This study attempts to determine whether midwall myocardial fibrosis burden is associated with adverse clinical outcomes in asymptomatic patients and whether those with more fibrosis derive greater benefit from early intervention. QuestionIn asymptomatic patients with severe aortic stenosis, is myocardial fibrosis burden associated with adverse events and potential benefits of early valve intervention?FindingsIn this post hoc analysis of a randomized clinical trial, higher midwall fibrosis burden was associated with increasing incidence of the primary composite end point of all-cause death or unplanned aortic stenosis-related hospitalization. However, the potential beneficial effects of early valve intervention demonstrated no significant heterogeneity by the degree of midwall fibrosis.MeaningIn this study, in asymptomatic patients with severe aortic stenosis, higher fibrosis burden was associated with adverse outcomes; benefits of early intervention were similar between patients with high and low fibrosis burden. ImportanceMyocardial fibrosis burden has been associated with adverse clinical outcomes in symptomatic patients with aortic stenosis.ObjectiveTo determine whether midwall myocardial fibrosis burden is associated with adverse clinical outcomes in asymptomatic patients and whether those with more fibrosis derive greater benefit from early intervention.Design, Setting, and ParticipantsThis post hoc analysis of a randomized clinical trial was conducted between August 2017 and October 2022. The trial took place at 24 cardiac centers across the United Kingdom and Australia. Participants included asymptomatic patients with severe aortic stenosis and midwall fibrosis on cardiac magnetic resonance. These data were analyzed from October 2024 through June 2025.InterventionEarly intervention with transcatheter or surgical aortic valve replacement.Main Outcomes and MeasuresPrimary outcome was all-cause death or unplanned aortic stenosis-related hospitalization. Secondary outcomes included the individual components of the primary outcome.ResultsIn 224 trial participants (mean [SD] age, 73 [9] years; 63 women and 161 men, and mean [SD] aortic valve peak velocity 4.3 [0.5] m per second) with a median follow-up of 42 months, fibrosis burden (per 1% increase) was associated with an increase in the primary end point (hazard ratio [HR], 1.23; 95% CI, 1.08-1.37) and its component of unplanned aortic stenosis-related hospitalizations (HR, 1.22; 95% CI, 1.03-1.40) but not all-cause death (HR, 1.17; 95% CI, 0.98-1.35). There were no interactions between randomization arm and the midwall fibrosis burden for the primary (P for interaction = .39) or secondary end points. In patients with high fibrosis burden above the median, the primary end point occurred in 12 of 59 (20%) of those randomized to early intervention and 17 of 53 (32%) of those randomized to guideline-directed conservative management (HR, 0.62; 95% CI, 0.29-1.28). For the individual components, all-cause death occurred in 9 (15%) and 10 (19%) patients, respectively (HR, 0.84; 95% CI, 0.33-2.07), and unplanned aortic stenosis-related hospitalization in 4 (7%) and 13 (25%) patients respectively (HR, 0.27; 95% CI, 0.08-0.77). In patients with low fibrosis burden below the median, there were no differences in the primary outcome (HR, 1.05; 95% CI, 0.39-2.86) or its components between intervention groups.Conclusions and RelevanceIn this study, in asymptomatic patients with severe aortic stenosis, higher midwall fibrosis burden was associated with adverse outcomes. There was no demonstrable heterogeneity by the degree of midwall fibrosis for the treatment effects of early surgical or transcatheter aortic valve replacement compared to clinical surveillance.Trial RegistrationClinicalTrials.gov Identifier: NCT03094143

Paravalvular leak (PVL) is a well-known complication of valve replacement, occurring in up to 10% of aortic and 17% of mitral prosthetic valves. Although many leaks are small and clinically insignificant, ≈1% to 5% of cases are associated with clinically relevant complications, such as heart failure symptoms and hemolytic anemia. Surgical reoperation is currently considered the first-line option; however, it encompasses high mortality and morbidity risks. In the past years, transcatheter PVL closure has proven to be highly effective when performed in experienced centers. Transcatheter PVL closure requires advanced imaging modalities, specialized materials, and techniques, reflecting the high complexity of the procedure. We review the complex nature of PVL, including its diagnostic workup and the available transcatheter treatment strategies, with a special focus on the treatment of mitral and aortic PVL using plugging devices.

Mitral valve transcatheter edge-to-edge repair (M-TEER) is an established treatment option for patients with severe mitral regurgitation (MR) at high risk for surgery. However, the rate of recurrent MR ≥ 3+ after M-TEER may be up to 10% at 1 year. As the volume of M-TEER procedures increases, the number of patients experiencing recurrent MR post-TEER is also rising. M-TEER reshapes valve anatomy and complicates further treatment strategies for MR. In this review, the authors provide practical management considerations for patients with residual or recurrent MR after M-TEER.

Importance:Myocardial fibrosis burden has been associated with adverse clinical outcomes in symptomatic patients with aortic stenosis. Objective:To determine whether midwall myocardial fibrosis burden is associated with adverse clinical outcomes in asymptomatic patients and whether those with more fibrosis derive greater benefit from early intervention. Design, Setting, and Participants:This post hoc analysis of a randomized clinical trial was conducted between August 2017 and October 2022. The trial took place at 24 cardiac centers across the United Kingdom and Australia. Participants included asymptomatic patients with severe aortic stenosis and midwall fibrosis on cardiac magnetic resonance. These data were analyzed from October 2024 through June 2025. Intervention:Early intervention with transcatheter or surgical aortic valve replacement. Main Outcomes and Measures:Primary outcome was all-cause death or unplanned aortic stenosis-related hospitalization. Secondary outcomes included the individual components of the primary outcome. Results:In 224 trial participants (mean [SD] age, 73 [9] years; 63 women and 161 men, and mean [SD] aortic valve peak velocity 4.3 [0.5] m per second) with a median follow-up of 42 months, fibrosis burden (per 1% increase) was associated with an increase in the primary end point (hazard ratio [HR], 1.23; 95% CI, 1.08-1.37) and its component of unplanned aortic stenosis-related hospitalizations (HR, 1.22; 95% CI, 1.03-1.40) but not all-cause death (HR, 1.17; 95% CI, 0.98-1.35). There were no interactions between randomization arm and the midwall fibrosis burden for the primary (P for interaction = .39) or secondary end points. In patients with high fibrosis burden above the median, the primary end point occurred in 12 of 59 (20%) of those randomized to early intervention and 17 of 53 (32%) of those randomized to guideline-directed conservative management (HR, 0.62; 95% CI, 0.29-1.28). For the individual components, all-cause death occurred in 9 (15%) and 10 (19%) patients, respectively (HR, 0.84; 95% CI, 0.33-2.07), and unplanned aortic stenosis-related hospitalization in 4 (7%) and 13 (25%) patients respectively (HR, 0.27; 95% CI, 0.08-0.77). In patients with low fibrosis burden below the median, there were no differences in the primary outcome (HR, 1.05; 95% CI, 0.39-2.86) or its components between intervention groups. Conclusions and Relevance:In this study, in asymptomatic patients with severe aortic stenosis, higher midwall fibrosis burden was associated with adverse outcomes. There was no demonstrable heterogeneity by the degree of midwall fibrosis for the treatment effects of early surgical or transcatheter aortic valve replacement compared to clinical surveillance. Trial Registration:ClinicalTrials.gov Identifier: NCT03094143.

Background Complications of percutaneous coronary intervention (PCI) remain infrequent but are associated with a risk of serious injury or death. The techniques and devices required to manage them may be unfamiliar or unavailable to operators. Simulation-based learning (SBL) and human factors training (HFT) may serve as tools to increase operator skills and confidence in complication prevention and management.Methods A survey was given to participants during an SBL program delivered at a major international cardiovascular intervention course in 2023 and 2024. Prior experience with complications, access to equipment, and confidence in managing procedural PCI complications were established. Confidence was then reassessed following SBL training.Results A total of 308 cardiologists, from over 50 countries, completed the survey. Access to emergency equipment varied, with half of the operators lacking access to embolic coils. Despite an overall significant procedural experience, many operators were not confident in managing complications. Only 36.9% had undergone any prior HFT, 28.7% reported a lack of confidence in relying on their team, and 26.2% had neutral or negative expectations of obtaining support from colleagues when encountering complications. Structured SBL/HFT significantly improved operator confidence in complication recognition and management.Conclusion Effective management of PCI complications requires a practical know-how of specific techniques and access to devices that may not be routinely available. We found that structured SBL and HFT increase operator confidence in complication prevention and management. Further research should seek to investigate long-term outcomes of SBL use in the clinical management of procedural complications.

Abstract Background Maladaptive inflammatory responses are associated with adverse cardiac remodelling after myocardial infarction (MI), but clinical methods for detecting residual myocardial inflammation post-MI are lacking. Purpose To investigate somatostatin receptor subtype 2 (SST2) positron emission tomography (PET)/magnetic resonance imaging (MRI) using 68Ga-DOTATATE after MI. Methods In a prospective observational cohort study, infarct-related myocardial inflammation detected by 68Ga-DOTATATE PET at 2wk and 3mo post-MI was compared with MRI characteristics including left ventricular (LV) volumetric changes at 1yr, as well circulating immune cell phenotyping and serum proteomic markers. Patients with a prior history of MI or heart failure were excluded. Histological SST2 expression was assessed in myocardial biopsies. Results 38 participants (mean age 60 [SD 9] years; 84% male) with recent MI were enrolled, of whom 58% had an ST-segment elevation MI. Mean peak Troponin I was 16,665 (range 408 to >25,000) ng/L and mean post-infarct LV ejection fraction was 51 (SD 9) %. 68Ga-DOTATATE maximum standardized uptake values (SUVmax) at 10 (SD 4) days accurately localised infarcted myocardial segments defined by late-gadolinium enhancement MRI (LGE; Fig. 1); were 14.2% higher in akinetic/hypokinetic vs. normo-kinetic segments (p<0.0001); and were correlated both with peak segmental strain (r=0.47, p=0.003) and segmental T1 values (r=0.51, p=0.02). Mean infarct SUVmax was 19.7% lower on repeat PET/MRI after a mean 102 (SD 22) days (p<0.0001), and this change was in keeping with parallel reductions in T2-weighted oedema signal on MRI and serum biomarkers of cardiac injury and systemic inflammation. Residual inflammation assessed by mean infarct SUVmax at 3mo was correlated with ΔLV indexed end-diastolic volume at 369 (SD 14) days, after adjustment for baseline infarct size and other clinical variables (p=0.038). The 3mo:2wk ratio of mean infarct SUVmax was an even stronger predictor of adverse myocardial remodelling (p=0.0025). Circulating SST2+ classical monocytes were correlated with infarct 68Ga-DOTATATE signal (r=0.47, p=0.02), and SST2 was co-expressed with CD68+ macrophages in inflamed myocardial specimens of patients with recent MI and ischaemic heart failure. After statistical feature selection and multiple comparisons adjustments, among the blood markers associated with 3mo:2wk infarct SUVmax was CCL25, a chemokine involved in macrophage recruitment which has been implicated in adverse cardiac remodelling. Conclusions Here, in the first prospective clinical study of serial SST2 PET/MRI after MI, we show that 68Ga-DOTATATE can identify and track resolving infarct-related myocardial inflammation. Moreover, residual inflammation detected by 68Ga-DOTATATE is associated with long-term adverse myocardial remodelling and could provide a potential future imaging biomarker to help stratify high-risk patients for emerging immunomodulatory therapies.Figure 1.68Ga-DOTATATE PET-MRI after MI

Abstract Background The modern epidemiology of heart failure (HF) with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF) is yet to be studied on a population-wide scale in the United Kingdom, particularly in the post-COVID-19 era. Purpose To explore the post-pandemic epidemiology and outcomes of HFrEF and HFpEF in population-wide electronic health records (EHRs). Methods We accessed data in the National Health Service England’s Secure Data Environment for England via the British Heart Foundation Data Science Centre CVD-COVID-UK/COVID-IMPACT Consortium. We used EHRs for 57 million individuals to identify patients aged ≥18 years, of known sex, who were diagnosed with HF as the primary condition in any inpatient hospital stay from 01 Jan 2020 to 27 Feb 2023. By linking HF admissions with the National Heart Failure Audit, six other National Institute for Cardiovascular Outcomes Research audits, and the General Practice Extraction Service Data for Pandemic Planning and Research, we classified HF into HFrEF and HFpEF based on recorded left ventricular ejection fraction (LVEF; ≤40% and >40% respectively) or documented diagnosis. We compared characteristics of these groups and used Cox proportional hazards models, adjusted for key confounders, to examine differences in cause-specific mortality and hospitalisation outcomes. Results Over 3.2 years, we identified 208815 patients with a HF hospitalisation. 86110 (41%) patients had HFrEF, 65735 (31%) had HFpEF, and 56970 (27%) could not be categorised. Compared to patients with HFrEF, patients with HFpEF were older (mean [SD], 80.5 [10.9] vs 75.6 [13.6] years), more often female (n [%], 35990 [54.8] vs 30835 [35.8]), and less deprived (n [%] in the least-deprived Index of Multiple Deprivation 2019 quintile, 12275 [18.7] vs 15055 [17.5]; Table). Over a median follow-up of 11 months among patients with HFrEF and HFpEF, 99740 patients were re-hospitalised (66%) and 71075 (47%) died. Risks of all-cause, cardiovascular, non-cardiovascular, and heart-failure re-hospitalisations were all higher in patients with HFpEF compared with patients with HFrEF (Figure). The risk of all-cause mortality was modestly higher in patients with HFpEF (HR 1.04, 95% CI 1.02–1.06; Figure). Risks of death due to cardiovascular disease overall, fatal myocardial infarction, and fatal HF were higher among patients with HFrEF. In contrast, risks of death due to non-cardiovascular causes were higher in patients with HFpEF. There were no differences in risk of death due to COVID-19. Conclusions Unlike previous epidemiological surveys of HF, patients with HFpEF appear to face worse prognosis and risk-adjusted disease trajectories compared with those with HFrEF after hospitalisation in this population-wide study. Excess mortality in HFpEF appears driven by higher risk of non-cardiovascular mortality. However, post-discharge survival is poor regardless of LVEF and represents an ongoing target for quality improvement efforts.

BACKGROUND:Heart failure is common, complex, and often associated with coexisting chronic medical conditions and a high mortality. We aimed to assess the epidemiology of people admitted to hospital with heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF), including the period covering the COVID-19 pandemic, which was previously not well characterised. METHODS:In this retrospective, cohort study, we used whole-population electronic health records with 57 million individuals in England to identify patients hospitalised with heart failure as the primary diagnosis in any consultant episode of an in-patient admission to a National Health Service (NHS) hospital. We excluded individuals with less than 1 year of medical history records in primary or secondary care; admissions to NHS hospitals for which less than 10% of heart failure cases were linkable to the National Heart Failure Audit (NHFA); individuals younger than 18 years at the time of the heart failure hospitalisation; and patients who died in hospital during the index heart failure admission. For patients with new onset heart failure, we assessed incidence rates of 30-day and 1-year all-cause and cause-specific (cardiovascular, non-cardiovascular, and heart failure-related) emergency rehospitalisation and mortality after discharge, and dispensed guideline-recommended medical therapy (GRMT). Follow-up occurred from the index admission to the earliest occurrence of the event of interest, death, or end of data coverage. We estimated adjusted hazard ratios (HRs) to compare HFrEF with HFpEF. We computed population-attributable fractions to quantify the percentage of outcomes attributable to coexisting chronic medical conditions. FINDINGS:Among 233 320 patients identified who survived the index heart failure admission across 335 NHS hospitals between Jan 1, 2019, and Dec 31, 2022, 101 320 (43·4%) had HFrEF, 71 910 (30·8%) had HFpEF, and 60 090 (25·8%) had an unknown classification. In patients with new onset heart failure, there were reductions in all-cause 30-day (-5·2% [95% CI -7·7 to -2·6] in 2019-22) and 1-year rehospitalisation rates (-3·9% [-6·6 to -1·2]). Declining 30-day rehospitalisation rates affected patients with HFpEF (-4·8% [-9·2 to -0·2]) and HFrEF (-6·2% [-10·5 to -1·6]), although 1-year rates were not statistically significant for patients with HFpEF (-2·2% [-6·6 to 2·3] vs -5·7% [-10·6 to -0·5] for HFrEF). There were no temporal trends in incidence rates of 30-day or 1-year mortality after discharge. The rates of all-cause (HR 1·20 [1·18-1·22]) and cause-specific rehospitalisation were uniformly higher in those with HFpEF than those with HFrEF. Patients with HFpEF also had higher rates of 1-year all-cause mortality after discharge (HR 1·07 [1·05-1·09]), driven by excess risk of non-cardiovascular death (HR 1·25 [1·21-1·29]). Rates of rehospitalisation and mortality were highest in patients with coexisting chronic kidney disease, chronic obstructive pulmonary disease, dementia, and liver disease. Chronic kidney disease contributed to 6·5% (5·6-7·4) of rehospitalisations within 1 year for HFrEF and 5·0% (4·1-5·9) of rehospitalisations for HFpEF, double that of any other coexisting condition. There was swift implementation of newer GRMT, but markedly lower dispensing of these medications in patients with coexisting chronic kidney disease. INTERPRETATION:Rates of rehospitalisation in patients with heart failure in England have decreased during 2019-22. Further population health improvements could be reached through enhanced implementation of GRMT, particularly in patients with coexisting chronic kidney disease, who, despite being at high risk, remain undertreated. FUNDING:Wellcome Trust, Health Data Research UK, British Heart Foundation Data Science Centre.

Background Cerebral amyloid angiopathy (CAA) is a common cause of intracerebral haemorrhage (ICH) with a high recurrence risk. Left atrial appendage occlusion (LAAO) is a method for ischaemic stroke prevention in patients with atrial fibrillation (AF), potentially reducing the risk of intracranial bleeding in CAA-associated ICH. We aimed to determine the outcomes of patients with AF with CAA-associated ICH undergoing LAAO.Methods We conducted a multicentre study of patients with CAA-associated ICH who underwent LAAO for stroke prevention. We pooled our findings with data from a systematic review of relevant published studies of LAAO for AF in ICH survivors reporting CAA diagnosis.Results We included data from two published studies (n=65) with CAA-specific data and our cohort study (n=37), providing a total of 102 participants (mean age 76.2 +/- 8.0 years, 74.6% male) with CAA-related symptomatic ICH and AF treated with LAAO. The median follow-up period was 9.4 months (IQR 4.2-20.6). Postprocedural antithrombotic regimens varied between single (73.0%) or dual antiplatelet therapy (16.2%), or direct oral anticoagulant (DOAC) (10.8%), with a median duration of 42 days (IQR 35-74). Postprocedural complications were uncommon, but included transient arrhythmias (2.1%) and non-life-threatening tamponade (2.1%). Pooled incidence rates of ischaemic stroke and ICH during follow-up were 5.16 (95% CI 1.36 to 17.48) and 2.73 (95% CI 0.41 to 13.94) per 100 patient years, respectively.Conclusions LAAO followed by short-term antithrombotic therapy might be a safe and effective ischaemic stroke preventive strategy in people with CAA-associated ICH and AF. However, randomised controlled trials are needed to determine how LAAO compares with long-term DOAC in this population.PROSPERO registration number CRD42023415354.

BackgroundTotal coronary atherosclerotic plaque activity across the entire coronary arterial tree is associated with patient-level clinical outcomes.ObjectivesWe aimed to investigate whether vessel-level coronary atherosclerotic plaque activity is associated with vessel-level myocardial infarction.MethodsIn this secondary analysis of an international multicenter study of patients with recent myocardial infarction and multivessel coronary artery disease, we assessed vessel-level coronary atherosclerotic plaque activity using coronary 18F-sodium fluoride positron emission tomography to identify vessel-level myocardial infarction.ResultsIncreased 18F-sodium fluoride uptake was found in 679 of 2,094 coronary arteries and 414 of 691 patients. Myocardial infarction occurred in 24 (4%) vessels with increased coronary atherosclerotic plaque activity and in 25 (2%) vessels without increased coronary atherosclerotic plaque activity (HR: 2.08; 95% CI: 1.16-3.72; P = 0.013). This association was not demonstrable in those treated with coronary revascularization (HR: 1.02; 95% CI: 0.47-2.25) but was notable in untreated vessels (HR: 3.86; 95% CI: 1.63-9.10; Pinteraction = 0.024). Increased coronary atherosclerotic plaque activity in multiple coronary arteries was associated with heightened patient-level risk of cardiac death or myocardial infarction (HR: 2.43; 95% CI: 1.37-4.30; P = 0.002) as well as first (HR: 2.19; 95% CI: 1.18-4.06; P = 0.013) and total (HR: 2.50; 95% CI: 1.42-4.39; P = 0.002) myocardial infarctions.ConclusionsIn patients with recent myocardial infarction and multivessel coronary artery disease, coronary atherosclerotic plaque activity prognosticates individual coronary arteries and patients at risk for myocardial infarction.

Ventricular septal defects are a rare complication after acute myocardial infarction with a mortality close to 100% if left untreated. However, even surgical or interventional closure is associated with a very high mortality and currently no randomized controlled trials are available addressing the optimal treatment strategy of this disease. This state-of-the-art review and clinical consensus statement will outline the diagnosis, hemodynamic consequences and treatment strategies of ventricular septal defects complicating acute myocardial infarction with a focus on current available evidence and a focus on major research questions to fill the gap in evidence.

There are sex differences in the extent, severity, and outcomes of coronary artery disease. We aimed to assess the influence of sex on coronary atherosclerotic plaque activity measured using coronary 18F-sodium fluoride (18F-NaF) positron emission tomography (PET), and to determine whether 18F-NaF PET has prognostic value in both women and men. In a post-hoc analysis of observational cohort studies of patients with coronary atherosclerosis who had undergone 18F-NaF PET CT angiography, we compared the coronary microcalcification activity (CMA) in women and men. Baseline 18F-NaF PET CT angiography was available in 999 participants (151 (15

Percutaneous left atrial appendage occlusion aims to reduce the risk of stroke in patients with AF, particularly those who are not good candidates for systemic anticoagulation. The procedure has been studied in large international randomised trials and registries and was approved by the National Institute for Health and Care Excellence in 2014 and by NHS England in 2018. This position statement summarises the evidence for left atrial appendage occlusion and presents the current indications. The options and consensus on best practice for pre-procedure planning, undertaking a safe and effective implant and appropriate post-procedure management and follow-up are described. Standards regarding procedure volume for implant centres and physicians, the role of multidisciplinary teams and audits are highlighted.

Post-infarction ventricular septal defect is a mechanical complication of acute MI. The incidence of this complication is low in the primary percutaneous coronary intervention era. However, the associated mortality is very high at 94% with medical management alone. Open surgical repair or percutaneous transcatheter closure still has an in-hospital mortality >40%. Retrospective comparisons between both closure methods are limited by observation and selection bias. This review addresses the assessment and optimisation of patients prior to repair, the optimal timing of repair, and the limitations in current data. The review considers techniques for percutaneous closure, and finally considers the path that future research should take to improve outcomes for patients.

ostinfarct inflammation and its resolution modulate ischemic injury after myocardial infarction (MI). While cardiac magnetic resonance imaging (MRI) is useful for assessing ventricular function, viability, and struc-tural complications after MI, as well as detecting edema associated with acute inflammation, it lacks specificity for immune cell activity and may be less sensitive for identifying persistent, low-grade inflammation. Positron emission tomography (PET)

BACKGROUND:Data regarding the safety and long-term effectiveness of percutaneous closure of paravalvular leak (PVL) after transcatheter aortic valve implantation (TAVI) are scarce. AIMS:This study aims to present a large multicentre international experience of percutaneous post-TAVI PVL closure. METHODS:All patients who underwent percutaneous post-TAVI PVL closure in 14 hospitals across Europe and North America between January 2018 and October 2022 were included. RESULTS:Overall, 45 patients (64% male) were enrolled. The median age was 80 years (75-84). Among them, 67% and 33% had self-expanding and balloon-expandable valve implantations, respectively. Baseline post-TAVI PVL was severe in 67% of cases and moderate in the rest. The time from index TAVI to PVL closure procedure was 16.1 (8.7-34.8) months. Most patients were in NYHA Class III and IV (73%) before the procedure, and 40% had referred hospitalisations for heart failure between TAVI and the PVL closure procedure. Successful PVL closure was achieved in 94%, reducing regurgitation to ≤mild in 91% and moderate in the rest. The Amplatzer Valvular Plug III was the most frequently used device (27 cases), followed by the Amplatzer Valvular Plug 4. The incidence of severe adverse events was 11%. None of the patients died during the index hospitalisation. During long-term follow-up (21.7±16.2 months), the all-cause mortality rate was 14%, and patients presented improvement in functional status and a significant reduction in the rate of hospitalisation for heart failure (from 40% to 6%). CONCLUSIONS:Percutaneous PVL closure is a feasible and safe option for treating post-TAVI leaks. Successful PVL reduction to mild or less could be associated with acute and long-lasting improvements in clinical outcomes.

Importance:Recurrent coronary events in patients with recent myocardial infarction remain a major clinical problem. Noninvasive measures of coronary atherosclerotic disease activity have the potential to identify individuals at greatest risk.Objective:To assess whether coronary atherosclerotic plaque activity as assessed by noninvasive imaging is associated with recurrent coronary events in patients with myocardial infarction.Design, Setting, and Participants:This prospective, longitudinal, international multicenter cohort study recruited participants aged 50 years or older with multivessel coronary artery disease and recent (within 21 days) myocardial infarction between September 2015 and February 2020, with a minimum 2 years' follow-up.Intervention:Coronary 18F-sodium fluoride positron emission tomography and coronary computed tomography angiography.Main Outcomes and Measures:Total coronary atherosclerotic plaque activity was assessed by 18F-sodium fluoride uptake. The primary end point was cardiac death or nonfatal myocardial infarction but was expanded during study conduct to include unscheduled coronary revascularization due to lower than anticipated primary event rates.Results:Among 2684 patients screened, 995 were eligible, 712 attended for imaging, and 704 completed an interpretable scan and comprised the study population. The mean (SD) age of participants was 63.8 (8.2) years, and most were male (601 [85%]). Total coronary atherosclerotic plaque activity was identified in 421 participants (60%). After a median follow-up of 4 years (IQR, 3-5 years), 141 participants (20%) experienced the primary end point: 9 had cardiac death, 49 had nonfatal myocardial infarction, and 83 had unscheduled coronary revascularizations. Increased coronary plaque activity was not associated with the primary end point (hazard ratio [HR], 1.25; 95% CI, 0.89-1.76; P = .20) or unscheduled revascularization (HR, 0.98; 95% CI, 0.64-1.49; P = .91) but was associated with the secondary end point of cardiac death or nonfatal myocardial infarction (47 of 421 patients with high plaque activity [11.2%] vs 19 of 283 with low plaque activity [6.7%]; HR, 1.82; 95% CI, 1.07-3.10; P = .03) and all-cause mortality (30 of 421 patients with high plaque activity [7.1%] vs 9 of 283 with low plaque activity [3.2%]; HR, 2.43; 95% CI, 1.15-5.12; P = .02). After adjustment for differences in baseline clinical characteristics, coronary angiography findings, and Global Registry of Acute Coronary Events score, high coronary plaque activity was associated with cardiac death or nonfatal myocardial infarction (HR, 1.76; 95% CI, 1.00-3.10; P = .05) but not with all-cause mortality (HR, 2.01; 95% CI, 0.90-4.49; P = .09).Conclusions and Relevance:In this cohort study of patients with recent myocardial infarction, coronary atherosclerotic plaque activity was not associated with the primary composite end point. The findings suggest that risk of cardiovascular death or myocardial infarction in patients with elevated plaque activity warrants further research to explore its incremental prognostic implications.