OBJECTIVES: Minimally invasive mitral valve repair (MVR) promises major advantages over median sternotomy regarding cosmetic results and faster recovery. However, the long-term functional outcome of minimally invasive MVR has been questioned by critics because the limited access may not exclusively promise high-quality repair. This study examines the long-term outcome regarding survival and reoperation rate. METHODS: All patients undergoing minimally invasive MVR from February 2000 until March 2020 were included in this study. Baseline clinical and surgical characteristics were summarized from the internal database. Primary end points were survival and freedom from reoperation, analysed via Kaplan–Meier curves. Secondary end points were periprocedural complications after minimally invasive MVR and incidence for recurrent mitral regurgitation >II°. RESULTS: A total of 1194 patients underwent minimally invasive MVR, in 17 cases mitral valve replacement was required. The mean age was 55.1 years [47.6; 62.7]. The successful minimally invasive repair rate was 97%. The 30-day mortality was 0.6%. Survival was 96.7% [standard deviation (SD): 5.8%], 91.6% (SD: 1.1%) and 80.0% (SD: 11.2%) at 5, 10 and 20 years. The incidence of reoperation was 4.4% (SD: 3.2%), 10.3% (SD: 7.4%) and 16.7% (SD : 7.4%) at 5, 10 and 20 years, respectively. Concomitant procedures such as tricuspid valve repair and modified Cryo-maze procedure were performed in 263 cases. CONCLUSIONS: Minimally invasive MVR for degenerative mitral regurgitation is safe, shows excellent functional long-term results and is associated with low perioperative and late mortality.

Patients with symptomatic mitral valve disease unsuitable for repair can be sufficiently treated with surgical mitral valve replacement (MVR). The decision between biological and mechanical MVR (bMVR/mMVR) can be difficult, especially due to the question of the lesser of two evils: anticoagulation versus reoperation. This single-center, retrospective study included all patients undergoing MVR between 2001 and 2020. Thirty-day mortality and periprocedural complications were analyzed. Propensity-score matching (PSM) adjusted for age, gender, weight, height, endocarditis, diabetes, hypertension, PAOD, AFib, CKD, cancer, and history of neurological disorders was performed. After PSM, survival and cumulative incidence of reoperation at time of follow-up were analyzed. The study included 2,027 patients in two main groups: 1,658 patients with bMVR, and 369 with mMVR; 51.2% were male. Age at surgery was 65.9±12.9 years. Median follow-up time was 6.83 years (IQR 1.11-10.61 years). Concomitant procedures were performed in 1,467 cases (72.4%). PSM yielded comparable groups of 339 pairs. Both groups showed comparable survival (p=0.203). Survival after mMVR and bMVR was comparable for all analyzed time points over the course of 20 years. Patients with mMVR showed a significantly lower cumulative incidence for reoperation (20-year: 15% vs. 59%, p < 0.001). Follow-up of 20 years at a high-volume center demonstrates comparable survival after mechanical or biological mitral valve replacement (MVR), while reoperation rates are significantly lower after mMVR.

Objectives: Pronounced mitral annular disjunction (pMAD ≥8 mm) in myxomatous mitral valve disease has been associated with ventricular arrhythmias in selected cohorts, whereas minor degrees of mural separation are frequently observed in structurally normal hearts. Its clinical relevance after mitral valve surgery remains unclear. We investigated whether pMAD is associated with postoperative symptom burden and rhythm outcomes. Methodsv: In this retrospective cohort with prospective follow-up, 246 adults undergoing mitral valve surgery for Barlow’s disease were classified intraoperatively as pMAD (≥8 mm) or non-pMAD (<8 mm). The primary end point was patient-reported postoperative palpitations. Propensity score–based inverse probability weighting was applied to adjust for baseline differences. Structured follow-up in pMAD patients included transthoracic echocardiography (TTE) and 24-hour Holter monitoring. Results: pMAD was present in 103 patients (41.9%). Surgery effectively reduced disjunction distance. At follow-up, palpitations were more frequent in pMAD compared with non-pMAD patients (40.8% vs 18.9%, P = .011), remaining significant after adjustment. In the pMAD follow-up cohort, atrial fibrillation prevalence decreased significantly after surgery. Holter monitoring did not demonstrate sustained malignant arrhythmias. Survival and major adverse events were comparable between groups. Conclusions: After mitral valve surgery for Barlow’s disease, pMAD is independently associated with increased postoperative palpitations despite anatomical correction. This association was not accompanied by excess malignant arrhythmias or adverse clinical end points, suggesting persistent symptom susceptibility rather than overt electrical instability.

Background: Outcomes of patients undergoing transcatheter aortic valve implantation (TAVI) for severe aortic stenosis with concomitant severe mitral regurgitation (MR) remain incompletely defined. This study aimed to quantify the evolution of high-grade MR after TAVI, compare changes using MR etiology, and assess associations between MR etiology, early improvement, or residual discharge MR and mortality. Methods: In a retrospective single-center cohort, 112 TAVI patients with baseline more-than-moderate MR were included (functional n = 94; degenerative n = 18). MR grade was assessed pre-TAVI, at discharge, and at last available follow-up (serial studies up to ≥5 years), and 5-year all-cause mortality was analyzed. Results: At discharge, 34% of patients improved by more than one MR grade, and 26% by one grade. Among 45 patients with available late echocardiographic follow-up, 62% improved by more than one grade, 24% by one grade. Exploratory five-year survival analyses did not demonstrate a significant difference for MR etiology (p = 0.23), discharge MR grade (p = 0.11), or MR improvement status (p = 0.12). Conclusions: Among patients surviving to longitudinal echocardiographic follow-up, MR reduction was frequently observed after TAVI. Exploratory analyses did not demonstrate statistically significant differences in 5-year survival according to MR etiology, early MR improvement, or discharge MR severity. However, limited sample size and incomplete follow-up preclude definitive prognostic conclusions. Overall, these findings are compatible with a surveillance-first management, and with individualized consideration of adjunctive mitral therapy for persistent higher-grade symptomatic MR.

Aims: Fibroelastic deficiency (FED) and Barlow's disease represent subtypes of degenerative mitral valve prolapse (MVP). Whether these two conditions represent opposite ends of an anatomic spectrum or rather distinct etiologies remains unclear. Methods and Results: To study this question from a genetic perspective, we conducted the first genome-wide association study (GWAS) on anatomical subtypes of MVP, exploring the MVP-Munich and MVP-France cohorts, including 1,064 FED and 821 Barlow’s disease cases, and 11,923 controls. Patients were stratified via echocardiographic and surgical reports. GWAS meta-analysis was performed separately for FED and Barlow’s disease. The identified risk loci were analyzed via gene set enrichment analysis (GSEA), targeted variant-phenotype association analysis, and mitral valve tissue was analyzed in single-nucleus RNA-sequencing. For FED, one risk locus achieved genome-wide significance (p<5e-8) at 5q23.3 (CHSY3). For Barlow’s disease, two independent loci with genome-wide significance were identified at 5q35.2 (CPLX2) and 10q26.12 (WDR11). Further 30 additional independent signals showed a suggestive association (p<5e-5) with FED, and 30 different independent signals with Barlow’s disease. Targeted variant-phenotype association analysis revealed an association of FED with atrial arrhythmias, while Barlow’s disease was associated with atrial and ventricular arrhythmias. In combination with GSEA, our results linked Barlow’s disease to changes in cell cycle, transcription, senescence, and ubiquitination. FED was connected to cardiac, valvular, mesoderm, and endoderm development. Conclusions: This study suggests genetic heterogeneity between FED and Barlow’s disease and identifies risk loci for future investigation.