Severe Mitral Regurgitation Secondary to Atresia of the Posterior Mitral Valve Leaflet in the Adult: Is Repair Always Best Practice?
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ABSTRACT:
SUBMITTER: Joshi V
PROVIDER: S-EPMC4670300 | biostudies-other | 2015 Dec
REPOSITORIES: biostudies-other
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Project description:Rationale: Ischemic mitral regurgitation (IMR) is frequently observed following myocardial infarction (MI) and is associated with higher mortality and poor clinical prognosis if left untreated. Accumulating evidence suggests that mitral valve (MV) leaflets actively remodel post-MI, yet the cellular mechanisms underlying these responses and how this affects tissue function remain largely unknown. Objective: We sought to elucidate MV remodeling post-MI at the tissue, cellular, and transcriptomic levels. Methods and Results: The mechanical behavior of ovine MV leaflets pre-MI and 8 weeks post-MI reveal a significant decrease in radial direction extensibility, which essentially eliminated the mechanical anisotropy typically observed in healthy MVs. Quantitative histology and ultrastructural assessment by transmission electron microscopy revealed altered leaflet composition and architecture at 8 weeks post-MI. Assessment of the MV interstitial cell (MVIC) nuclear aspect ratio, a metric of cellular deformation, revealed that MVICs were on average rounder following MI. RNA sequencing (RNA-seq) indicated that YAP-induced genes were elevated at 4 weeks post-MI and genes related to extracellular matrix organization were some of the most downregulated in sheep with IMR compared to sheep without IMR at 4 weeks post-MI. Additionally, RNA-seq revealed the possible recruitment of immune cells in this remodeling process due to the drastic elevation of CXCL9 and CLEC10A. Conclusions: This multiscale assessment revealed significant mechanical and microstructural changes due to MI. RNA-seq provided a baseline for global gene expression changes in response to MI with and without IMR and suggests YAP-induced mechanotransduction, altered expression of ECM-related genes, and recruitment of immune cells as mechanisms contributing to altered MV biomechanics post-MI. Conclusions: This multiscale assessment revealed significant mechanical and microstructural changes due to MI. RNA-seq provided a baseline for global gene expression changes in response to MI with and without IMR and suggests YAP-induced mechanotransduction, altered expression of ECM-related genes, and recruitment of immune cells as mechanisms contributing to altered MV biomechanics post-MI.
2020-05-06 | GSE139921 | GEO
Project description: Not available
| S-EPMC8298853 | biostudies-literature
Project description: Not available
| S-EPMC10954669 | biostudies-literature
Project description:OBJECTIVES:The Cardiothoracic Surgical Trials Network recently reported no difference in the primary end point of left ventricular end-systolic volume index at 1 year postsurgery in patients randomized to repair (n = 126) or replacement (n = 125) for severe ischemic mitral regurgitation. However, patients undergoing repair experienced significantly more recurrent mitral regurgitation than patients undergoing replacement (32.6% vs 2.3%). We examined whether baseline echocardiographic and clinical characteristics could identify those who will develop moderate/severe recurrent mitral regurgitation or die. METHODS:Our analysis includes 116 patients who were randomized to and received mitral valve repair. Logistic regression was used to estimate a model-based probability of recurrence or death from baseline factors. Receiver operating characteristic curves were constructed from these estimated probabilities to determine classification cut-points maximizing accuracy of prediction based on sensitivity and specificity. RESULTS:Of the 116 patients, 6 received a replacement before leaving the operating room; all other patients had mild or less mitral regurgitation on intraoperative echocardiogram after repair. During the 2-year follow-up period, 76 patients developed moderate/severe mitral regurgitation or died (53 mitral regurgitation recurrences, 13 mitral regurgitation recurrences and death, and 10 deaths). The mechanism for recurrent mitral regurgitation was largely mitral valve leaflet tethering. Our model (including age, body mass index, sex, race, effective regurgitant orifice area, basal aneurysm/dyskinesis, New York Heart Association class, history of coronary artery bypass grafting, percutaneous coronary intervention, or ventricular arrhythmias) yielded an area under the receiver operating characteristic curve of 0.82. CONCLUSIONS:The model demonstrated good discrimination in identifying patients who will survive 2 years without recurrent mitral regurgitation after mitral valve repair. Although our results require validation, they offer a clinically relevant risk score for selection of surgical candidates for this procedure.
| S-EPMC4687890 | biostudies-literature
Project description:BACKGROUND:Carpentier's techniques for degenerative posterior mitral leaflet prolapse have been established with excellent long-term results reported. However, residual mitral regurgitation (MR) occasionally occurs even after a straightforward repair, though the involved mechanisms are not fully understood. We sought to identify specific preoperative echocardiographic findings associated with residual MR after a posterior mitral leaflet repair. METHODS AND RESULTS:We retrospectively studied 117 consecutive patients who underwent a primary mitral valve repair for isolated posterior mitral leaflet prolapse including a preoperative 3-dimensional transesophageal echocardiography examination. Twelve had residual MR after the initial repair, of whom 7 required a corrective second pump run, 4 underwent conversion to mitral valve replacement, and 1 developed moderate MR within 1 month. Their preoperative parameters were compared with those of 105 patients who had an uneventful mitral valve repair. There were no hospital deaths. Multivariate analysis identified preoperative anterior mitral leaflet tethering angle as a significant predictor for residual MR (odds ratio, 6.82; 95% confidence interval, 1.8-33.8; P=0.0049). Receiver operator characteristics curve analysis revealed a cut-off value of 24.3° (area under the curve, 0.77), indicating that anterior mitral leaflet angle predicts residual MR. In multivariate regression analysis, smaller anteroposterior mitral annular diameter (P<0.001) and lower left ventricular ejection fraction (P=0.002) were significantly associated with higher anterior mitral leaflet angle, whereas left ventricular and left atrial dimension had no significant correlation. CONCLUSIONS:Anterior mitral leaflet tethering in cases of posterior mitral leaflet prolapse has an adverse impact on early results following mitral valve repair. The findings of preoperative 3-dimensional transesophageal echocardiography are important for consideration of a careful surgical strategy.
| S-EPMC6015386 | biostudies-literature
Project description:Ischaemic mitral regurgitation (IMR), a frequent complication following myocardial infarction (MI), leads to higher mortality and poor clinical prognosis if untreated. Accumulating evidence suggests that mitral valve (MV) leaflets actively remodel post MI, and this remodelling increases both the severity of IMR and the occurrence of MV repair failures. However, the mechanisms of extracellular matrix maintenance and modulation by MV interstitial cells (MVICs) and their impact on MV leaflet tissue integrity and repair failure remain largely unknown. Herein, we sought to elucidate the multiscale behaviour of IMR-induced MV remodelling using an established ovine model. Leaflet tissue at eight weeks post MI exhibited significant permanent plastic radial deformation, eliminating mechanical anisotropy, accompanied by altered leaflet composition. Interestingly, no changes in effective collagen fibre modulus were observed, with MVICs slightly rounder, at eight weeks post MI. RNA sequencing indicated that YAP-induced genes were elevated at four weeks post MI, indicating elevated mechanotransduction. Genes related to extracellular matrix organization were downregulated at four weeks post MI when IMR occurred. Transcriptomic changes returned to baseline by eight weeks post MI. This multiscale study suggests that IMR induces plastic deformation of the MV with no functional damage to the collagen fibres, providing crucial information for computational simulations of the MV in IMR.
| S-EPMC7276554 | biostudies-literature
Project description: Not available
| S-EPMC9366867 | biostudies-literature
Project description:Ischemic mitral regurgitation (IMR) is a prevalent cardiac disease associated with substantial morbidity and mortality. Contemporary surgical treatments continue to have limited long-term success, in part due to the complex and multi-factorial nature of IMR. There is thus a need to better understand IMR etiology to guide optimal patient specific treatments. Herein, we applied our finite element-based shape-matching technique to non-invasively estimate peak systolic leaflet strains in human mitral valves (MVs) from in-vivo 3D echocardiographic images taken immediately prior to and post-annuloplasty repair. From a total of 21 MVs, we found statistically significant differences in pre-surgical MV size, shape, and deformation patterns between the with and without IMR recurrence patient groups at 6 months post-surgery. Recurrent MVs had significantly less compressive circumferential strains in the anterior commissure region compared to the recurrent MVs (p = 0.0223) and were significantly larger. A logistic regression analysis revealed that average pre-surgical circumferential leaflet strain in the Carpentier A1 region independently predicted 6-month recurrence of IMR (optimal cutoff value - 18%, p = 0.0362). Collectively, these results suggest greater disease progression in the recurrent group and underscore the highly patient-specific nature of IMR. Importantly, the ability to identify such factors pre-surgically could be used to guide optimal treatment methods to reduce post-surgical IMR recurrence.
| S-EPMC9134826 | biostudies-literature
Project description:BackgroundIschemic mitral regurgitation is associated with a substantial risk of death. Practice guidelines recommend surgery for patients with a severe form of this condition but acknowledge that the supporting evidence for repair or replacement is limited.MethodsWe randomly assigned 251 patients with severe ischemic mitral regurgitation to undergo either mitral-valve repair or chordal-sparing replacement in order to evaluate efficacy and safety. The primary end point was the left ventricular end-systolic volume index (LVESVI) at 12 months, as assessed with the use of a Wilcoxon rank-sum test in which deaths were categorized below the lowest LVESVI rank.ResultsAt 12 months, the mean LVESVI among surviving patients was 54.6±25.0 ml per square meter of body-surface area in the repair group and 60.7±31.5 ml per square meter in the replacement group (mean change from baseline, -6.6 and -6.8 ml per square meter, respectively). The rate of death was 14.3% in the repair group and 17.6% in the replacement group (hazard ratio with repair, 0.79; 95% confidence interval, 0.42 to 1.47; P=0.45 by the log-rank test). There was no significant between-group difference in LVESVI after adjustment for death (z score, 1.33; P=0.18). The rate of moderate or severe recurrence of mitral regurgitation at 12 months was higher in the repair group than in the replacement group (32.6% vs. 2.3%, P<0.001). There were no significant between-group differences in the rate of a composite of major adverse cardiac or cerebrovascular events, in functional status, or in quality of life at 12 months.ConclusionsWe observed no significant difference in left ventricular reverse remodeling or survival at 12 months between patients who underwent mitral-valve repair and those who underwent mitral-valve replacement. Replacement provided a more durable correction of mitral regurgitation, but there was no significant between-group difference in clinical outcomes. (Funded by the National Institutes of Health and the Canadian Institutes of Health; ClinicalTrials.gov number, NCT00807040.).
| S-EPMC4128011 | biostudies-literature
Project description:ObjectiveMitral valve repair is superior to replacement for degenerative disease, but long-term outcomes of anterior versus posterior leaflet repair remain poorly defined. We propensity matched anterior and posterior repairs to compare long-term outcomes.MethodsPatients undergoing first-time degenerative mitral repair between 1992 and 2018 were identified. Primary outcome was overall survival. Secondary outcomes were postprocedural residual mitral regurgitation and reoperation. From 1025 patients, 1:1 propensity score matching was performed, yielding 309 anterior (isolated anterior = 85, bileaflet = 224) and 309 isolated posterior repairs.ResultsAge was 58 ± 15 years, ejection fraction was 57% ± 10%, and matched groups were well balanced. Anterior repairs had longer bypass (122 ± 53 vs 109 ± 43 minutes, P = .001) and crossclamp (94 ± 44 vs 85 ± 62 minutes, P = .033) times. Mean residual mitral regurgitation grade was 0.44 (95% confidence interval, 0.24-0.65) for anterior repair and 0.30 (95% confidence interval, 0.13-0.47) for posterior repair (P = .31). Overall, 92% (569/618) of matched patients had no residual mitral regurgitation, with no differences in mitral regurgitation grade between groups (P = .77). Survival did not differ between anterior (10 years: 72% ± 7%; 15 years: 63% ± 7%) and posterior (10 years: 74% ± 7%; 15 years: 60% ± 8%) groups (log-rank P = .93). Linearized incidence of reoperation was 0.62% per patient-year, including 0.74% for anterior and 0.48% for posterior repairs. Cumulative incidence of reoperation at 15 years was 7.5% after anterior repair and 4.9% after posterior repair (Gray's test P = .26).ConclusionsNo long-term survival or reoperation difference was found between posterior and anterior repair. On the basis of these findings, surgeons at centers of excellence should aim for repair of both anterior and posterior leaflet pathology with the same decision-making threshold over valve replacement for degenerative mitral disease.
| S-EPMC7483316 | biostudies-literature