Papillary Muscle Displacement Research Articles

Contemporary review of the evolution of various treatment modalities for mitral regurgitation.

Mitral regurgitation is one of the commonest valvular heart diseases for which there have been several innovative treatment strategies that have developed over the last several decades. We describe the various treatment modalities that have been used for the last several decades. All articles in PubMed, Cochran and Embase were screened from inception to August 2024 for the following - 'Mitral valve regurgitation' 'Mitral valve repair' 'Mitral valve replacement' 'Robotic mitral surgery' 'Transcatheter mitral valve repair.' Mitral regurgitation (MR) is classified into primary and secondary MR. Causes of primary MR include degenerative disease, rheumatic heart disease, and infective endocarditis. Secondary MR is observed in the setting of left ventricle (LV) pathology, including ischemic or dilated cardiomyopathy. In secondary MR, annular dilation, papillary muscle displacement, tethering of chordae tendineae and/or mitral valve (MV) leaflets result in leaflet restriction and malcoaptation. In this review, we discuss various modalities for treatment of mitral regurgitation, as well as newer treatment options for MR including robotic MV repair and other minimally invasive procedures. Several ongoing randomized controlled trials in this topic will help shed more light and provide guidance to deliver the optimal care for our patients.

Comparison of mitral valve apparatus anomalies between sarcomeric hypertrophic cardiomyopathy and Fabry disease cardiomyopathy

Abstract Background Despite different etiopathogenesis, Fabry disease (FD) cardiomyopathy and sarcomeric hypertrophic cardiomyopathy (HCM) share a similar hypertrophic phenotype. Cardiac magnetic resonance (CMR) plays a pivotal role in distinguishing between these two clinical conditions, thanks to the thorough morphological definition of the phenotype and non-invasive tissue characterization. A high prevalence of mitral apparatus anomalies has been previously described both in sarcomeric HCM and FD cardiomyopathy. Purpose This study systematically compares the morphology of the mitral apparatus in sarcomeric HCM and FD cardiomyopathy, to add new insights into differential diagnosis. Methods CMR images of 120 patients were retrospectively analyzed and divided as follows: healthy controls CTRL (n=40), HCM (n=40), and FD (n=40) with left ventricular hypertrophy (LVH). The analyses included the measurement of I) papillary muscles’ hypertrophy, expressed as the maximum diameter (D max) of the anterolateral (AL) and posteromedial (PM) papillary muscles (see Figure 1 A and B); II) the anteriorization of the anterolateral papillary muscle defined as the distance between the anterolateral papillary muscle and the anterior interventricular junction (Anteriorization of AL) (Fig. 1 C); III) the length of the anterior mitral leaflet (MVL length) (Fig. 1 D). All measurements were performed on cine-SSFP sequences in diastole. Results Compared to healthy controls, HCM and FD patients showed significant hypertrophy of both papillary muscles (p<0.001) and elongation of the anterior mitral leaflet (p<0.001). Both papillary muscles in FD patients showed greater hypertrophy compared to HCM patients (D max AL p=0.017 and D max PM p=0.039). No significant differences were observed between FD and HCM regarding MVL length (p=0.078). Compared to FD (p=0.028) and healthy controls (p<0.001), HCM patients showed greater anteriorization of the anterolateral papillary muscle. (Results are summarized in Table 1). Conclusions From the comparison of mitral valve apparatus anomalies between HCM and FD, it emerged that patients with FD cardiomyopathy show a higher degree of papillary muscle hypertrophy, while patients with sarcomeric HCM display a greater anterior displacement of the anterolateral papillary muscle. The systematic analysis of the morphology of mitral apparatus can be integrated in the differential diagnosis between these two pathologies.Fig.1 Representation of MeasurementsTable 1.Summary results table

Papillary Muscle Maneuvers: Pathophysiology-based Approach in Secondary Mitral Regurgitation.

The treatment of secondary mitral regurgitation (SMR) remains challenging despite the implementation of modern heart failure medication and established catheter-based techniques. Only a subgroup of SMR patients benefit from mitral valve (MV) intervention, and the long-term prognostic benefit of different therapeutic approaches in SMR remains controversial. A literature search was conducted through PubMed and Embase databases to identify relevant studies addressing the pathophysiological background for papillary muscle maneuvers in SMR and currently available surgical techniques. Furthermore, the studies evaluating patients' selection criteria for papillary muscle maneuvers were specifically considered. Articles were selected based on quality and relevance. Over the last two decades, papillary muscle maneuvers have evolved as a pathophysiology-based treatment strategy to address left ventricular (LV) remodeling in SMR. In particular, patients with severe leaflet tenting and moderate heart failure phenotype seem to benefit most from papillary muscle maneuvers that improve LV geometry and thereby the durability of MV repair. We conclude that papillary muscle maneuvers are an evolving pathophysiology-based treatment strategy of ventricular SMR which target papillary muscle displacement due to LV remodeling.

Association of Mitral Valve Geometry at CT with Secondary Mitral Regurgitation after Transcatheter Aortic Valve Replacement in Patients with Aortic Regurgitation.

The improvement rate and predictors of secondary mitral regurgitation in patients with aortic regurgitation undergoing transcatheter aortic valve replacement (TAVR) remain unclear. This study aimed to identify predictors of persistent moderate to severe secondary mitral regurgitation after TAVR in patients with aortic regurgitation by assessing mitral valve geometry with computed tomography (CT). This retrospective cohort study reviewed 242 consecutive patients with aortic regurgitation who underwent TAVR between May 2014 and December 2022. Patients with primary or less than moderate mitral regurgitation were excluded. Mitral annular dimensions (area, perimeter, anteroposterior, intercommissural, and trigone-to-trigone diameter), mitral valve tenting geometry (mitral valve tenting area [MVTA] and mitral valve tenting height [MVTH]), and papillary muscle displacement were systematically measured at CT. Mitral regurgitation improvement was assessed at 3 months after TAVR by echocardiography. Logistic regression was performed to explore the association of mitral valve geometry with mitral regurgitation improvement after TAVR. A total of 75 patients (mean age, 74 7 years; 32.0% female) with moderate to severe secondary mitral regurgitation were included in the final analysis. Mitral regurgitation improved in 49 patients and remained unchanged in 26 patients. Mitral annular dimensions, including area, perimeter, anteroposterior, and intercommissural diameter, were associated with mitral regurgitation improvement. MVTA and MVTH were risk factors for sustained mitral regurgitation. In addition, QRS duration 120 ms and atrial fibrillation had an impact on the mitral regurgitation improvement. Mitral annular area (odds ratio [OR], 1.41; 95% confidence interval [CI]: 1.05, 1.90; p = 0.02) and MVTA (OR, 7.24; 95% CI: 1.72, 30.44; p = 0.007) were independent predictors of persistent secondary mitral regurgitation after TAVR. Mitral annular area and MVTA were independent predictors of persistent secondary mitral regurgitation after TAVR.

Development and validation of an ex vivo porcine model of functional tricuspid regurgitation

Background and Aim: Ex vivo models of functional tricuspid regurgitation (FTR) are needed for pre-clinical testing of novel surgical and interventional repair strategies, but current options are costly or have not been formally validated. The objective of this research was to create and validate an ex vivo model to test novel repair methods for FTR. Methods: In explanted porcine hearts, the right atrium was excised to visualize the tricuspid valve. The pulmonary artery and aorta were clamped and cannulated, the coronary arteries ligated, and the right and left ventricles statically pressurized with air to 30 mmHg and 120 mmHg, respectively. FTR was induced by increasing right ventricular pressure to 80 mmHg for 3 h, which resulted in progressive tricuspid annular enlargement, right ventricular dilation, papillary muscle displacement, and central tricuspid malcoaptation. A structured light scanner was used to image the 3D topography of the tricuspid valve in both the native and FTR state, and images were exported into scan-to-computer-aided design software, which allowed for high-resolution 3D computational reconstruction. Relevant geometric measurements were sampled including annular circumference and area, major and minor axis diameter, and tenting height, angle, and area. Geometric measurements from the ex vivo model were compared to clinical transthoracic echocardiographic (TTE) measurements using two-sample t-tests. Results: A total of 12 porcine hearts were included in the study. Annular measurements of the native valve were comparable to published TTE data, except for the minor axis diameter, which was shorter in the ex vivo model (2.5 vs. 3.1 cm, P = 0.007). Induction of FTR in the ex vivo model resulted in annular enlargement (FTR vs. native: circumference 13.7 vs.11.8 cm, P = 0.012; area 14 vs. 11 cm2, P = 0.011). Ex vivo leaflet measurements in both the native and FTR model differed from published TTE data, but demonstrated comparable directional changes between the native and regurgitant states, including increased tenting height, area, and volume. Conclusion: The ex vivo pneumatically-pressurized porcine model closely recapitulates the geometry of both the native and regurgitant tricuspid valve complex in humans and holds promise for testing novel FTR repair strategies. Relevance for Patients: Currently available interventions for the tricuspid valve have a risk of permanent conduction abnormalities and are insufficient in addressing tricuspid disease for a subset of patients. This ex vivo model provides a platform for testing of novel interventions that address the deficiencies of current tricuspid therapies.

Echocardiographic quantification of mitral apparatus morphology and dynamics in patients with dilated cardiomyopathy.

Mitral regurgitation is among the most common valvular heart diseases. Mitral regurgitation in patients with dilated cardiomyopathy is a complex pathology involving annular dilatation, papillary muscle displacement, systolic leaflet tethering, and left ventricular remodeling. Quantification of mitral apparatus damage in these patients is essential for successful interventional and surgical therapy. Mitral regurgitation in the presence of dilated cardiomyopathy is classified as Carpentier type IIIB, with restricted leaflet mobility as a standard feature. Echocardiography allows accurate evaluation of the complex anatomy and function of the mitral apparatus. Updated guidelines recommend two-dimensional followed by systematic three-dimensional echocardiographic evaluation in patients with mitral regurgitation. New three-dimensional echocardiographic software packages provide many parameters that help identify the precise morphology and function of the various components of the mitral apparatus, helping to determine the etiology of mitral regurgitation and evaluate disease severity. This review provides the first point-by-point approach to the assessment of all old and new echocardiographic methods, from the simplest to the most complex, used to examine the components of the mitral valve apparatus in patients with dilated cardiomyopathy. Although these parameters are still under research, this information will be helpful for establishing therapeutic procedures in a disease with a poor prognosis.

Papillary muscle approximation in chronic ovine functional tricuspid regurgitation

ObjectiveIsolated tricuspid ring annuloplasty remains the surgical standard for functional tricuspid regurgitation repair but offers suboptimal results when right ventricular dilation and remodeling along with papillary muscle displacement is present. Addressing subvalvular remodeling with papillary muscle approximation may improve clinical outcomes. MethodsFunctional tricuspid regurgitation and biventricular dysfunction were induced in 8 healthy sheep by rapid ventricular pacing (200-240 bpm) for 27 ± 6 days. Subsequently, animals underwent cardiopulmonary bypass for implantation of sonomicrometry crystals on the tricuspid annulus, right ventricle, and papillary muscle tips. Papillary approximation sutures were anchored between anterior-posterior and anterior-septal papillary muscles and externalized through right ventricular free wall to epicardial tourniquets. After weaning from cardiopulmonary bypass, sequential papillary muscle approximations were performed. Simultaneous hemodynamic, sonomicrometry, and echocardiographic data were collected at baseline and after each papillary muscle approximation. ResultsWith rapid pacing, right ventricular fractional area change decreased from 59 ± 6% to 38 ± 8% (P < .001), whereas tricuspid annulus diameter increased from 2.4 ± 0.3 cm to 3.3 ± 0.6 cm (P = .003). Tricuspid regurgitation (0-4+) increased from +0 ± 0 to +3.3 ± 0.7 (P < .001). Both anterior–posterior and anterior–septal papillary muscle approximation significantly reduced functional tricuspid regurgitation from +3.3 ± 0.7 to +2 ± 0.5 and +1.9 ± 0.6, respectively (P < .001). Reduction of tricuspid insufficiency with both subvalvular interventions was associated with decreased distance of the anterior papillary muscle to the annular centroid. ConclusionsPapillary muscle approximations were effective in reducing severe ovine functional tricuspid regurgitation associated with right ventricular dilation and papillary muscle displacement. Further studies are needed to evaluate efficacy of this adjunct to ring annuloplasty in repair of severe functional tricuspid regurgitation.

Apical papillary muscle displacement is a prevalent feature and a phenotypic precursor of apical hypertrophic cardiomyopathy.

Papillary muscle (PM) abnormalities are considered part of the phenotypic spectrum of hypertrophic cardiomyopathy (HCM). The aim of this study was to evaluate the presence and frequency of PM displacement in different HCM phenotypes. We retrospectively analysed cardiovascular magnetic resonance (CMR) findings in 156 patients (25% females, median age 57 years). Patients were divided into three groups: septal hypertrophy (Sep-HCM, n = 70, 45%), mixed hypertrophy (Mixed-HCM, n = 48, 31%), and apical hypertrophy (Ap-HCM, n = 38, 24%). Fifty-five healthy subjects were enrolled as controls. Apical PM displacement was observed in 13% of controls and 55% of patients, which was most common in the Ap-HCM group, followed by the Mixed-HCM and Sep-HCM groups (respectively: inferomedial PM 92 vs. 65 vs. 13%, P < 0.001; anterolateral PM 61 vs. 40 vs. 9%, P < 0.001). Significant differences in PM displacement were found when comparing healthy controls with patients with Ap- and Mixed-HCM subtypes but not when comparing them with patients with the Sep-HCM subtype. T-wave inversion in the inferior and lateral leads was more frequent in patients with Ap-HCM (100 and 65%, respectively) when compared with Mixed-HCM (89 and 29%, respectively) and Sep-HCM (57 and 17%, respectively; P < 0.001 for both). Eight patients with Ap-HCM had prior CMR examinations because of T-wave inversion [median interval 7 (3-8) years], and in the first CMR study, none showed apical hypertrophy [median apical wall thickness 8 (7-9) mm], while all of them presented with apical PM displacement. Apical PM displacement is part of the phenotypic Ap-HCM spectrum and may precede the development of hypertrophy. These observations suggest a potential pathogenetic, mechanical link between apical PM displacement and Ap-HCM.

Abnormal Mechanics Relate to Myocardial Fibrosis and Ventricular Arrhythmias in Patients With Mitral Valve Prolapse.

The relation between ventricular arrhythmia and fibrosis in mitral valve prolapse (MVP) is reported, but underlying valve-induced mechanisms remain unknown. We evaluated the association between abnormal MVP-related mechanics and myocardial fibrosis, and their association with arrhythmia. We studied 113 patients with MVP with both echocardiogram and gadolinium cardiac magnetic resonance imaging for myocardial fibrosis. Two-dimensional and speckle-tracking echocardiography evaluated mitral regurgitation, superior leaflet and papillary muscle displacement with associated exaggerated basal myocardial systolic curling, and myocardial longitudinal strain. Follow-up assessed arrhythmic events (nonsustained or sustained ventricular tachycardia or ventricular fibrillation). Myocardial fibrosis was observed in 43 patients with MVP, predominantly in the basal-midventricular inferior-lateral wall and papillary muscles. Patients with MVP with fibrosis had greater mitral regurgitation, prolapse, and superior papillary muscle displacement with basal curling and more impaired inferior-posterior basal strain than those without fibrosis (P<0.001). An abnormal strain pattern with distinct peaks pre-end-systole and post-end-systole in inferior-lateral wall was frequent in patients with fibrosis (81 versus 26%, P<0.001) but absent in patients without MVP with basal inferior-lateral wall fibrosis (n=20). During median follow-up of 1008 days, 36 of 87 patients with MVP with >6-month follow-up developed ventricular arrhythmias associated (univariable) with fibrosis, greater prolapse, mitral annular disjunction, and double-peak strain. In multivariable analysis, double-peak strain showed incremental risk of arrhythmia over fibrosis. Basal inferior-posterior myocardial fibrosis in MVP is associated with abnormal MVP-related myocardial mechanics, which are potentially associated with ventricular arrhythmia. These associations suggest pathophysiological links between MVP-related mechanical abnormalities and myocardial fibrosis, which also may relate to ventricular arrhythmia and offer potential imaging markers of increased arrhythmic risk.

Subannular repair in secondary mitral regurgitation with restricted leaflet motion during systole

ObjectiveVentricular secondary mitral regurgitation (SMR) (Carpentier type IIIb) results from left ventricular (LV) remodelling, displacement of papillary muscles and tethering of mitral leaflets. The most appropriate treatment approach remains controversial....

Abstract 15014: Aberrant, Elevated Papillary Muscle and Left Ventricular Wall Forces Associated With Mitral Valve Prolapse Are Normalized by Surgical Neochordal Repair but Not by Transcatheter Edge-to-Edge Repair

Introduction: Recent studies have linked mitral valve prolapse (MVP) to localized myocardial fibrosis and ventricular arrhythmia, and early imaging work has shown altered ventricular motion with papillary muscle (PM) traction in MVP and MitraClip patients. We aimed to biomechanically compare MitraClip and neochordal repair for MVP on PM forces ex vivo . Methods: We developed a force transduction system to measure the forces exerted on the PMs throughout the cardiac cycle in a left heart simulator ( Fig A ) with consistent pressures. Using a randomized, paired procedure with porcine MVs (n=4), we measured the hemodynamics and forces for control, diseased (P2 prolapse via chordal rupture), MitraClip repair ( Fig B, C, D ) (single P2 clip), and neochordal repair (P2 primary neochord on each PM) conditions. Results: We found that MitraClip PM forces (7.19 ± 0.31 N) are higher by 9.34% compared with those of controls (6.58 ± 0.21 N, p&lt;0.001 ). This result is similar to MVP valves modeled by superior PM displacement, which showed 9.23% higher forces than those of controls (n=10, p&lt;0.001 ). Moreover, MitraClip repaired valves showed PM force increases of 6.4% compared with forces of neochordal repair (6.76 ± 0.22 N, p&lt;0.001 ), despite having similarly reduced regurgitation fractions (5.05% ± 1.98% vs. 4.25% ± 1.51%, respectively, p&gt;0.05 ) compared with those of the diseased state (16.96% ± 3.04%, p&lt;0.001 ) and controls (2.66% ± 0.87%). Additionally, neochordal repair valves had 2.79% higher forces compared to those of control valves ( p&lt;0.001 ). Conclusions: We discovered that MitraClip, while reducing regurgitation, does not restore aberrant forces on the PM induced in MVP to baseline or reduced levels, while neochordal repair does. Our work suggests that these elevated forces, associated with MVP and MitraClip, predisposes the MV to continued traction, which may present a long-term harm to patients by catalyzing localized fibrosis and ventricular arrhythmia.

Different mechanisms of mitral regurgitation in hypertrophic cardiomyopathy: A clinical case and literature review.

Abnormalities of the mitral valve (MV) apparatus are typical features of hypertrophic cardiomyopathy (HCM). These abnormalities include leaflet elongation, thick leaflets, displacement of papillary muscle, and systolic anterior motion (SAM) of the MV anterior leaflet. Mitral valve chordal rupture associated with HCM is a rare but serious issue capable of change the clinical apparence and the prognosis of the patient. A 57-year-old lady with a history of diabetes, dyslipidemia, and a previous single episode of atrial fibrillation (treated with pharmacological cardioversion), presented to the Emergency Department for worsening dyspnea (New York Heart Association Classification class IV). A trans-thoracic echocardiogram (TTE) showed a significant, septal, and asymmetric left ventricular hypertrophy (basal anteroseptal wall diastolic thickness of 19 mm) with normal left ventricle systolic function. A SAM of AML was evident together with a left ventricular outflow tract gradient of 56 mmHg at rest, rising to 136 mmHg during the Valsalva maneuver. In addition, there was evidence of moderate to severe mitral regurgitation (MR) with an anteriorly directed jet, not very typical of MR related to SAM. A 2D-3D trans-esophageal echocardiogram (2D-3D TEE) revealed a combined MR mechanism based on PML degenerative prolapse with P2-flail from ruptured chordae with related eccentric anteriorly directed regurgitant jet, together with a second regurgitant posteriorly directed jet, related to SAM of AML. The patient underwent MV repair together with septal myectomy, with a good final outcome. Pre-operative echocardiography (both TTE and 2D-3D TEE) is an essential tool in order to detect different MV abnormalities in patients with HCM. These types of patients should never be treated by septal reduction alone. Surgical MV repair or replacement, together with septal myectomy, may be the preferred approach.

ISCHEMIC MITRAL REGURGITATION - TO REPAIR OR REPLACE? LOOKING BEYOND THE VALVE.

Ischemic mitral regurgitation (IMR) is a frequent and serious complication of coronary artery disease, associated with considerable patient increased mortality and morbidity. While the benefits of optimal medical therapy and surgical revascularization, when indicated, are uncontested in moderate to severe cases, the ideal surgical approach to the valve, if any, is yet to be established. Mitral valve repair has established benefits over replacement in primary mitral regurgitation, but its superiority in the treatment of functional regurgitation has not been replicated. Differing outcomes likely stem from the distinct IMR pathophysiology. Unlike its degenerative counterparts, IMR does not derive from direct damage to the valve leaflets, but rather from dysfunction of its sub-valvular apparatus and the left ventricular wall, in the context of acute or chronic ischaemia. Echocardiographic data points to remodelling of the left ventricle, with subsequent papillary muscle displacement, increased leaflet tethering and inefficient coaptation, as the main responsible mechanism for ischemic mitral regurgitation. Neither mitral valve repair nor replacement directly address these issues, with the appearance of the first randomized trials supporting replacement as the more durable option. However, new subvalvular procedures are improving the stability of repair techniques and the debate is long from settled. The purpose of this review is to analyse the currently available data, couple it with our understanding of IMR's pathophysiology and compare the different outcomes for mitral valve repair and replacement.

Changes in Mitral Valve Apparatus with Continuous Flow LVAD

<h3>Purpose</h3> The purpose of this research was to study the changes in mitral valve apparatus after placement of continuous flow LVAD. These data can help determine if additional mitral valve intervention is needed at the time of LVAD placement. <h3>Methods</h3> A retrospective review of data of all the LVAD placed in the hospital from 2012 through March 31^st 2020 were done. Demographic, clinical variables and clinical outcomes were obtained from electronic medical records. The echocardiographic variables were obtained by two authors with standardized guidelines agreed upon before initiation of the study; this required review of all the images and identification of some unique variables dedicated to the study of mitral valve apparatus. The echocardiogram performed closest before LVAD placement and the last echocardiogram performed within one year after LVAD placement were evaluated to allow reflection of the worst pre-LVAD and the best post-LVAD state of the mitral valve apparatus. <h3>Results</h3> Of total of 145 patients who had LVAD during the study period, 88 patients were identified with pre-specified minimum available echocardiographic variables. 9 did not have significant pre-existing mitral regurgitation (MR). 69 patients had improvement from "moderate or severe" to "mild or none". 10 patients did not show any improvement in the severity of MR: 8 from mild and 2 from moderate MR. All severe MR improved. The changes in mitral valve apparatus included (all reduction): left ventricular end diastolic dimension by 9 (+/-14.98) mm; left atrial volume index by 16.2 (+/- 14.73) ml/m2; annulus size by 5 (+/- 7.94) mm; apical displacement by 2 (+/- 3.91) mm; posterior displacement by 2 (+/- 4.7) mm; tethering area by 85 (+/- 104.94) mm2 and papillary muscle displacement by 2 (+/- 9.55) mm. Changes in mitral valve apparatus were similar in those who had improvement of MR or not except the reduction in posterior displacement happened more in those who had improvement in MR severity. <h3>Conclusion</h3> Continuous flow LVAD favorably improves mitral valve apparatus and MR severity. Prevalence of clinically significant residual MR is low. More data is needed to understand the changes in mitral valve apparatus and guide if any concomitant mitral valve intervention is needed with LVAD placement.

Efficacy of a Novel Posterior Leaflet Repair Device to Treat Secondary Mitral Regurgitation Using an Ex Vivo Heart Model

Mitral regurgitation is one of the most prevalent valvular disorders. It has numerous etiologies grouped as primary typically because of underlying degenerative leaflet disease, or secondary mitral regurgitation (SMR), most commonly because of geometrical distortion of the left ventricle (LV) impacting the functional integrity of the valvular apparatus.1 Specifically for SMR, LV dilation and dysfunction lead to papillary muscle displacement, annular dilation, and apical tethering of the leaflets with restricted mobility, predominantly affecting the posterior leaflet.

Echocardiographic characteristics of non‐resectional ring‐only valve repair in mitral valve prolapse

AbstractBackgroundSimple mitral valve repair (MVR) using a ring‐only approach (ROA) was recently proposed for some complex forms of bileaflet myxomatous mitral valve prolapse (MVP). Nevertheless, few data are available concerning the characteristics of MVP patients that may benefit from this simple repair technique.MethodsBased on 39 consecutive patients (28 men; mean age 57 ± 15) with severe primary Mitral regurgitation (MR) caused by bileaflet MVP referred for MVR, we sought to identify the preoperative echocardiographic parameters associated with successful ROA repair.ResultsTwenty‐three patients (59%) underwent standard resectional MVR (SMVR) while 16 (41%) underwent ROA. Cardiopulmonary bypass and cross clamp times were lower in ROA than in SMVR (74 ± 27 min vs 99 ± 42 min and 49 ± 19 min vs 70 ± 25 min, respectively, p = 0.03 and p = 0.005). ROA patients were more frequently women (50% vs 13%, p = 0.027). Echocardiographic characteristics of successful ROA were mid‐late systolic MR, a paradoxical systolic papillary muscle displacement, and paradoxical systolic annulus expansion (PAE). A prolapsing depth &lt;10 mm, the absence of flail leaflet and ruptured chordae, the presence of multiple jets, more often in the central part of the valve were also associated with ROA. Non hemodynamic systolic anterior motion and residual trivial MR tended to be more frequent in ROA than in SMVR.ConclusionSimple and fast MVR using a ROA is feasible in 4/10 patients with complex forms of bileaflet MVP. Successful ROA patients were more frequently women, with mid‐late systolic central multiple jet, low prolapse depth, absence of chordal rupture or flail leaflet and PAE.

Geometric differences of the mitral valve apparatus in atrial and ventricular functional mitral regurgitation

BackgroundFunctional mitral regurgitation (FMR) occurs in patients with annular dilation (atrial, aFMR) or patients with left ventricular (LV) disease (ventricular, vFMR). Meticulous understanding of the mechanisms underpinning regurgitation is crucial to optimize therapeutic strategies. MethodsPatients with moderate-severe FMR were identified from a registry of patients referred for transcatheter mitral valve intervention. In addition, controls without cardiovascular disease were identified. Differences in the geometry of the LV and mitral valve apparatus (including leaflet and tenting geometry, papillary muscle displacement and movement, annular dimensions, and dynamism) between atrial and ventricular FMR, and control subjects, were assessed using multiphasic cardiac CT. ResultsOf 183 FMR patients, 18 patients (10%) were found to have aFMR. The remaining patients had either ischemic or non-ischemic ventricular FMR. In aFMR, both increasing LV end-systolic volume (rho 0.701, p ​< ​0.01) and left atrial volume (rho 0.909, p ​< ​0.01) were associated with larger annular area. By contrast, in vFMR larger annular area was most strongly associated with larger left atrial volume (rho 0.63, p ​< ​0.01). In controls, increased annular area was associated with larger LVEDV (rho 0.78, p ​< ​0.01) and LVESV (rho 0.824, p ​< ​0.01), but not left atrial size (rho 0.16, p ​= ​0.45).Ventricular FMR comprised apicolaterally displaced, akinetic posteromedial papillary muscles, resulting in pronounced leaflet tethering, leaflet elongation compared to controls, and only modest relative LA dilatation. Compared to vFMR, aFMR was characterised by marked relative annular dilation, smaller but discernible mitral valve tenting, shorter leaflet lengths when related to annular size, but normal papillary geometry. ConclusionFMR is characterised by multiple changes within the mitral valve complex. Atrial and ventricular FMR differ significantly in terms of the drivers of annular size, and geometry and function of the subvalvular apparatus. This highlights the need to consider these as separate disease entities.

Mitral Valve Translocation: Optimization of Patch Geometry in an Ex Vivo Model of Secondary Mitral Regurgitation.

Optimal translocation patch width for functional mitral regurgitation (FMR) treatment was evaluated in an air-filled ex vivo system. FMR was created in 19 isolated swine hearts by annular dilation and papillary muscle displacement. Frustum-shaped pericardial patches of varying widths (Group 1 = 0.5cm; Group 2 = 1.0cm; Group 3 = 1.5cm) were implanted and imaged via a 3D-structured light scanner. Median leaflet coaptation decreased (P < 0.001) from 5.5 ± 2.0mm at baseline to 2.4 ± 1.3mm following FMR creation. Translocation repair increased coaptation length over FMR levels by 2.2mm in Group 1 (P < 0.001), 4.6mm in Group 2 (P < 0.001), and 4.7mm in Group 3 (P < 0.001). After repair, no significant differences were found between groups for annular height, circularity index, tenting height, tenting area, and non-coapting surface area. The supranormal coaptation and minimal valve geometric changes support using a 1.0- or 1.5-cm translocation patch for FMR treatment. Implantation of a 1.0-cm or 1.5-cm circumferential pericardial patch (mitral valve translocation) increases leaflet coaptation length without significantly altering valve geometry.

Transcatheter mitral valve repair (TMVR) using MitraClip in patients younger than 65 years: a multicenter analysis of 2-years outcomes

Abstract Background TMVR using MitraClip became a well-established interventional therapy for severe MR. However, TMVR has been almost only applied to old aged patients rejected from surgical therapy. Objective To present 2-years outcomes of 36 patients younger than 65 years with no surgical options treated by TMVR. Methods A retrospective clinical and TEE study was conducted to evaluate 36 patients younger than 65 years treated by TMVR in 3 heart centers. Results Mean age of the 36 study patients was 56.3±6.6 years, male gender was 72.2%. High operative risk was estimated by STS score (mean = 8.73±2.97) and EuroSCORE (mean = 24.71±12.79). All patients were refused for surgery by heart team decision, therefore admitted to TMVR. Baseline severity of MR was assessed by 3D-TEE based biplane vena contracta width (mean = 8.35±1.87 mm). Baseline transmitral mean pressure gradient was 1.81±0.78 mmHg. 21 patients showed mitral annular dilatation as the main cause of MR, 8 patients had leaflet prolapse, 4 patients exhibited papillary muscle displacement leading to leaflet tethering and 3 patients showed mitral leaflet thickening and/or retraction due to fibrosis. Procedural success was achieved in all patients with 1/2/3 clips implanted in 52.8%/44.4%/2.8% of cases with a mean of 1.5 clip per case. Two grades or more reduction in severity of MR (MR grade ≤ II/IV) was accomplished in 88.9% of patients. Mean postprocedural MPG was 3.78±1.96 mmHg. Average follow-up (FU) period was 25,8 months and the median was 20 months (25th–75th percentile: 12–36 months). During 2-years FU, statistically significant difference (p value &amp;lt;0.002) was detected for NT-proBNP levels compared to baseline (mean = 9870±10819, median = 7748, 25th–75th percentile: 2702–14237 pg/ml) and at follow up visits (mean = 7645±11292, median = 3263, 25th-75th percentile: 883–8078 pg/ml). Furthermore, persistent symptomatic improvement during FU, defined as NYHA functional class improvement by 2 or more Grades, was achieved in 69% of patient in parallel with efficient reduction of MR in 34 patients so that a second intervention by reclipping was required in 2 patients to correct recurrent significant MR. Only two patients experienced procedure-related complications by large puncture site hematoma. No procedure-related mortality during the first 30 days was detected. However, mortality was recorded in 2 patients during the first month and was attributed to severe advanced heart failure in one case and septicemia after exclusion of infective endocarditis in another case. Over 2 years FU, other 5 patients passed away, 3 cases owing to advanced heart failure, one case due to multi-organ failure and one because of tumor disease. Conclusion TMVR in patients younger than 65 years refused from surgical repair provides satisfactory clinical and echocardiography outcomes at 2 years. Future studies should evaluate the outcomes of MitraClip in this population in a larger cohort. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Hassan M.H. Mohammed received a scholarship grant from the Egyptian ministry of higher education and Minia University, Egypt.

Surgical Treatment of Left Ventricular Aneurysm Combined with Ischemic Mitral Regurgitation Using a Modified Technique

Background. Ischemic mitral regurgitation (IMR) is the second most common cause of mitral regurgitation (MR). IMR occurs in patients with myocardial infarction due to a rupture of the subvalvular apparatus. Pathological remodel-ing, dilatation and dysfunction of the left ventricle (LV) play a significant role in the development of IMR. The presence of a postinfarction LV aneurysm can lead to the development of MR due to dysfunction, relative and true shortening of the papillary muscles. There are various methods of surgical correction of IMR. The aim. To show the effectiveness of surgical treatment of left ventricular aneurysm combined with ischemic mitral regurgitation using a modified technique. Materials and methods. From January 2011 to December 2019, 20 patients with IMR combined with LV aneurysm underwent surgical intervention using a modified technique at the National Amosov Institute of Cardiovascular Surgery of the NAMS of Ukraine. According to this technique, access to the mitral valve was performed through the left ventricle. The mean age of the patients was 61.2 ± 10.1 years. Among patients with IMR, the majority were men (60.0%). The overwhelming majority of patients (80.0%) had the history of hypertension. Diabetes mellitus was detected in 35.0% of patients. Mitral ring dilatation was observed in 25.0% (5) of the cases, papillary muscle displacement in 40.0% (8), chords rupture in 15.0% (3), papillary muscle infarction in 20.0% (4) of the cases. All the patients had reduced LV ejection fraction with a mean value of 34.5 ± 7.8%. Results. Aortic cross-clamp time through ventricular access was 112.9 ± 18.7 minutes. The duration of mechanical ventilation was 19.1 ± 20.6 hours. The length of stay of patients in the ICU was 99.2 ± 43.5 hours. There were no signs of acute heart failure in the early postoperative period in one in five patients (20.0%). The rate of degree III heart failure after intervention using the modified technique was 20.0% (4). The study of the incidence of cardiac arrhythmias after combined intervention showed that 85.0% (17) of patients operated using the modified technique had no cardiac arrhythmias. Conclusions. In patients who underwent surgery using the modified technique, the mortality rate was 5.0%. This is 1.6-2.8 times less than that in patients undergoing conventional operation. Postoperative occurrence of arrhythmias is much less common than that described in the literature.