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This study aims to compare 1-year outcomes after transcatheter aortic valve replacement (TAVR) between patients with moderate–severe MR and severe MR preoperatively using the Japan Transcatheter Valve Therapy (J-TVT) registry. Patients undergoing TAVR for aortic stenosis between August 2013 and December 2019 with preoperative mitral regurgitation of moderate–severe (group MR3) or severe (group MR4) were included. Patients with a history of valve surgery and dialysis patients were excluded. A total of 2017 patients were included, and 1-year follow-up data were obtained from the registry (follow-up rate 98.5%). Propensity-score matching between MR3 and MR4 groups was performed. All-cause mortality and the composite outcome of death and/or heart failure events were compared. Crude data showed that 1-year survival was significantly higher in the MR 3 (89.8%) than MR 4 (84.7%) groups, and freedom from 1-year mortality and heart failure events was also higher in the MR 3 (87.1%) than MR 4 (80.5%) groups ( p  = 0.0001). After propensity-score matching, 452 cases (226 cases each in MR 3 group and MR 4 group) were extracted. Cox regression model showed no statistical difference in the 1-year survival rate between MR 3 group (84.5%) and MR 4 group (85.5%) ( p  = 0.84), nor in freedom from 1-year death and/or heart failure events between MR 3 group (80.2%) and MR 4 group (81.6%) ( p  = 0.72). The 1-year survival rate and freedom from death and/or heart failure events were found to be similar between patients undergoing TAVR with MR grade 3 and MR grade 4.

IntroductionHeart failure occasionally develops after transcatheter aortic valve implantation (TAVI) for severe aortic stenosis (AS), despite procedural success. Most cases present with mildly reduced or preserved left ventricular ejection fraction (LVEF), underscoring the role of diastolic dysfunction. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown benefits across the heart failure spectrum, independent of LVEF. The purpose of this randomised controlled trial is to determine whether adding a SGLT2 inhibitor to conventional medications improves LV diastolic function in patients with preserved LVEF after TAVI.Methods and analysisThis study is a prospective, single-centre, open-label, randomised, parallel-group, two-arm trial enrolling patients with mildly reduced or preserved LVEF (≥40%) undergoing TAVI for severe AS. Participants will be randomised in a 1:1 ratio to receive either conventional medications plus empagliflozin or conventional medications alone. In the empagliflozin group, participants will receive conventional medical therapy plus empagliflozin 10 mg orally once daily, initiated 4 weeks after TAVI. Empagliflozin treatment will continue throughout the study period. Participants in the control group will receive conventional medications without empagliflozin. The primary endpoint is the change in E/e’, assessed by echocardiography from treatment initiation at 4 weeks post TAVI (day 1) to day 168 (week 24). Each group will include 50 patients, totalling 100 patients.Ethics and disseminationEthical approval for this study has been obtained from the Chiba University Hospital Certified Clinical Research Review Board (CRB0111-25).Trial registration numberjRCT1031250190.

IntroductionThere are a substantial number of patients developing heart failure after transcatheter aortic valve implantation (TAVI) for severe aortic stenosis (AS), even though AS has been successfully treated. The purpose of this randomised controlled trial was to determine whether the addition of an angiotensin receptor–neprilysin inhibitor (ARNI), sacubitril/valsartan, is superior to conventional medications in lowering N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels in patients undergoing TAVI for AS.Methods and analysisThe study design is a prospective, single-centre, open-label, randomised, parallel-group, two-arm study, in which participants will be randomised in a 1:1 ratio to receive either conventional medications plus ARNI or conventional medications only. In the ARNI group, if a patient was on an ACE inhibitor or angiotensin II receptor blocker before TAVI, it will be switched to ARNI 100 mg/day (50 mg two times per day) on the first postoperative day. If not, candesartan 4 mg/day will be started 1–2 days before TAVI, and switched to ARNI 100 mg/day on the first postoperative day. As the patient has tolerability to ARNI, dosage will be increased stepwise to 400 mg/day 2–4 weeks apart. ARNI will be continued until at least 6-month follow-up. In the control group, the patient will receive conventional medications. The primary endpoint is the serum NT-proBNP value at 6-month follow-up after TAVI. Each group includes 42 patients (84 total patients).Ethics and disseminationEthical approval for this study has been obtained from the Chiba University Hospital Certified Clinical Research Review Board (CRB3180015). The study is ongoing. Findings from this study will be disseminated through peer-reviewed publications and conference presentations.Trial registration numberThis trial has been registered on the Japan Registry of Clinical Trials: jRCT1031220344.

Abstract A 74-year-old woman with a history of interstitial pneumonia, who had been taking oral corticosteroids for the past 9 years, was diagnosed with severe aortic stenosis. The patient underwent transfemoral transcatheter aortic valve replacement (TAVR) with a balloon-expandable valve under local anesthesia. After deploying a 26-mm SAPIEN 3 valve with 1.5 ml less balloon inflation, transesophageal echocardiography revealed a hemorrhage in the aortic annulus. Intraoperative angiography revealed a small contrast leakage around the ascending aorta. Emergent surgical aortic valve replacement was performed successfully, with a tear at the non-left commissure closed using interrupted sutures. The patient was discharged on postoperative day 14 with no paravalvular leakage. Chronic corticosteroid use may be a risk factor for annular ruptures during TAVR. Careful balloon dilation may be necessary, especially when balloon-expandable valves are used in patients receiving long-term corticosteroids.

Abstract We report a false lumen stent graft technique to close the intimal tears at the visceral segment for post-dissection thoracoabdominal aneurysm after initial thoracic endovascular aortic repair. Following abdominal endovascular aortic repair, a stent graft was then deployed in the false lumen, and successfully closed the intimal tears at the visceral segment. The residual re-entries at the iliac level were closed 2 years after the prior endovascular aortic repair, once a collateral network for spinal cord perfusion had developed, minimizing the risk of spinal cord ischemia. This endovascular strategy successfully reduced a size of post-dissection thoracoabdominal aneurysm.

Cellular senescence is deeply involved in physiological homeostasis, development, tissue repair, aging, and diseases. Senescent cells (SnCs) accumulate in aged tissues and exert deleterious effects by secreting proinflammatory molecules that contribute to chronic inflammation and aging-related diseases. We revealed that an aberrant interaction between glycolytic PGAM1 and Chk1 kinase is augmented in SnCs associated with increased glycolysis, whose byproduct, lactate, promotes this binding in a noncell autonomous manner. The pseudo-Warburg effect of SnCs with enhanced PPP (pentose phosphate pathway) activity is maintained by HIF-2α phosphorylation by Chk1 and subsequent upregulation of glycolytic enzymes, creating a vicious cycle reprogramming the glycolytic pathway in SnCs. HIF-2α also activates FoxM1 expression, which transcriptionally suppresses proapoptotic profiles, including BIM, and upregulates DNA repair machineries in SnCs. FoxM1 thus supports the genomic integrity and survival capacity of SnCs during their glycolytic changes. Chemical abrogation of PGAM1-Chk1 binding reverts these phenotypes and eliminates SnCs through senolysis. Inhibition of the PGAM1-Chk1 interaction improves physiological parameters during aging and inhibits lung fibrosis in mouse models. Our study highlights a novel pathway contributing to the metabolic reprogramming of SnCs and how the use of a new senolytic molecule that targets the PGAM-Chk1 interaction creates a specific vulnerability of those cells to potentially fight age-related diseases.