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Background: 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. Methods: 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). Results: 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 P 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. Conclusions: 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.

OBJECTIVES Patients undergoing surgical mitral valve repair (MVr) for degenerative mitral regurgitation are at risk of even late postoperative atrial fibrillation (AF). Left atrial (LA) function has been shown superior to LA volume in evaluating the risk of AF in diverse cardiac conditions. We therefore investigated the prognostic value of LA function and volume in predicting mid-to-late postoperative AF after MVr (>30 days postoperatively). METHODS We retrospectively identified all patients who underwent MVr for degenerative mitral regurgitation between 2012 and 2019 at our institution. Exclusion criteria were preoperative AF, concomitant procedures, re-operations, missing or insufficiently processable preoperative echocardiograms and missing follow-up. LA function and volume measurements were conducted using speckle-tracking strain echocardiographic analysis. Postoperative LA function was measured in a subgroup with sufficient postoperative echocardiograms. RESULTS We included 251 patients, of whom 39 (15.5%) experienced AF in the mid-to-late postoperative period. Reduced LA strain parameters and more than mild preoperative tricuspid regurgitation were independently associated with mid-to-late postoperative AF. LA volume index had no association with mid-to-late postoperative AF in univariable analysis and did not improve the performance of multivariable models. Patients with mid-to-late AF exhibited diminished improvement in LA function after surgery. CONCLUSIONS In MVr patients, LA function (but not volume) showed independent predictive value for mid-to-late postoperative AF. Including LA function into surgical decision-making and approach may identify patients who will benefit from earlier intervention with the aim to prevent irreversible LA damage with consequent risk of postoperative AF.

The prevalence of mitral annular calcium (MAC) is increasing in our aging population. However, data regarding prognostication in MAC-related mitral valve (MV) disease remain limited. This retrospective observational study aims to explore the prognostic impact of systolic pulmonary artery pressure (SPAP) in MAC-related MV dysfunction and define its determinants. We identified 4,384 patients (mean age 78 ± 11 years and 69% female) with MAC-related MV dysfunction (documented transmitral gradient ≥3 mm Hg) from a large institutional echocardiographic database between 2001 and 2019. In Cox regression analysis, higher SPAP strongly associated with all-cause mortality, independent of cardiovascular risk factors and indices of MV dysfunction (adjusted hazard ratio 1.22 per 10 mm Hg SPAP increase, 95% confidence interval 1.17 to 1.27). Patients with SPAP ≥50 mm Hg had significantly higher mortality compared with SPAP50 mm Hg (log-rank p0.001), a finding that was consistent across different transmitral gradient subgroups (≤5, 5 to 10, and ≥10 mm Hg). Independent determinants of SPAP included the mean transmitral gradient, mitral regurgitation severity, left ventricular ejection fraction, and ≥moderate aortic stenosis (adjusted p0.05), and atrial fibrillation and left atrial dimension. The impact of concomitant mitral regurgitation on SPAP decreased at higher transmitral gradients and was no longer significant at gradients ≥10 mm Hg (p = 0.100). In conclusion, SPAP strongly associates with mortality in MAC, independent of cardiovascular risk factors and indices of MAC-related MV dysfunction. These findings suggest an incremental role for SPAP in the risk stratification and prognostication in this increasingly prevalent condition with expanding the scope of possible interventions.

BACKGROUND: Evaluation of aortic stenosis (AS) requires calculation of the aortic valve area (AVA), which relies on the assumption of a circular-shaped left ventricular outflow tract (LVOT). However, the LVOT is often elliptical, and the circular assumption underestimates the true LVOT area. Biplane imaging using transthoracic echocardiography (TTE) allows for direct planimetry of the LVOT area. We aim to assess the feasibility of obtaining LVOT area by this technique, and its impact on the discordance between AVA and gradient criteria in AS grading. METHODS: We prospectively studied 134 patients (median age 80 years, interquartile range (IQR) 73–87 years; 39% female) with AS, including 82 (61%) with severe AS and 52 (39%) with mild or moderate AS. LVOT area was traced by direct planimetry (LVOTA(biplane)) and compared with LVOT area calculated by circular assumption (LVOTA(circ)). In a subset of patients who underwent cardiac computed tomography (CT), direct planimetry of LVOT area (LVOTA(CT)) was used as a reference standard. RESULTS: LVOTA(biplane) was significantly larger than LVOTA(circ) (4.20 cm(2) (IQR 3.66–4.90 cm(2)) vs 3.73 cm(2) (IQR 3.14–4.15 cm(2)), p < 0.001). Among 30 patients who underwent cardiac CT, LVOTA(biplane) had better agreement with LVOTA(CT) than LVOTA(circ) (mean bias −0.45 ± 0.63 cm(2) vs −1.02 ± 0.63 cm(2), p < 0.0001). Of 82 patients with severe AS (AVA ≤ 1 cm(2) using LVOTA(circ)), 40 (49%) had discordant mean gradient (MG < 40 mmHg). By using LVOTA(biplane), patients with discordant AVA and MG decreased from 49% to 27% (p = 0.004), and 29% of patients with severe AS were reclassified as moderate AS, with the highest percentage of reclassification in the low-gradient AS with preserved left ventricular ejection fraction group. CONCLUSIONS: Direct planimetry by biplane imaging avoids the inherent underestimation of LVOT area using the circular assumption. LVOT area obtained by biplane planimetry can lead to better concordance between AVA and MG, and classification of AS severity.

Background To review the efficacy of a minimally invasive surgical technique for mitral valve (MV) repair, we analyzed a nonresectional technique for degenerative mitral regurgitation. Methods A retrospective analysis was performed on 101 consecutive patients who underwent a minimally invasive MV repair for severe degenerative mitral regurgitation between 2014 and 2017. All patients underwent a right lateral minithoracotomy and femoral cannulation and were repaired by a nonresectional technique using neochord loop implantation and ring annuloplasty. Patients were followed with longitudinal echocardiograms. Results The median age was 58 years (interquartile range [IQR], 49-64), and 31% were women. The procedure was successfully performed using a right minithoracotomy in all patients except for 1 who required an extended thoracotomy. A median of 4 neochords were placed. The median length was 16 mm (IQR, 14-18), and ring size was 34 mm (IQR, 32-36). Concomitant procedures included left atrial appendage exclusion in 10 patients (10%) and patent foramen ovale closure in 13 (13%). Median cardiopulmonary bypass time was 152 minutes (IQR, 142-164), and aortic cross-clamp time was 90 minutes (IQR, 81-98). Operative mortality was 0% and 1-year survival 100%. At 3 years freedom from recurrent at least moderate mitral regurgitation was 100%, and no patient required a valve-related reoperation. At 1 year the median left atrial diameter decreased by 15% (44 vs 37 mm, P Conclusions Minimally invasive MV repair using a nonresectional technique can be performed for severe degenerative mitral regurgitation with a low complication rate, excellent durability, and promising left ventricular reverse remodeling.

Background Left atrial appendage closure (LAAC) is an alternative to long-term anticoagulation for thromboembolic protection in patients with atrial fibrillation (AF) and high bleeding risk. Short-term Warfarin use following LAAC is well-studied, while data pertaining to novel oral anticoagulant (NOAC) use in this setting is less robust. Specifically, data regarding the safety and efficacy of postprocedural NOAC use in high-risk patients is lacking. Objective To compare the safety and efficacy of Warfarin and NOAC use in a high-risk patient population undergoing LAAC with the WATCHMAN device. Methods From November 2015 to October 2017, 97 patients underwent LAAC with the WATCHMAN device. All patients were discussed at a multidisciplinary meeting prior to device implantation. Longitudinal data were collected and analyzed for a composite endpoint of stroke and death at 8 months, and major bleeding at 3 and 6 months. Results Among the 90 patients included in the safety and efficacy analysis, 43 were prescribed Warfarin and 47 were prescribed NOACs. Baseline characteristics were comparable between study groups. There were no procedural complications and no significant differences in the incidence of death and stroke at 8 months or major bleeding at 3 and 6 months. Conclusion For patients with AF at high risk of both thromboembolic and hemorrhagic events, NOACs as compared to Warfarin, seem to be safe and effective for short-term anticoagulation following LAAC with the WATCHMAN device. Further validation in large randomized controlled trials is required.

Background: Surgical or percutaneous occlusion of the left atrial appendage (LAA) is increasingly used for thromboembolic protection in atrial fibrillation. Incomplete LAA closure may increase risk of thrombosis and thromboembolism, and therefore approaches to address residual communications are needed. Objective: To analyze the technique of closing an incompletely occluded LAA and subsequent patient outcomes. Methods: We performed a retrospective analysis of 5 consecutive patients who presented for completion of LAA closure. Results: Four patients were male, mean age 75, average CHA2DS2-VASc score 5.4, and four had prior surgical LAA ligation. One patient had previously had a WATCHMAN device placed for whom a 3D printed model was created from preprocedural imaging data to guide Amplatzer occluder device selection for closure. The residual LAA communication maximal diameter averaged 6.2 mm (range 5-8mm). In 4 of 5 cases, an ablation catheter was used to enter the LAA. The residual LAA communication was closed with either an Amplatzer occluder (n=3) or a WATCHMAN device (n=2). No procedural complications occurred, and no residual leak remained afterwards. No neurologic events occurred during follow up (average 603 days, range 155-1177 days). Anticoagulation or dual antiplatelet therapy was stopped following a transesophageal echo (TEE) ³ 6 weeks after the procedure demonstrated no residual communication in 4 of 5 patients, and after 20 weeks in the fifth patient without a follow up TEE. Conclusion: Large residual LAA communications after LAA occlusion attempts can be successfully and safely closed percutaneously using either Amplatzer occluder devices or WATCHMAN devices.

Introduction: Acute rheumatic fever (ARF) results from autoimmune responses to group A streptococcus. ARF can cause chronic rheumatic heart valve disease (RHVD), a major public health burden in low- and middle-income countries. Although ARF affects both sexes equally, females have a higher prevalence of RHVD. We identified a target protein, ProTα, that may contribute to pathophysiology of and gender predisposition in RHVD. Estradiol regulates ProTα, which influences transcriptional activity of the estrogen receptor (ER). Methods: Human heart valves (n=120) obtained from heart transplantation and valve replacement surgeries, including non-diseased mitral and aortic valves (NDMV and NDAV, n=17/group), rheumatic mitral and aortic valves (RMVD, n=45; RAVD, n=8) and calcifying valves from patients with calcific aortic valve disease (CAVD, n=33) underwent proteomic and network analyses, and immunohistochemical assessment of CD68, CD4, CD8 and ProTα. ProTα levels were measured in plasma and peripheral mononuclear cells (PBMCs) from RHVD patients and healthy donors (n=14/group) by ELISA and flow cytometry. Results: A comparison of proteomes from NDMV and NDAV established the baseline differences between valve types. 12 proteins were enriched (q Conclusion: We propose that ProTα is a novel contributor to the immunopathogenesis of RHVD and may regulate sex predisposition in this disease.

Infective endocarditis (IE), including prosthetic valve and device infections, are highly morbid conditions with a diversity of clinical presentations, etiologies, and complications. Due to changing patterns of antibiotic resistance and an increasingly complex patient population, there has been a shift to managing this disease with a multidisciplinary team including cardiologists, surgeons, microbiologists, infectious disease specialists, and neurologists.

To provide a new and practical approach for clinicians assessing and managing patients with low-gradient severe aortic stenosis (AS) using recent data highlighting the importance of transvalvular flow rate in AS assessment. Recent data have highlighted the unifying underpinning of low-gradient severe AS to be low transvalvular flow rate, and shown the impact that flow rate has on diagnostic and prognostic utility in AS. Additional developments in echocardiographic measurement technique and non-echocardiographic modalities have also been made which can help tackle this clinical conundrum. Low-gradient severe AS is a challenging condition to diagnose and manage. Here we provide a new approach using transvalvular flow rate, with a practical clinically oriented guide, and a summary of recent evidence.

The aim of this study was to assess the incidence, mechanisms, and outcomes of mitral regurgitation (MR) after percutaneous mitral valvuloplasty (PMV).Significant MR continues to be a major complication of PMV, with a wide range in clinical presentation and prognosis.Consecutive patients with mitral stenosis undergoing PMV were prospectively enrolled. MR severity was evaluated by using quantitative echocardiographic criteria, and its mechanism was characterized by 3-dimensional transesophageal echocardiography, divided broadly into 4 categories based on the features contributing to the valve damage. B-type natriuretic peptide levels were obtained before and 24 h after the procedure. Endpoints estimated cardiovascular death or mitral valve (MV) replacement due to predominant MR.A total of 344 patients, ages 45.1 ± 12.1 years, of whom 293 (85%) were women, were enrolled. Significant MR after PMV was found in 64 patients (18.6%). The most frequent mechanism of MR was commissural, which occurred in 22 (34.4%) patients, followed by commissural with posterior leaflet in 16 (25.0%), leaflets at central scallop or subvalvular damage in 15 (23.4%), and central MR in 11 (17.2%). During the mean follow-up period of 3 years (range 1 day to 10.6 years), 60 patients reached the endpoint. The event-free survival rates were similar among patients with mild or commissural MR, whereas patients with damaged central leaflet scallop or subvalvular apparatus had the worst outcome, with an event-free survival rate at 1 year of only 7%. Long-term outcome was predicted by net atrioventricular compliance (CSignificant MR following PMV is a frequent event, mainly related to commissural splitting, with favorable clinical outcome. Parameters that express the relief of valve obstruction and the mechanism by which MR develops were predictors of long-term outcomes.

Rheumatic mitral stenosis remains a common disease in the developing world. Percutaneous mitral balloon valvuloplasty is an important therapy for rheumatic mitral stenosis. Echocardiography plays a critical role in the diagnosis of rheumatic mitral stenosis and the assessment of suitability for and guidance of percutaneous mitral valvuloplasty.

Aims Secondary mitral regurgitation (MR) drives adverse remodelling towards late heart failure stages. Little is known about the evolution of MR under guideline-directed therapy (GDT) and its relation to cardiac remodelling and outcome. We therefore aimed to assess incidence, impact, and predictors of progressive secondary MR in patients under GDT. Methods and results We prospectively enrolled 249 patients with chronic heart failure and reduced ejection fraction receiving GDT in this long-term observational study. Of patients with non-severe MR at baseline 81% remained stable whereas 19% had progressive MR. Those patients were more symptomatic (P

IMPORTANCE: Pulmonary hypertension (pHTN) is associated with increased risk of mortality after mitral valve surgery for mitral regurgitation. However, its association with clinical outcomes in patients undergoing transcatheter mitral valve repair (TMVr) with a commercially available system (MitraClip) is unknown. OBJECTIVE: To assess the association of pHTN with readmissions for heart failure and 1-year all-cause mortality after TMVr. DESIGN, SETTING, AND PARTICIPANTS: This retrospective cohort study analyzed 4071 patients who underwent TMVr with the MitraClip system from November 4, 2013, through March 31, 2017, across 232 US sites in the Society of Thoracic Surgery/American College of Cardiology Transcatheter Valve Therapy registry. Patients were stratified into the following 4 groups based on invasive mean pulmonary arterial pressure (mPAP): 1103 with no pHTN (mPAP

See Article by Nishino et al Ischemic mitral regurgitation (IMR) is a common complication of ischemic heart disease that doubles mortality after myocardial infarction (MI) and is a major driving factor increasing heart failure.1,2 IMR is caused by post-MI left ventricle (LV) remodeling: inferior wall bulging displaces the papillary muscle, tethering the leaflets into the LV cavity, and restricting their closure.3 The mitral valve (MV) has been thought of as an unchanging structure. However, its ability to adapt to expansion of the remodeling LV is increasingly recognized.4–7 Although mechanically displacing the papillary muscles without MI causes compensatory MV growth,8 this adaptive process is altered in the infarcted ventricle by excessive profibrotic processes, impairing closure, and augmenting MR.9–11 There is a need to understand the timing of compensatory valve growth versus counterproductive fibrosis and the potential effects of therapy on these competing processes.12 IMR can vary from early post-MI to the chronic stage, but previous studies have mainly focused on IMR in the subacute or chronic setting, and little is known about the mechanism of acute IMR. The study by Nishino et al13 in this issue of Circulation: Cardiovascular Imaging provides new insights into the mechanism of acute IMR. This sophisticated 3-dimensional echocardiographic study included 80 patients with significant IMR (44 patients with acute IMR; 36 with chronic IMR) compared with 3 …

After myocardial infarction (MI), mitral valve (MV) tethering stimulates adaptive leaflet growth, but counterproductive leaflet thickening and fibrosis augment mitral regurgitation (MR), doubling heart failure and mortality. MV fibrosis post-MI is associated with excessive endothelial-to-mesenchymal transition (EMT), driven by transforming growth factor (TGF)-β overexpression. In vitro, losartan-mediated TGF-β inhibition reduces EMT of MV endothelial cells.This study tested the hypothesis that profibrotic MV changes post-MI are therapeutically accessible, specifically by losartan-mediated TGF-β inhibition.The study assessed 17 sheep, including 6 sham-operated control animals and 11 with apical MI and papillary muscle retraction short of producing MR; 6 of the 11 were treated with daily losartan, and 5 were untreated, with flexible epicardial mesh comparably limiting left ventricular (LV) remodeling. LV volumes, tethering, and MV area were quantified by using three-dimensional echocardiography at baseline and at 60 ± 6 days, and excised leaflets were analyzed by histopathology and flow cytometry.Post-MI LV dilation and tethering were comparable in the losartan-treated and untreated LV constraint sheep. Telemetered sensors (n = 6) showed no significant losartan-induced changes in arterial pressure. Losartan strongly reduced leaflet thickness (0.9 ± 0.2 mm vs. 1.6 ± 0.2 mm; p 0.05; 0.4 ± 0.1 mm sham animals), TGF-β, and downstream phosphorylated extracellular-signal-regulated kinase and EMT (27.2 ± 12.0% vs. 51.6 ± 11.7% α-smooth muscle actin-positive endothelial cells, p 0.05; 7.2 ± 3.5% sham animals), cellular proliferation, collagen deposition, endothelial cell activation (vascular cell adhesion molecule-1 expression), neovascularization, and cells positive for cluster of differentiation (CD) 45, a hematopoietic marker associated with post-MI valve fibrosis. Leaflet area increased comparably (17%) in constrained and losartan-treated sheep.Profibrotic changes of tethered MV leaflets post-MI can be modulated by losartan without eliminating adaptive growth. Understanding the cellular and molecular mechanisms could provide new opportunities to reduce ischemic MR.

Pulmonary hypertension (pHTN) is associated with increased mortality after mitral valve surgery for mitral regurgitation. However, its prognostic impact on patients undergoing transcatheter mitral valve repair with MitraClip is unknown. We sought to assess the impact of pHTN on 1-year all-cause

Aortic valve area (AVA) and LV stroke volume index (SVi) calculations assume a circular-shaped LV outflow tract (LVOT). However, the LVOT is often ellipsoid rather than circular, resulting in underestimation of the true LVOT area. Biplane imaging of LVOT allows direct planimetry of LVOT area. We

Symptomatic severe aortic stenosis (AS) is associated with dismal prognosis without aortic valve replacement (AVR), yet the utilization of AVR within the transcatheter AVR era has not been examined. Consecutive patients with high gradient severe AS (aortic valve area [AVA] ≤1 cm2and mean aortic

The mitral valve apparatus is a complex 3-dimensional (3D) functional unit that is critical to unidirectional heart pump function. This review details the normal anatomy, histology, and function of the main mitral valve apparatus components: mitral annulus, mitral valve leaflets, chordae tendineae, and papillary muscles. Two-dimensional and 3D echocardiography is ideally suited to examine the mitral valve apparatus and has provided important insights into the mechanism of mitral valve disease. An overview of standardized echocardiography image acquisition and interpretation is provided. Understanding normal mitral valve apparatus function is essential to comprehend alterations in mitral valve disease and the rationale for repair strategies.

Rationale : Ischemic mitral regurgitation, a complication after myocardial infarction (MI), induces adaptive mitral valve (MV) responses that may be initially beneficial but eventually lead to leaflet fibrosis and MV dysfunction. We sought to examine the MV endothelial response and its potential contribution to ischemic mitral regurgitation. Objective : Endothelial, interstitial, and hematopoietic cells in MVs from post-MI sheep were quantified. MV endothelial CD45, found post MI, was analyzed in vitro. Methods and Results : Ovine MVs, harvested 6 months after inferior MI, showed CD45, a protein tyrosine phosphatase, colocalized with von Willebrand factor, an endothelial marker. Flow cytometry of MV cells revealed significant increases in CD45 + endothelial cells (VE-cadherin + /CD45 + /α-smooth muscle actin [SMA] + and VE-cadherin + /CD45 + /αSMA− cells) and possible fibrocytes (VE-cadherin − /CD45 + /αSMA + ) in inferior MI compared with sham-operated and normal sheep. CD45 + cells correlated with MV fibrosis and mitral regurgitation severity. VE-cadherin + /CD45 + /αSMA + cells suggested that CD45 may be linked to endothelial-to-mesenchymal transition (EndMT). MV endothelial cells treated with transforming growth factor-β1 to induce EndMT expressed CD45 and fibrosis markers collagen 1 and 3 and transforming growth factor-β1 to 3, not observed in transforming growth factor-β1–treated arterial endothelial cells. A CD45 protein tyrosine phosphatase inhibitor blocked induction of EndMT and fibrosis markers and inhibited EndMT-associated migration of MV endothelial cells. Conclusions : MV endothelial cells express CD45, both in vivo post MI and in vitro in response to transforming growth factor-β1. A CD45 phosphatase inhibitor blocked hallmarks of EndMT in MV endothelial cells. These results point to a novel, functional requirement for CD45 phosphatase activity in EndMT. The contribution of CD45 + endothelial cells to MV adaptation and fibrosis post MI warrants investigation.

Ischemic mitral regurgitation (IMR) is associated with poor outcomes. It is unknown what factors contribute to progression of IMR and how progressive IMR affects outcomes. We sought to determine imaging predictors of IMR progression and to determine if progressive IMR is an independent predictor of survival in patients with advanced ischemic cardiomyopathy.Consecutive advanced ischemic cardiomyopathy patients who underwent cardiac magnetic resonance and echocardiograms at baseline with echocardiographic follow-up were studied. Cardiac magnetic resonance was used to assess left ventricular volumes, infarct size, and mitral valve geometry. The effective regurgitant orifice area (EROA) was calculated from the proximal isovelocity surface area by echocardiography. Repeated measures mixed effects and Cox proportional hazards regression models were built to identify predictors of IMR progression and survival. We evaluated 336 patients (age, 62±11 years) over a median follow-up time of 54 months: 154 patients were subsequently revascularized, and 182 patients were medically treated. Ninety-eight patients (29%) demonstrated an increase in EROA values of ≥0.1 cm(2). There were 87 adverse events (death or transplant). On multivariable analysis, infarct size (P0.001), progression in IMR (P=0.008), age (P=0.003), and baseline EROA (P=0.010) were independently associated with adverse events. Independent predictors of IMR progression were as follows: baseline EROA (P0.001), left ventricular end-systolic volume index (P=0.014), and total scar (P=0.036).IMR frequently increases in severity, and progression is independently associated with adverse left ventricular remodeling and infarct size, as assessed by cardiac magnetic resonance. Furthermore, IMR progression is a powerful independent predictor of adverse events, even after controlling for the severity of IMR at baseline.

Transcatheter mitral valve (MV) repair with the MitraClip safely reduces mitral regurgitation (MR) in patients who are not appropriate for MV surgery. The procedural success of transcatheter MV repair is highly dependent on advanced Echo imaging and team communication. This chapter discusses the basic mechanisms of MR, MitraClip specific MV Echo screening criteria, and offers a detailed, step-by-step approach explaining optimal MitraClip procedure Echo guidance.

International audience; Mitral valve disease is a frequent cause of heart failure and death. Emerging evidence indicates that the mitral valve is not a passive structure, but−even in adult life−remains dynamic and accessible for treatment. This concept motivates efforts to reduce the clinical progression of mitral valve disease through early detection and modification of underlying mechanisms. Discoveries of genetic mutations causing mitral valve elongation and prolapse have revealed that growth factor signalling and cell migration pathways are regulated by structural molecules in ways that can be modified to limit progression from developmental defects to valve degeneration with clinical complications. Mitral valve enlargement can determine left ventricular outflow tract obstruction in hypertrophic cardiomyopathy, and might be stimulated by potentially modifiable biological valvular-ventricular interactions. Mitral valve plasticity also allows adaptive growth in response to ventricular remodelling. However, adverse cellular and mechanobiological processes create relative leaflet deficiency in the ischaemic setting, leading to mitral regurgitation with increased heart failure and mortality. Our approach, which bridges clinicians and basic scientists, enables the correlation of observed disease with cellular and molecular mechanisms, leading to the discovery of new opportunities for improving the natural history of mitral valve disease.

Background— Previous studies have demonstrated that mitral annulus early diastolic (e′) velocity is increased in constrictive pericarditis (CP) and reduced in restrictive cardiomyopathy. However, those studies did not comprehensively evaluate mitral and tricuspid annular velocities before and after pericardiectomy. Methods and Results— We performed comprehensive echocardiography before and after pericardiectomy in 99 patients with CP, 52 with primary (idiopathic or postpericarditis etiology) and 47 with secondary CP (due to surgery or radiation). Overall, mean±SD mitral medial, mitral lateral, and tricuspid lateral e′ velocities were 12.2±4.2, 10.0±5.4, and 11.6±3.5 cm/s, respectively; annular late diastolic velocities were 10.3±4.3, 12.2±4.9, and 11.7±5.4 cm/s, respectively; and annular systolic (s′) velocities were 7.8±2.8, 8.2±2.1, and 11.2±3.8 cm/s, respectively. Medial e′ was equal to or greater than mitral lateral e′ in 74% of analyzable cases. With the exception of tricuspid s′, there were significant differences in all s′ and e′velocities between primary and secondary CP before pericardiectomy. After pericardiectomy, all annular velocities decreased significantly ( P P P =0.0004, respectively), and the mitral lateral/medial e′ ratio normalized ( P =0.0002). Conclusions— The mitral lateral/medial e′ ratio is reversed in three fourths of patients with CP. All annular velocities are lower in secondary compared to primary CP before pericardiectomy. After pericardiectomy, there is reduction of all annular velocities and normalization of the mitral lateral/medial e′ ratio.

To assess left ventricular (LV) function and brain-type natriuretic peptide (BNP) in patients with first-time flash pulmonary edema (FPE).We retrospectively studied all patients presenting to Mayo Clinic's site in Rochester, MN, from January 5, 2000, to December 30, 2004, with FPE. Only patients with first-time FPE who had undergone BNP assessment and echocardiography within 24 hours of presentation were included. Patients were divided into 2 groups: those with reduced LV ejection fraction (LVEF) (less than 50%) and those with preserved LVEF (equals 50%).Thirty-seven patients met the inclusion criteria (22 female, 15 male). Mean plus or minus SD LVEF was 41% plus or minus 13%. The LVEF was reduced in 73% (group 1, n equals 27; mean plus or minus SD age, 75 plus or minus 8 years) and preserved in 27% (group 2, n equals 10; mean plus or minus SD age, 75 plus or minus 13 years). Most frequent underlying causes for first-time FPE were coronary artery disease and hypertension. Patients with preserved LVEF had significantly lower BNP levels at presentation (535 pg/mL [interquartile range, 352-1210 pg/mL]) vs 1320 pg/mL (interquartile range, 768-2000 pg/mL; P equals .01), despite similar elevated LV filling pressures as measured by echocardiography. The mean plus or minus SD ratio of early diastolic mitral valve inflow velocity to early diastolic mitral annulus velocity was 23 plus or minus 8 vs 22 plus or minus 10; P equals .78. Early diastolic mitral annulus velocity, a surrogate measurement for myocardial relaxation, was reduced in all patients with preserved LVEF and in 95% of patients with reduced LVEF.Coronary artery disease and hypertension are the most common precipitating factors for first-time FPE. Reduced myocardial relaxation in almost all patients regardless of LVEF supports the notion that diastolic dysfunction is a prerequisite for FPE. Levels of BNP were elevated in every patient regardless of LVEF but were significantly lower in patients with preserved LVEF despite similarly elevated LV filling pressures.

Calcification of normal tricuspid and congenital bicuspid valves is the most common cause of aortic stenosis in industrialized countries. There is compelling evidence that thickening and calcification in aortic valve disease is a complex inflammatory process and not simply age-related degeneration. Both aortic sclerosis and stenosis represent phenotypic expressions of one disease continuum. Patients with symptomatic severe aortic stenosis benefit from aortic valve replacement. However, management in the absence of symptoms remains challenging. While a delay of aortic valve replacement due to lack of symptom recognition may result in a dismal outcome, unselected premature aortic valve replacement may be associated with unbalanced risks of cardiac surgery. Echocardiography is the standard for evaluating the severity of aortic stenosis; however, most of the current echocardiographic parameters have limitations in predicting the onset of symptoms. This review summarizes the current guidelines and the emerging application of echocardiographic techniques in the management of asymptomatic severe aortic stenosis.

In recent years, minimally invasive mitral valve surgery (MIMVS) has established itself as an alternative and increasingly used option for patients with mitral valve (MV) pathology. MIMVS is associated with a very low perioperative morbidity and mortality rate in appropriately selected patients, comparable to a full sternotomy approach. Besides superior cosmetic results, patients after MIMVS enjoy shorter recovery times and earlier returns to full activity. A number of approaches are branded as minimally invasive, but the most widely used one entails peripheral cardiopulmonary bypass and a small right anterolateral mini-thoracotomy. The operative technique and outcomes of this approach are summarized in the current update.

Surgical mitral valve (MV) repair remains the gold standard to treat patients with significant degenerative mitral regurgitation (DMR). Medical therapy was the only option for patients found to be not appropriate for MV surgery until the development of percutaneous/transcatheter MV repair options that now allow to reduce MR less invasively and safely. This article discusses the basic mechanisms of MR and the rationale for MR intervention and offers a detailed review on percutaneous/transcatheter MV repair with the MitraClip.

With the mitral valve (MV) leaflet bases arising from the mitral annulus (MA) and the leaflet body and tips connected via the chordae and papillary muscles (PM) to the left ventricular (LV) wall, the anterior and posterior MV leaflets are hoisted like sails. The precise systolic spatial and temporal three-dimensional (3D) interplay of all these structures ensures optimal MV leaflet coaptation within the LV cavity just at the level of the MA, while preventing leaflet displacement into the left atrium (LA; prolapse) or the LV outflow tract (systolic anterior motion, SAM). Any change in form or function that leads to an imbalance of this interplay can result in mechanical leaflet stretch, and if leaflet redundancy is exhausted, to a relative leaflet tissue to MA area deficit and therefore mitral regurgitation (MR).1 Gradually evolving changes that do not unsettle this balance, such as fetal to adulthood growth, seem to allow the MV leaflets to adapt, grow and match the needs of the enlarging LV and MA (×20 area increase).2 The …

Innovations in physics and its applications often enable medical advances. Collaboration between physicists who developed a high-frame-rate ultrasound system and cardiovascular investigators has allowed non-invasive measurement of vascular and myocardial stiffness.1,2 In this current issue of the European Heart Journal—Cardiovascular Imaging , members of these groups, using a related technology, have employed ultrasound to treat as well as to image the heart3 in mitral regurgitation (MR) secondary to myocardial infarction (MI) that causes mitral valve (MV) leaflet tethering mediated by chordae to the displaced papillary muscles (PMs).4 This is a condition for which a strong need is perceived for improved approaches.5 Although there is evidence for adaptive MV growth in secondary MR,6,7 this extra leaflet tissue is often insufficient to compensate adequately for mitral annular (MA) enlargement and chordal tethering.8 The MV leaflets thus become increasingly taut, being pulled by the annulus towards the base, and by chordae towards the left ventricular (LV) apex. The normally convex MV closing configuration towards left atrium becomes concave, and the anterior MV leaflet appears like a ‘hockey stick’ on Echo.9 Once the necessary leaflet tissue redundancy for MV coaptation is …

In functional mitral regurgitation (FMR), increased leaflet area has been described as a remodelling compensatory mechanism. We hypothesized that chordae tendineae elongation would also occur as part of this remodelling. In this study, the lengths of primary chords and measurements of mitral leaflets and annulus were compared with varying degrees of mitral regurgitation (MR).We studied 58 patients who underwent three-dimensional (3D) transoesophageal echocardiography, including 38 with FMR and 20 with normal mitral valves (NL). The FMR group was divided into two subgroups according to two-dimensional vena contracta width (VCW). Three-dimensional datasets from transgastric or mid-oesophageal approach were used to measure primary chordal length, coaptation length, inter-papillary muscle distances, and quantitative 3D measurements of the annulus and leaflets. Leaflet surface area was increased and coaptation length was decreased in FMR compared with NL. While no difference in other 3D measurement of annulus/leaflets was noted between the FMR subgroups, averaged chordal length was shorter in patients with more severe FMR. Chords of the anterior leaflet in FMR with larger VCW were shorter compared with both NL and FMR with smaller VCW. In contrast, the chords of the posterior leaflet were longer in FMR with smaller VCW compared with the other two groups.Our results suggest the posterior leaflet chords possibly remodel by elongating and contribute to reduced MR and that in a subgroup of FMR patients, the primary chords may remodel by shortening, resulting in augmented MR. This information could be useful in choosing strategy for FMR correction.

BACKGROUND: In patients with myocardial infarction (MI), leaflet tethering by displaced papillary muscles induces mitral regurgitation (MR), which doubles mortality. Mitral valves (MVs) are larger in such patients but fibrosis sets in counterproductively. The investigators previously reported that experimental tethering alone increases mitral valve area in association with endothelial-to-mesenchymal transition. OBJECTIVES: The aim of this study was to explore the clinically relevant situation of tethering and MI, testing the hypothesis that ischemic milieu modifies mitral valve adaptation. METHODS: Twenty-three adult sheep were examined. Under cardiopulmonary bypass, the papillary muscle tips in 6 sheep were retracted apically to replicate tethering, short of producing MR (tethered alone). Papillary muscle retraction was combined with apical MI created by coronary ligation in another 6 sheep (tethered plus MI), and left ventricular remodeling was limited by external constraint in 5 additional sheep (left ventricular constraint). Six sham-operated sheep were control subjects. Diastolic mitral valve surface area was quantified by 3-dimensional echocardiography at baseline and after 58 ± 5 days, followed by histopathology and flow cytometry of excised leaflets. RESULTS: Tethered plus MI leaflets were markedly thicker than tethered-alone valves and sham control subjects. Leaflet area also increased significantly. Endothelial-to-mesenchymal transition, detected as α-smooth muscle actin-positive endothelial cells, significantly exceeded that in tethered-alone and control valves. Transforming growth factor-β, matrix metalloproteinase expression, and cellular proliferation were markedly increased. Uniquely, tethering plus MI showed endothelial activation with vascular adhesion molecule expression, neovascularization, and cells positive for CD45, considered a hematopoietic cell marker. Tethered plus MI findings were comparable with external ventricular constraint. CONCLUSIONS: MI altered leaflet adaptation, including a profibrotic increase in valvular cell activation, CD45-positive cells, and matrix turnover. Understanding cellular and molecular mechanisms underlying leaflet adaptation and fibrosis could yield new therapeutic opportunities for reducing ischemic MR.

Aortic stenosis (AS) induces adaptive left ventricular (LV) remodeling, the patterns of which impact clinical outcomes. However, data regarding the prevalence of LV remodeling patterns and associated clinical factors in patients with AS are limited. The PARTNER randomized trial and continued access

Aortic stenosis (AS) induces adaptive left ventricular (LV) remodeling, with some geometric patterns associated with increased morbidity and mortality after surgical aortic valve replacement (AVR). Whether the geometric pattern of LV remodeling at baseline impacts outcomes after transcatheter AVR (