant of ERO on the multivariate model. Displacement of the anterior papillary muscle and consequent MV tenting remained the strongest determinants of the degree of ERO. These findings suggested that the distorted geometric change of the LV with MV tenting is a necessary condition for the development of FMR, whereas mechanical dyssynchrony could have a minor role. There are several limitations of the study by Choi et al.6) First, the study had a relatively small sample size (n = 53), a mild degree (ERO = 0.17 ± 0.10 cm2) of FMR and a small percentage of left bundle branch block (18%) as compared to the previous studies. These factors might affect the results between mechanical dyssynchrony and the degree of FMR. Second, they measured the geometric parameters using 3D echocardiography and the multi-planar reconstruction (MPR) mode of a 3D image analysis program. This method is ideal to measure the mitral apparatus at a specific angle compared with that of 2D echocardiography. But the reproducibility is modest (the intra-observer correlation coefficients were 0.69-0.73 for the measurement of the mitral apparatus). This might also have affected the results. Despite the limitations, Choi et al's study is the first trial to estimate the distances of both papillary muscles using MPR by 3D echocardiography. This method is promising to evaluate the mechanism of FMRs if the technical issues related to the image resolution of 3D echocardiography and the learning curve can be resolved.

Ischaemic mitral regurgitation: pathophysiology, outcomes and the conundrum of treatment

Ischaemic mitral regurgitation is a frequent complication of left ventricular global or regional pathological remodelling due to chronic coronary artery disease. It is not a valve disease but represents the valvular consequences of increased tethering forces (papillary muscles displacement leading to a more apical position of the leaflets and their coaptation point) and reduced closing forces (reduced contractility, dyssynchrony of the papillary muscles, intra-left ventricular dyssynchrony). Although mitral regurgitation has an unloading effect and reduces impedance, the volume overload begets further left ventricular dilatation, increases ventricular wall stress leading to worsened performance. Ischaemic mitral regurgitation is characteristically dynamic: its severity may vary with haemodynamic conditions. Both the severity of ischaemic mitral regurgitation and its dynamic component worsen prognosis. There are numerous possible treatment modalities, but the management of the individual patient remains difficult. Medical therapy is mandatory; revascularization procedures are frequently not sufficient to reduce mitral regurgitation; the role of combined surgical therapy by mitral valve repair is not yet defined in the absence of large randomized trial. Some patients are good candidates for cardiac resynchronization therapy that may reduce the amount of regurgitation. New therapeutic targets are under investigation.

Response of Two Annular Prostheses to Functional Mitral Regurgitation Main Determinants: An In Vitro Evaluation

Functional mitral regurgitation (FMR) is usually treated through annuloplasty, i.e., the restriction of the mitral annulus by implanting an undersized prosthetic ring. We conceived a steady-state fluid-dynamic mock simulator that allows for controlling the main mechanic determinants of FMR: transmitral pressure and papillary muscle (PM) apical and lateral dislocation. We used our system to compare the FMR-specific Geoform ring with the general purpose Physio ring in the treatment of FMR. Each ring was implanted on 10 excised fresh porcine valves. Different transmitral pressures (40, 80, 120, 140, and 160 mm Hg) and symmetrical PM apical displacements (2.5-15 mm, step 2.5 mm) were imposed with submillimetric precision. In each configuration, the regurgitant flow through the valve was measured. For PM apical displacement ≥7.5 mm, the regurgitant flow was lower (p < 0.05) with the Geoform ring than with the Physio ring. Differences and their statistical significance increased as PM displacement or transmitral pressure increased. Regression analysis showed that this outcome did not depend on the morphology of the valves. The adopted approach proved itself simple and reliable and allowed to highlight the differences between the two examined annuloplasty devices in countering the two main determinants of FMR: high apical PM dislocation and transvalvular pressure.

In Vivo Measurement of Mitral Leaflet Surface Area and Subvalvular Geometry in Patients With Asymmetrical Septal Hypertrophy

Background— Analyzing the determinants of systolic anterior motion of the mitral valve and consequent left ventricular outflow tract (LVOT) obstruction in patients with asymmetrical septal hypertrophy requires a comprehensive 3-dimensional analysis of mitral leaflet (ML) area, papillary muscle (PM) geometry, and the distribution of left ventricular hypertrophy. Methods and Results— Real-time 3-dimensional echocardiography was performed in 47 patients with asymmetrical septal hypertrophy and 32 normal controls. Patients included 20 with resting LVOT obstruction (group I) and 27 without (group II). Customized software (Omni 4D) provided a validated measure of ML surface area, LVOT area, mitral annular area and nonplanarity, LVOT hypertrophy index by topography (percent area with wall thickness &gt;16 mm), and 3-dimensional PM positions relative to annulus. ML area was more than twice as large in group I than normal and 1.4 times normal in group II ( P &lt;0.001). Group I patients were also characterized by higher LVOT hypertrophy index and medial and anterior displacements of both PMs, resulting in a shorter inter-PM distance. Independent determinants of LVOT obstruction were indexed total ML area (adjusted odds ratio, 5.651; 95% confidence interval, 1.573 to 20.304; P =0.008) and inter-PM distance (adjusted odds ratio, 0.416; 95% confidence interval, 0.203 to 0.854; P =0.0169). Minimal LVOT area during systole correlated well with peak LVOT pressure gradient ( R 2 =0.83, P &lt;0.001); its independent determinants were left ventricular end-systolic volume ( P =0.0183), indexed total ML area ( P =0.0108), inter-PM distance ( P =0.0378), annular height ( P =0.0047), and LVOT hypertrophy index ( P =0.0098). Conclusions— Myocardium is not the only tissue affected in patients with asymmetrical septal hypertrophy, and primary changes of the mitral apparatus, including ML area increase and PM displacement, are independent determinants of LVOT obstruction and provide a comprehensive mechanism that determines leaflet slack and anteriorly directed motion. Abnormal PM–mitral valve geometry assessed by real-time 3-dimensional echocardiography can provide reasonable new targets for individualized intervention.

Dynamic RING + STRING for ischemic mitral regurgitation: Papillary muscle repositioning and modification of the septal–lateral diameter in the loaded beating heart under echocardiographic guidance

Ischemic mitral regurgitation (MR) involves annular dilatation in all cases. Some patients, however, also exhibit severe leaflet tethering due to papillary muscle displacement. Leaflet tethering is the strongest predictor of repair failure in up to 30% of patients treated by undersized ring annuloplasty (RING). These failures emphasize the need for subvalvular strategies. Several adjunctive techniques have been proposed, but only 3 techniques have received clinical acceptance. Borger and associates reported initial results of cutting second-order chordae. The impact of this technique on left ventricular systolic function, however, has been discussed controversially. Leaflet extension has been performed successfully in a case series by de Varennes and associates. We have reported a technique (RING þ STRING) that allows repositioning of the posterior papillary muscle under transesophageal echocardiographic (TEE) guidance. Even though midterm results with this technique have been encouraging, we have been looking for further improvement. Reduction of the septal–lateral diameter has been the key to reduction of ischemic MR in the experimental setting. This observation has been the basis for the use of aggressively undersized complete rings used clinically. Recently, however, Magne and colleagues documented functional mitral stenosis with associated pulmonary hypertension and reduced functional capacity as result of aggressive undersizing, the equivalent of patient–prosthesis mismatch in mitral valve repair.

Invited Commentary

What is the best technique for mitral valve replacement in patients with ischemic mitral regurgitation and left ventricular (LV) dysfunction? The authors [1Yousefnia M.A. Dehestani A. Saidi B. Roshanali F. Mandegar M.H. Alaeddini F. Papillary muscle repositioning in valve replacement for left ventricular dysfunction: ischemic mitral regurgitation.Ann Thorac Surg. 2010; 90: 497-502Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar] show us that preserving both anterior and posterior chordal attachments does not give the good results we would have expected. LV function certainly improves over time, but only in modest proportions. A different operation is presented, this time attaching the tip of the anterior and posterior papillary muscles to the mitral annulus, therefore essentially correcting posterior and downward displacement of the posterior papillary muscles, as a significantly improved option in terms of reversal of adverse LV remodeling.It is interesting to point out that valve replacement associating complete chordal preservation mimics mitral repairs in that no direct interventions on the LV are required. The second type of operation, on the contrary, intervenes immediately on LV variables. Aligning here both papillary muscles and restoring a more normal LV geometry seems to enhance a durable restoration of LV function. In terms of ejection fraction, volume reduction, and sphericity index, the results here parallel those reported for mitral repair using the papillary muscle sling that addresses the intraventricular component of ischemic mitral dysfunction.However impressive, the authors' dissimilar results must be tempered because we do not know how many patients in each group were expected, according to the Leyden algorithm, to experience reversal of adverse remodeling. The preoperative LV volumes were, however, not significantly different between groups. Such data do not seem to indicate that patients could be foreseen as poor responders.Confirmation is needed from a larger cohort of patients and also from different surgical groups. Continuing investigations may well result in a new type of operation for ischemic mitral regurgitation. What is the best technique for mitral valve replacement in patients with ischemic mitral regurgitation and left ventricular (LV) dysfunction? The authors [1Yousefnia M.A. Dehestani A. Saidi B. Roshanali F. Mandegar M.H. Alaeddini F. Papillary muscle repositioning in valve replacement for left ventricular dysfunction: ischemic mitral regurgitation.Ann Thorac Surg. 2010; 90: 497-502Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar] show us that preserving both anterior and posterior chordal attachments does not give the good results we would have expected. LV function certainly improves over time, but only in modest proportions. A different operation is presented, this time attaching the tip of the anterior and posterior papillary muscles to the mitral annulus, therefore essentially correcting posterior and downward displacement of the posterior papillary muscles, as a significantly improved option in terms of reversal of adverse LV remodeling. It is interesting to point out that valve replacement associating complete chordal preservation mimics mitral repairs in that no direct interventions on the LV are required. The second type of operation, on the contrary, intervenes immediately on LV variables. Aligning here both papillary muscles and restoring a more normal LV geometry seems to enhance a durable restoration of LV function. In terms of ejection fraction, volume reduction, and sphericity index, the results here parallel those reported for mitral repair using the papillary muscle sling that addresses the intraventricular component of ischemic mitral dysfunction. However impressive, the authors' dissimilar results must be tempered because we do not know how many patients in each group were expected, according to the Leyden algorithm, to experience reversal of adverse remodeling. The preoperative LV volumes were, however, not significantly different between groups. Such data do not seem to indicate that patients could be foreseen as poor responders. Confirmation is needed from a larger cohort of patients and also from different surgical groups. Continuing investigations may well result in a new type of operation for ischemic mitral regurgitation. Papillary Muscle Repositioning in Valve Replacement for Left Ventricular Dysfunction: Ischemic Mitral RegurgitationThe Annals of Thoracic SurgeryVol. 90Issue 2PreviewThe aim of this study was to investigate the feasibility of performing papillary muscle repositioning (PMR) for subvalvular-sparing mitral valve replacement procedures in patients with ischemic mitral regurgitation and to determine the early and late effects of this procedure on the clinical outcome and left ventricular mechanics. Full-Text PDF

Changes in functional mitral regurgitation after cardiac resynchronization therapy

This editorial refers to ‘Impact of reduction in early- and late-systolic functional mitral regurgitation on reverse remodelling after cardiac resynchronization therapy, by Y. Liang et al. , doi:10.1093/eurheartj/ehq134 Functional mitral regurgitation (MR) is a common finding in patients with global left ventricular (LV) dilatation and dysfunction.1 In these patients, the mitral leaflets are structurally normal and leaflet coaptation failure results from an imbalance between valve closing forces and valve tethering forces.2,3 Impaired LV contractility, global LV dyssynchrony, and reduced mitral annulus systolic contraction lead to a significant reduction in valve closing forces. In turn, valve tethering forces are increased due to mitral annulus dilatation, LV remodelling, and papillary muscle displacement.4 Furthermore, MR per se induces additional adverse ventricular remodelling through volume overload, and plays an important role in the progression of the cardiomyopathy. The presence of significant functional MR also has important prognostic implications,5,6 and is associated with a relatively high morbidity and mortality. Surgery is the preferred therapeutic option, but several recent studies demonstrated that cardiac resynchronization therapy (CRT) might also be able to reduce functional MR.7–10 Reduction of MR following CRT was shown to be related to various issues. First, the reduction in LV dyssynchrony and the improvement in LV contraction immediately after CRT can significantly increase valve closing forces.7,10 Secondly, LV reverse remodelling and changes in mitral apparatus geometry can further reduce MR by reducing … *Corresponding author. Tel: +31 71 5262020, Fax: +31 71 5266809, Email: j.j.bax{at}lumc.nl

Altered right ventricular papillary muscle position and orientation in patients with a dilated left ventricle

To investigate the impact of left ventricular dilatation on right ventricular papillary muscle displacement. Thirteen patients underwent high-resolution cardiac magnetic resonance imaging at Emory University Hospital: Seven patients with congestive heart failure and a dilated left ventricle composed the dilated left ventricular group, and 6 normal subjects were used as a control. A total of 120 cardiac magnetic resonance imaging slices were acquired in a short-axis view at end diastole for each subject. Cardiac magnetic resonance imaging slices were used to identify the papillary muscle tip position in 3-dimensional coordinates for the septal, posterior, and anterior papillary muscles. The centroid of the papillary muscle coordinates was used as the reference point for comparison between subjects. The relative orientation between the right ventricular papillary muscles was evaluated and compared between the dilated left ventricular group and normal subjects. Dilatation of the left ventricle resulted in a significant (P = .05) displacement of the septal right ventricular papillary muscle toward the centroid: normal group, 0.0285 ± 0.036 mm/mm versus dilated left ventricular group, 0.1437 ± 0.026 mm/mm. More specifically, the septal papillary muscle significantly (P = .03) moved away from the septal wall (normal group: 0.61 ± 0.09 mm/mm, dilated left ventricular group: 0.379 ± 0.037 mm/mm). Specific locations of all 3 right ventricular papillary muscles were reported for normal subjects and patients with a dilated left ventricle. Patients with a dilated left ventricle have significantly increased displacement of the septal right ventricular papillary muscle away from the septum when compared with normal controls. This demonstrates pathophysiologic contribution of the left ventricle to specific papillary muscle alterations within the right ventricle.