Mitral Valve Annulus Diameter Research Articles

Mutation in PDGFRbeta: a potential new pathogenic variant for acquired mitral valve prolapse

Abstract Funding Acknowledgements None. Background Mitral valve prolapse (MVP) due to myxomatous degeneration is characterized by familial clustering, but few pathogenic genes have been identified. In a genetic screening program for MVP patients, we identified a platelet-derived growth factor receptor β (PDGFRβ)-E162K missense variant in a family with a bi-leaflet MVP phenotype in four affected family members. PDGFRβ is a receptor tyrosine kinase, which plays an important role in vascular development. Purpose In this study, we investigated whether the E162K substitution in PDGFRβ could lead to mitral valve abnormalities. Methods To assess the functional effects of the missense variant, proliferation and migration assays were performed using HeLa cells overexpressing wild-type (WT) or mutant PDGFRβ. Immunostainings were performed to determine PDGFRβ expression in the diseased valves from a family member undergoing surgical operation and from additional patients operated for MVP. Mouse models were created with the mouse equivalent of the human PDGFRβ-E162K variant (PDGFRβ-E161K) using CRISPR/CAS9. The variant was not lethal and transthoracic echocardiography was performed on adult homozygous PDGFRβE161K/E161K mice, heterozygous PDGFRβE161K/- mice, and WT mice . In addition, histology was performed in adult and neonatal mice to detect potential valvular defects. Results HeLa cells expressing PDGFRβ-E162K and stimulated with PDGFD showed reduced proliferation and migration, suggesting a loss of function of the mutant receptor. PDGFRβ was expressed in human diseased mitral valves. Echocardiographic evaluation revealed a significant larger mitral valve annulus diameter in both PDGFRβE161K/- and PDGFRβE161K/E161K compared to WT (WT: 1.97 mm; PDGFRβE161K/-:2.13, p=0.031; PDGFRβE161K/E161K:2.42 mm, p<0.0001). Histological data in PDGFRβE161K/E161K mice showed significant leaflet thickening in the free edge (FE) of the posterior mitral valve leaflet (PMVL) compared to WT (WT: 72.34 ɥm; PDGFRβE161K/E161K: 109.6 ɥm, p=0.040) and a larger leaflet area of the PMVL compared to WT (WT: 25280 ɥm²; PDGFRβE161K/E161K: 44494 ɥm², p=0.020). Moreover, an altered organization of the extracellular matrix reminiscent of the myxomatous degeneration in MVP was observed. These alterations were not observed in mutant neonatal hearts. Conclusions The PDGFRβ-E162K variant is associated with familial MVP and alters the function of PDGFRβ. Mice harboring this mutation display acquired mitral valve defects.

Mutation in PDGFRbeta: a potential new pathogenic variant for mitral valve prolapse

Abstract Background Mitral valve prolapse (MVP) due to myxomatous degeneration is characterized by familial clustering, but few pathogenic genes have been identified. In a genetic screening program for MVP patients, we identified a platelet-derived growth factor receptor β (PDGFRβ)-E162K missense variant in a family with a bi-leaflet MVP phenotype in four affected family members. PDGFRβ is a receptor tyrosine kinase, which plays an important role in vascular development. Purpose In this study, we investigated whether the E162K substitution in PDGFRβ could lead to mitral valve abnormalities. Methods To assess the functional effects of the missense variant, proliferation and migration assays were performed using HeLa cells overexpressing wild-type (WT) or mutant PDGFRβ. Immunostainings were performed to determine PDGFRβ expression in the diseased valves from a family member undergoing surgical operation and from additional patients operated for MVP. Mouse models were created with the mouse equivalent of the human PDGFRβ-E162K variant (PDGFRβ-E161K) using CRISPR/CAS9. The variant was not lethal and a total of 12 homozygous PDGFRβ-E161K-/- mice, 11 heterozygous PDGFRβ-E161K+/- mice, and 7 WT mice were subjected to transthoracic echocardiography. In addition, histology was performed in all 30 mice to detect potential valvular defects. Results Stimulated HeLa cells expressing PDGFRβ-E162K showed reduced proliferation and migration, suggesting a loss of function of the mutant receptor. PDGFRβ was expressed in human diseased mitral valves. Echocardiographic evaluation revealed a significant larger mitral valve annulus diameter in both PDGFRβ-E161K+/- and PDGFRβ-E161K-/- compared to WT (WT: 1.97 mm; PDGFRβ-E161K+/-:2.13, p=0.031; PDGFRβ-E161K-/-: 2.42 mm, p<0.0001). Histological data in PDGFRβ-E161K-/- mice showed significant leaflet thickening in the free edge (FE) of the posterior mitral valve leaflet (PMVL) compared to WT (WT: 72.34 ɥm; PDGFRβ-E161K-/-: 109.6 ɥm, p=0.040) and a larger leaflet area of the PMVL compared to WT (WT: 25280 ɥm²; PDGFRβ-E161K-/-: 44494 ɥm², p=0.020). Moreover, an altered organization of the extracellular matrix reminiscent of the myxomatous degeneration in MVP was observed. Conclusions The PDGFRβ-E162K variant is associated with familial MVP and alters the function of PDGFRβ. Mice harboring this mutation display mitral valve defects and can be used as a model for mitral valve disease.

EMCAPT study: the effect of MitraClip treatment on the mitral annulus and left atrial appendage evaluation by transoesophageal echocardiography.

Data on the change in mitral valve annulus diameter (MAD), and left atrial appendage (LAA) structure and function after transcatheter edge-to-edge repair (TEER) of the mitral valve in patients with secondary mitral regurgitation (MR) are lacking. To evaluate the change in these parameters just after the clip insertion and its relationship with prognosis in the long term. A total of 50 patients (age: 71.5 ±11.3 years, 70% male) with moderate-to-severe or severe MR were included in the study. Transthoracic (TTE) and transoesophageal echocardiography (TEE) were performed before and after the procedure. Prognostic data were recorded with post-procedure telephone calls and follow-up visits. TEE performed during the procedure showed that LAA contraction and filling velocity significantly increased (p < 0.001 for all). Systolic pulmonary artery pressure (SPAP), MAD, and LAA landing zone dimension significantly decreased (p < 0.001 for all). There was only a significant correlation between the MAD before clip placement and the MAD change after clip placement (r = 0.6, p < 0.001). During a mean follow-up period of 10.5 ±8.9 months, no significant correlation was found between MAD change, LAA contraction and filling velocity change, and LAA landing zone dimension change and rehospitalization, stroke, mortality, and composite outcome. The contraction and filling velocity of LAA, SPAP, MAD, and LAA landing zone dimension changed significantly immediately after the MitraClip procedure. Although these parameters are not related to composite outcome in our study, MAD, LAA diameter, and velocity need to be compared between successful and unsuccessful procedures to predict their clinical relevance.

Anatomy and Topography of Coronary Sinus and Mitral Valve Annulus in Functional Mitral Regurgitation.

BackgroundWe aimed to investigate the anatomical relationship of the coronary sinus (CS) and the mitral valve annulus (MVA) in patients with or without functional mitral regurgitation (FMR) using a multislice CT (MSCT) software to determine (a) the distance and angle of both CS and MVA plane and (b) the mitral annulus geometry.MethodsA total of 215 patients with MSCT and CS to MVA topography evaluation were enrolled in this retrospective study.ResultsThis patient cohort included 145 patients without FMR (67.4%, FMR ≤ 1+) and 70 patients (32.6%) with clinically relevant FMR (FMR ≥ 2+). Distance and angulation of CS to MVA planes were highly variable. In all groups, no significant correlation was documented between the distance or angle of CS to MVA planes and left ventricular ejection fraction, left ventricular end-diastolic diameter, or left atrial volume. A significant increase in total CS length could be found in patients with FMR ≥ 2+ compared to the FMR ≤ 1+ group. MVA diameter, area, and perimeter were significantly increased in FMR ≥ 2+ compared to FMR ≤ 1+. In the FMR ≥ 2+ cohort 61% showed a distance of CS to MVA plane <7.8 mm and 58% revealed an angle of CS to MVA plane <14.2°.ConclusionDistance and angulation of CS to MVA topography using an MSCT approach are similar between patients with or without FMR, while CS length, MVA area, MVA perimeter, anterior-posterior diameter, and intercommissural diameter are significantly increased in all FMR subgroups. However, ~60% of FMR ≥ 2+ patients showed favorable CS to MVA topography for indirect mitral annuloplasty.

Computational estimates of annular diameter reveal genetic determinants of mitral valve function and disease.

The fibrous annulus of the mitral valve plays an important role in valvular function and cardiac physiology, while normal variation in the size of cardiovascular anatomy may share a genetic link with common and rare disease. We derived automated estimates of mitral valve annular diameter in the 4-chamber view from 32,220 MRI images from the UK Biobank at ventricular systole and diastole as the basis for GWAS. Mitral annular dimensions corresponded to previously described anatomical norms, and GWAS inclusive of 4 population strata identified 10 loci, including possibly novel loci (GOSR2, ERBB4, MCTP2, MCPH1) and genes related to cardiac contractility (BAG3, TTN, RBFOX1). ATAC-Seq of primary mitral valve tissue localized multiple variants to regions of open chromatin in biologically relevant cell types and rs17608766 to an algorithmically predicted enhancer element in GOSR2. We observed strong genetic correlation with measures of contractility and mitral valve disease and clinical correlations with heart failure, cerebrovascular disease, and ventricular arrhythmias. Polygenic scoring of mitral valve annular diameter in systole was predictive of risk mitral valve prolapse across 4 cohorts. In summary, genetic and clinical studies of mitral valve annular diameter revealed genetic determinants of mitral valve biology, while highlighting clinical associations. Polygenic determinants of mitral valve annular diameter may represent an independent risk factor for mitral prolapse. Overall, computationally estimated phenotypes derived at scale from medical imaging represent an important substrate for genetic discovery and clinical risk prediction.

Evolution from mitral annular dysfunction to severe mitral regurgitation in Barlow's disease.

Barlow's disease (BD) is characterized by thick, redundant mitral valve (MV) leaflets, which can lead to prolapse and significant mitral regurgitation (MR). MV annular abnormalities are also commonly observed and increasingly recognized as possible primary pathology, with leaflet thickening being secondary to increased stress on the MV apparatus. To provide more insights into this hypothesis, the evolution of MV abnormalities over time in patients with BD was assessed. A total of 64 patients (54 ± 12 years, 72% male) with BD who underwent MV surgery and had multiple transthoracic echocardiograms (TTE) before surgery were included. In total, 186 TTE were analysed (median time interval 4.2, interquartile range 2.2-6.5 years) including specific MV characteristics. At baseline, MV leaflet length, thickness, billowing height and annular diameter were larger in patients with BD compared to 59 healthy subjects. Systolic outward motion (curling) of the annulus was observed in 77% and severe mitral annular disjunction (≥5 mm) in 38% of patients with BD. Forty (63%) patients had MR grade I-II and 24 (37%) MR grade III-IV; at baseline, the 2 groups only differed in left atrial volume and in thickness and billowing height of the posterior leaflet, showing comparable MV annular abnormalities and dilatation despite different grades of MR. Over time, MV annulus diameter, leaflet length and billowing height increased significantly along with MR grade. In patients with BD, MV annulus abnormalities are present at an early stage and precede the development of significant MR, suggesting their substantial role in the pathophysiology of this disease and as an important target for surgical treatment.

Mitral Annular Disjunction: A Diagnosis to Save Lives

Introduction Mitral annular disjunction (MAD) is caused by a variation in the attachment of posterior mitral valve (MV) leaflet causing a wide separation between the left atrial wall-MV junction and left ventricular (LV) wall. Longitudinal MAD distance from left atrial wall-MV junction to LV wall during end-systole in the echocardiographic parasternal long axis view should be in excess of 2mm to suspect MAD. Recent evidence suggests that MAD magnitude is linked to higher incidence of ventricular arrhythmias. We present a case of an individual presenting with unexplained syncope, MAD and multiple episodes of non sustained ventricular tachycardia (NSVT). Case description 68 year old male with history of hypertension presented to ER with syncope. Initial EKG showed sinus bradycardia without ischemic changes. His troponins were negative and electrolytes were normal. Exercise stress test for chronotropic competence revealed premature ventricular contractions (PVCs) and an episode of 9 beats NSVT. Patient continued to have multiple episodes of NSVT with significant PVC burden. Echo showed normal systolic-diastolic function, myxomatous MV, bileaflet mitral valve prolapse (MVP), mild mitral regurgitation and MAD with magnitude of 12mm. Myocardial perfusion imaging did not reveal any defects. Cardiac MRI (CMR) showed delayed enhancement of basal mid-lateral and mid-septal walls. He received a dual chamber implantable cardioverter defibrillator to decrease the risk of sudden cardiac death related to MAD. Discussion Papillary muscle fibrosis and MAD magnitude are markers for severe arrhythmic events. Both are commonly seen with bileaflet MVP. Typical findings seen on echocardiogram are curling motion of the basal lateral LV wall from hypercontraction of regional area which causes paradoxical increase in the MV annulus diameter during systole. It also causes myxomatous MV and myocardial stretch in the LV inferobasal segment eventually causing fibrosis as identified on CMR. MVP is associated with MAD but MAD can also occur without underlying MVP and should be considered an independent risk factor for arrhythmias. Physicians should consider MAD in patients with no apparent cause for PVCs and refer them for echocardiogram. There is currently no consensus regarding pharmacological or device therapy for MAD. Conclusion Identification and recognition of MAD, with or without MVP, as an independent arrhythmic risk factor should be routinely done by non invasive methods.

The Early “Unnatural” History Following Surgical Repair of Ventricular Septal Defects

Surgical outcomes for simple ventricular septal defects (VSD) have been excellent in the past three decades. For this project, the timing of resolution of left-sided dilation and mitral regurgitation (MR) following VSD repair was assessed. Echocardiographic data surrounding surgery of 42 consecutive children who underwent surgical patch repair of a VSD were reviewed. The echocardiograms were reviewed up to a mean of 12 months post-operatively (range 9 - 14 months). Quantitative data indexed to body surface area including left atrial (LA) volume, mitral valve annulus diameter, and left ventricular end-diastolic dimension (LVEDD) was analyzed. The majority of our pre-surgical cohort had only trace (44%) or no MR (31%), with a small proportion having mild (16%) or moderate MR (9%). No patients had moderate or greater MR following repair at follow-up. The median mitral valve annular Z-score was 1.8 (SD 1.6; range: -1.2 to 4.1) pre-operatively, improving to a 0.6 (range: -1.7 to 2.4; p < 0.001) at follow-up. LA dilation was present in 70% of patients, with a median LA volume Z-score of 1.1 (range: -2.6 to 15.5), decreasing to 13% median Z-score -1.2 (range: -3.5 to 2.9; p < 0.001) at follow-up. LV dilation was present in 81% of pre-operative patients with a median LVEDD Z-score of 3.0 (range: -2.0 to 7.9). There was significant improvement in qualitative assessment of LV enlargement (25%) with a median LVEDD Z-score of 0.5 (range: -2.1 to 2.9; p < 0.001) at follow-up. Discharge echocardiogram was performed at a mean of 5.7 days (range: 3 - 12 days) following surgery. Normalization of LA, mitral valve annulus, and LV size occurred within the first three months in the majority of patients, with significant changes occurring within the first post-operative week following surgical repair for VSD.

P3764Morphological mechanisms of atrial functional mitral regurgitation in patients with atrial fibrillation

Abstract Background Atrial functional mitral regurgitation (AFMR) occurs in patients with atrial fibrillation. However, morphological mechanisms of AFMR are poorly understood. Purpose The purpose of this study was to examine the morphological characteristics in patients with AFMR. Methods Among consecutive 795 patients undergoing initial radiofrequency catheter ablation (RFCA) at our hospital, twenty-five patients with persistent AF accompanied by AFMR (≥ moderate) before RFCA (AFMR group) were studied. Age-matched 25 patients with persistent AF without MR were defined as a control group. Results Left ventricular ejection fraction (LVEF) was lower and left atrium volume index was larger in the AFMR group (Table). Mitral valve annulus diameter and length of anterior mitral leaflet (AML) were similar between groups, whereas length of posterior mitral leaflet (PML) was significantly shorter in the AFMR group. Smaller tethering angle of AML (γ in the figure) and shorter tethering height were significantly associated with the occurrence of AFMR, which were different from morphology of functional mitral regurgitation in patients with dilated LV. Multiple regression analysis revealed that less tenting height (p&lt;0.05) and LA dilatation toward the posterior (p&lt;0.01) were significantly related to AFMR. Echocardiographic parameters AFMR (n=25) Control (n=25) P value Age, y 69±8 66±10 NS Male, n (%) 9 (36) 20 (80) P=0.001 LVEF,% 60±9 67±6 P=0.004 LAD, mm 44±5 41±7 NS LAVI, ml/m2 56±17 41±13 P&lt;0.001 MV diameter, mm 3.9±0.4 3.8±0.5 NS α angle, ° 34±9 35±7 NS β angle, ° 48±9 50±8 NS γ angle, ° 32±5 37±5 P=0.0005 AML length, mm 3.0±0.5 3.0±0.5 NS PML length, mm 2.1±0.1 2.4±0.1 P=0.03 Tenting height, mm 1.5±0.1 1.8±0.1 P=0.02 D, mm 0.8±0.3 0.5±0.3 P=0.001 LVEF: left ventricular ejection fraction; LAD: left atrial diameter; LAVI: left atrial volume index; AML: anterior mitral leaflet; PML: posterior mitral leaftlet. Conclusions AFMR occurs in patients with unique morphological features, such as less tethering height and LA dilatation toward the posterior.

Multimodality registration of two-dimensional echocardiography and cardiac CT for mitral valve diagnosis and surgical planning.

A registration method to fuse two-dimensional (2-D) echocardiography images with cardiac computed tomography (CT) volume is presented. The method consists of two major procedures: temporal and spatial registrations. In temporal registration, the echocardiography frames at similar cardiac phases as the CT volume were interpolated based on electrocardiogram signal information, and the noise of the echocardiography image was reduced using the speckle reducing anisotropic diffusion technique. For spatial registration, an intensity-based normalized mutual information method was applied with a pattern search optimization algorithm to produce an interpolated cardiac CT image. The proposed registration framework does not require optical tracking information. Dice coefficient and Hausdorff distance for the left atrium assessments were [Formula: see text] and [Formula: see text], respectively; for left ventricle, they were [Formula: see text] and [Formula: see text], respectively. There was no significant difference in the mitral valve annulus diameter measurement between the manually and automatically registered CT images. The transformation parameters showed small deviations ([Formula: see text] deviation in translation and [Formula: see text] for rotation) between manual and automatic registrations. The proposed method aids the physician in diagnosing mitral valve disease as well as provides surgical guidance during the treatment procedure.

Non-ischaemic mitral valve suture annuloplasty: late follow-up results.

To evaluate late outcomes after posterior mitral valve (MV) annulus double-suture annuloplasty for degenerative (non-ischaemic) MV insufficiency. Between 2005 and 2011, 138 patients underwent MV repair using posterior MV double-suture annuloplasty and an additional 105 patients underwent tricuspid valve repair. The study protocol included operative mortality, reoperation rate and reasons, as well as echocardiographic parameters at pre- and postoperative and follow-up periods (2-9 years). In-hospital mortality was 2/138 (1.45%). Early post operation, no regurgitation was noted in 74/136 (54.4%) patients, I(o) regurgitation was observed in 55/136 (40.4%), II(o) was observed in 6/136 (4.4%) and III(o) was observed in 1/136 (0.7%); during late follow-up (from 2 to 9 years), no regurgitation was observed in 21.6% patients, I(o) was observed in 58%, II(o) was observed in 17% and III(o) was observed in 3.4%. The mean preoperative anterolateral diameter of the MV annulus was 39.02±4.97 mm and, at late follow-up, it was 27.66±3.94 mm (p=0.000); at these same time points, left ventricular end-diastolic diameter (LVEDD) was 55.74±7.29 mm and 49.17±6.01 mm (p=0.000), respectively, and the left ventricular ejection fraction (LVEF) was 53.08±8.93% and 50.92±6.78%, respectively (p=0.007). This study demonstrates suture annuloplasty to be an effective treatment up to 9 years for degenerative mitral valve disease. This technique enables preservation of the posterior mitral valve annulus diameter with stable long-term (up to 9 years) reduction, a competent (no regurgitation/⩽II(o) regurgitation) MV in 96.6% of cases and positive left ventricular (LV) remodelling.

Association between Body Mass Index and Mitral Valve Prolapse

Introduction: Body mass index (BMI) can affect cardiac morphology; however, the relationship between BMI and valvular heart diseases has not been thoroughly evaluated. This study aimed to determine the relationship between BMI and mitral valve prolapse (MVP) as one of the most common valve diseases worldwide. It can help us to better understand pathophysiology of this common disease. Materials and Methods: In this descriptive study we enrolled 200 patients with isolated MVP. This patient was referred from 2014 to 2015 to our cardiology clinic in Mashhad, Iran, with chief complaint of chest pain, dyspnea, and palpitation. patients underwent transthoracic echocardiography. We document the patients’ height, weight, and demographics data. BMI distribution was categorized as higher and lower than 18.5 kg/m2. Chi- square and independent samples t-test were performed using SPSS version 19 to analyze the data. Results: The results showed that 92 (46%) and 108 (54%) of the samples were male and female, respectively, and their mean age was 24.29±3.75 years. Most of the patients(n=110) had low BMI (55% of the patients had BMI lower than 18.5 kg/m2). Left atrial and ventricular diameters had a significant relationship with BMI of all the underweight patients(n=110) (P=0.026 and 0.032, respectively). The main complaints were chest pain (n=55,50%) and dyspnea (n=58,64.44%) in the patients with low and normal BMI, respectively. Conclusion: Symptoms and echocardiographic features in MVP patients vary with BMI. While mitral valve annulus diameter was the same in both BMI groups, the results showed that left atrial and ventricular diameters in the underweight patients were less than those with normal BMI.

Fate of Mitral Regurgitation After Transcatheter Closure of Atrial Septal Defect in Adults

Although the volume overload of pulmonary circulation improves after atrial septal defect (ASD) closure, the increasing left ventricular preload may contribute to mitral regurgitation (MR) deterioration. We aimed to evaluate the impact of MR after transcatheter ASD closure on clinical outcomes in adults. A total of 288 consecutive patients who underwent transcatheter ASD closure were enrolled. Changes in MR were assessed at 1 month after the procedure. The end point was defined as cardiovascular events. After the procedure, MR ameliorated in 3 patients and unchanged in 253, whereas MR deteriorated in 32. During a median follow-up of 24 months, patients with MR deterioration had no cardiovascular events, and the event-free survival rate was not different between patients with MR deterioration and those with MR amelioration or no-change (p = 0.355). Even in patients with MR deterioration, the New York Heart Association functional class improved after the procedure, with no cases of worsening functional class. Multivariate logistic regression analysis showed that MR deterioration was independently related to advanced age and female gender. The degree of enlargement of mitral valve annulus diameter after the procedure was greater in patients with MR deterioration than in those with MR amelioration or no-change, and it was correlated with the degree of MR deterioration. In conclusion, MR deterioration occurs in a minority of adult patients after transcatheter ASD closure; however, it is not linked with adverse outcomes. MR deterioration may be provoked by geometric changes in mitral valve annulus, especially in women with advanced age.

Mid- to long-term aortic valve-related outcomes after conventional repair for patients with interrupted aortic arch or coarctation of the aorta, combined with ventricular septal defect: the impact of bicuspid aortic valve

Bicuspid aortic valve (BAV) is a common risk factor for valve-related problems and occurs more frequently in patients with an interrupted aortic arch (IAA) or coarctation of the aorta (CoA), combined with a ventricular septal defect (VSD), than in the general population. We have been using conventional repair for patients with IAA/CoA+VSD, including those with a very small aortic valve (AV). We retrospectively investigated the outcomes of these patients from the perspective of valve morphology. Between 2000 and 2012, 50 consecutive patients underwent conventional repair for CoA/IAA with VSD [one-stage repair, 44 (88%); staged repair, 6 (12%)]. The criteria for conventional repair were as follows: an AV annulus diameter (AVD) z-score of >-6.0; mitral valve annulus diameter z-score of >-3.0; without retrograde flow in the proximal arch. Sixteen (32%) patients had BAV (Group B); the remaining 34 (68%) patients had a tricuspid AV (Group T). The surgical outcomes in both groups were investigated. No mortality occurred in the cohort. The median follow-up times were 6 years and 3 months (6 months to 11 years and 8 months) and 6 years and 2 months (4 months to 11 years and 4 months) in Groups B and T, respectively (P > 0.05). The preoperative data (median age at repair, median body weight and median AVD) were comparable in the two groups (P > 0.05). Two patients (4%) underwent reintervention in the aortic arch: 1 patient underwent balloon angioplasty for re-coarctation; the other removal of the interposed graft because of somatic growth. In both groups, the AVD became significantly larger at the 1-year follow-up, approximating the normal value. Three (6%) patients underwent a total of eight valve-related reinterventions (balloon angioplasty, 6; Ross operation, 1; valve replacement, 1). All three had BAV, and the AVD was 3.8-5.6 mm (z-score, -3.4 to -1.6). The 5-year valve-related reintervention-free survival rate was 76% and 100% in Groups B and T, respectively (P < 0.01). The long-term outcomes after conventional repair under our criteria were acceptable. BAV was a significant risk factor for valve-related reinterventions after conventional repair for IAA/CoA with VSD.

Percutaneous closure of an atrial septal defect in an infant with shone's syndrome

Rarely is closure of the atrial septal defect indicated in infants. Yet, an atrial septal defect in the presence of congenital mitral stenosis may cause significant congestive heart failure in infancy. We present the case of an infant with Shone's syndrome, left ventricular hypoplasia, and a large ostium secundum atrial septal defect who developed pulmonary overcirculation following repair of coarctation of the aorta. The infant underwent cardiac catheterization, hemodynamic assessment, and successful percutaneous closure of the atrial septal defect. The patient improved dramatically following the intervention. Follow-up echocardiograms have demonstrated growth of mitral valve annulus diameter and left ventricular dimensions. Atrial septal defect closure in this small infant was associated with immediate improved clinical status, and improved growth of the left heart structures.

Clinical implications of thrombocytopenia among patients undergoing intra-aortic balloon counterpulsation in the coronary care unit

Clinical implications of thrombocytopenia among patients undergoing intra-aortic balloon counterpulsation in the coronary care unit

Mitral annular reduction with subablative therapeutic ultrasound

Mitral annular reduction with subablative therapeutic ultrasound

Evaluation of sirolimus-eluting stents and Titan2 bio-active stents performance by optical coherence tomography: a window on the importance of nitric oxide for strut coverage

Evaluation of sirolimus-eluting stents and Titan2 bio-active stents performance by optical coherence tomography: a window on the importance of nitric oxide for strut coverage

Remodeling of the mitral valve using radiofrequency energy: review of a new treatment modality for mitral regurgitation

Mitral regurgitation (MR) is a common valvular pathology with significant morbidity and mortality implications. Mechanical treatment of this condition is more effective than medical treatment and surgical correction has traditionally been the mechanical method of choice. Following major advances and wide acceptance of percutaneous interventions for coronary artery diseases, the field of valvular heart disease became an attractive target for transcatheter treatment modalities. Significant steps have been achieved in the field of percutaneous treatment of mitral stenosis as well as aortic stenosis, and lately, mitral regurgitation has been the focus of interest for many investigators looking for transcatheter solutions. Percutaneous edge-to-edge techniques and annuloplasty are innovative but have many disadvantages including the inability to reintervene and leaving a foreign body behind, respectively. Since the mitral and tricuspid annuli have dense collagen, a treatment modality targeting that collagen is logical. Observing the thermal effect on collagen, which causes conformational changes and shrinkage, radiofrequency energy was tested to evaluate its effect on the collagen-rich structure that is the mitral valve annulus. The potential of shrinking the mitral annulus by applying direct thermal source could be a promising modality for the treatment of mitral regurgitation with potential open and percutaneous applications. This paper presents an overview of the recent advances in transcatheter treatment of mitral regurgitation focusing on a new treatment modality that aims at reducing the mitral valve annulus diameter through the direct application of thermal energy using a radiofrequency energy probe.

Mitral annular reduction with subablative therapeutic ultrasound: pre-clinical evaluation of the ReCor device

To evaluate the potential for mitral annular (MA) size reduction using a novel device utilising therapeutic ultrasound (TU).The ReCor device (ReCor Medical, Inc., Ronkonkoma, NY, USA, Investigational device, not for use in human application) was studied in a closed chest canine animal model (35 dogs). Under fluoroscopy, a 12 Fr TU balloon catheter was advanced into the left atrium (transseptal approach). The TU balloon was inflated with contrast-saline, positioned at the MA and energy delivered circumferentially, to heat the tissue locally. Five TU applications were delivered (at least 60W for at least 40 sec). Relative to baseline, mitral valve annular diameter reduction (measured by transthoracic echocardiography) was 8.4% immediately post procedure(p<0.001), 8.6% at one week (p<0.001), 8.8% at two weeks (p<0.001), 9.3% at three weeks (p<0.001), 10.8% at four weeks (p<0.001), 8.6% at three months (p<0.001) and 5.7% at six months (p<0.001). Histology showed an increase in elastin associated with tissue thickening at the annular level. Transmission electron microscopy demonstrated a decrease in diameter of individual collagen fibres in treated regions compared to controls.Therapeutic ultrasound (TU) energy application to the mitral annulus is feasible percutaneously. A reduction in annular dimensions occurs immediately and appears to be durable without peri-annular damage.