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Constantinos Kallis,1– 3 Amit Kaura,1,3 Nathan A Samuel,4 Abdulrahim Mulla,3 Ben Glampson,3 Kevin O’Gallagher,5 Jim Davies,4 Dimitri Papadimitriou,3 Kerrie J Woods,4 Anoop D Shah,6,7 Bryan Williams,6,7 Folkert W Asselbergs,6,7 Erik K Mayer,3,8 Richard W Lee,1,9 Christopher Herbert,10 Stuart W Grant,11 Nick Curzen,12 Iain B Squire,13 Thomas Johnson,14 Ajay M Shah,15 Divaka Perera,5 Rajesh K Kharbanda,4 Riyaz S Patel,6 Keith M Channon,4 Jamil Mayet,1,3 Jennifer K Quint1– 3 1National Heart and Lung Institute, Imperial College London, London, UK; 2School of Public Health, Imperial College London, London, UK; 3NIHR Imperial Biomedical Research Centre, Imperial College London and Imperial College Healthcare NHS Trust, London, UK; 4NIHR Oxford Biomedical Research Centre, University of Oxford and Oxford University Hospitals NHS Foundation Trust, Oxford, UK; 5NIHR King’s Biomedical Research Centre, King’s College London and King’s College Hospital NHS Foundation Trust, London, UK; 6NIHR University College London Biomedical Research Centre, University College London and University College London Hospitals NHS Foundation Trust, London, UK; 7Institute of Health Informatics, University College London, London, UK; 8Imperial Clinical Analytics, Research & Evaluation (iCARE) and Department of Surgery & Cancer, Imperial College London, London, UK; 9Early Diagnosis and Detection Centre, NIHR BRC at The Royal Marsden and Institute of Cancer Research, London, UK; 10NIHR Leeds Clinical Research Facility, Leeds Teaching Hospitals Trust and University of Leeds, Leeds, UK; 11NIHR Manchester Biomedical Research Centre, Manchester University NHS Foundation Trust and the University of Manchester, Manchester, UK; 12NIHR Southampton Clinical Research Facility and Biomedical Research Centre, Faculty of Medicine, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, UK; 13NIHR Leicester Biomedical Research Centre, Glenfield Hospital, and Department of Cardiovascular Sciences, University of Leicester, Leicester, UK; 14NIHR Bristol Biomedical Research Centre, University of Bristol and University Hospitals Bristol NHS Foundation Trust, Bristol, UK; 15NIHR Guys & St Thomas’ Hospital Clinical Research Facility, King’s College Hospital, and King’s College London British Heart Foundation Centre of Excellence, London, UKCorrespondence: Jennifer K Quint, School of Public Health, Imperial College London, Floor 9, Sir Michael Uren Building, 86 Wood Ln, London, W12 0BZ, United Kingdom, Email j.quint@imperial.ac.ukBackground: No single biomarker currently risk stratifies chronic obstructive pulmonary disease (COPD) patients at the time of an exacerbation, though previous studies have suggested that patients with elevated troponin at exacerbation have worse outcomes. This study evaluated the relationship between peak cardiac troponin and subsequent major adverse cardiac events (MACE) including all-cause mortality and COPD hospital readmission, among patients admitted with COPD exacerbation.Methods: Data from five cross-regional hospitals in England were analysed using the National Institute of Health Research Health Informatics Collaborative (NIHR-HIC) acute coronary syndrome database (2008– 2017). People hospitalised with a COPD exacerbation were included, and peak troponin levels were standardised relative to the 99th percentile (upper limit of normal). We used Cox Proportional Hazard models adjusting for age, sex, laboratory results and clinical risk factors, and implemented logarithmic transformation (base-10 logarithm). The primary outcome was risk of MACE within 90 days from peak troponin measurement. Secondary outcome was risk of COPD readmission within 90 days from peak troponin measurement.Results: There were 2487 patients included. Of these, 377 (15.2%) patients had a MACE event and 203 (8.2%) were readmitted within 90 days from peak troponin measurement. A total of 1107 (44.5%) patients had an elevated troponin level. Of 1107 patients with elevated troponin at exacerbation, 256 (22.8%) had a MACE event and 101 (9.0%) a COPD readmission within 90 days from peak troponin measurement. Patients with troponin above the upper limit of normal had a higher risk of MACE (adjusted HR 2.20, 95% CI 1.75– 2.77) and COPD hospital readmission (adjusted HR 1.37, 95% CI 1.02– 1.83) when compared with patients without elevated troponin.Conclusion: An elevated troponin level at the time of COPD exacerbation may be a useful tool for predicting MACE in COPD patients. The relationship between degree of troponin elevation and risk of future events is complex and requires further investigation.Keywords: COPD, CVD, exacerbation

Objective: To examine whether endogenous bradykinin mediates the endothelium-dependent vasomotor dysfunction induced by ischaemia-reperfusion injury, or the protection afforded by remote ischaemic preconditioning in vivo in man.Design: Randomised double-blind, cross-over study.Settings: Royal Infirmary of Edinburgh, Wellcome Trust Clinical Research Facility.Patients: Twenty healthy male volunteers.Interventions: Subjects were randomised to intravenous infusion of the bradykinin B(2) receptor antagonist, HOE-140 (100 μg/kg), or saline placebo in a double-blind, crossover trial. Ischaemia-reperfusion injury was induced in the non-dominant arm by inflating a cuff to 200 mm Hg for 20 min in all subjects. Ischaemia-reperfusion injury was preceded by three cycles of remote ischaemic preconditioning in the dominant arm in 10 subjects.Main Outcome Measures: Bilateral forearm blood flow was assessed using venous occlusion plethysmography during intra-arterial infusion of acetylcholine (5-20 μg/min).Results: Acetylcholine caused vasodilatation in all studies (p<0.05) that was attenuated by ischaemia-reperfusion injury, both in the presence (p=0.0002) and absence (p=0.04) of HOE-140. Remote ischaemic preconditioning abolished the impairment of endothelium-dependent vasomotor function induced by ischaemia-reperfusion injury. HOE-140 had no effect on the protection afforded by remote ischaemic preconditioning.Conclusions: These findings do not support a major role for endogenous bradykinin, acting via the B(2) kinin receptor, in the mechanism of ischaemia-reperfusion injury or the protective effects of remote ischaemic preconditioning in man.Clinical Trial Registration Information: NCT00965120 and NCT00965393. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We assessed the causes of imbalance of oxygen transport by continuously measuring oxygen consumption (VO2) during hypothermic cardiopulmonary bypass (CPB) in pigs. METHODS: Six pigs (17.2+/-1.6 kg) underwent hypothermic (32 degrees C) CPB for 180 min with 120 min of aortic crossclamping (ACC). An AMIS 2000 mass spectrometer was adapted for the on-line measurement of VO2. Arterial lactate was measured at the beginning of CPB, the end of hypothermia, before and 10 min after ACC release, 20 min later, and at the end of CPB. RESULTS: Arterial lactate increased from 1.8+/-0.7 to 5.1+/-1.8 mmol/L during CPB. Hypothermia reduced VO2 by 0.63+/-0.29 mlmin/kg per degrees C, but lactate increased to 4.2+/-1.5 mmol/L (p <0.05). The most rapid rise of VO2 and lactate occurred during the first 10 min after ACC removal, accounting for 26% and 68%, respectively, of the total rise during rewarming. CONCLUSIONS: Inadequate tissue oxygenation persists throughout hypothermic CPB. The rise in systemic VO2 and lactate immediately after ACC release may reflect inadequate oxygen transport within the myocardium during ischemia and manifest on reperfusion. This simple technique may be used to provide important information regarding the dynamic balance of systemic and myocardial oxygen transport during ischemia-reperfusion. [ABSTRACT FROM AUTHOR]

Cerebrovascular events (CVEs) are a dreaded complication of transcatheter aortic valve replacement (TAVR). They are associated with significant mortality, morbidity, and reduced quality of life and impose a significant burden to health care systems. Although the rates of clinical stroke have reduced since the advent of TAVR, it remains an important complication, particularly as TAVR is increasingly utilized. CVE may occur at the time of the TAVR, as a direct consequence of the procedure, or may occur later, related to thrombosis of the prosthetic valve, atrial fibrillation, and other comorbidities. Imaging of the brain has revealed a high prevalence of subclinical cerebral infarcts (68%-98%) associated with the TAVR procedure. Although their clinical significance has not been fully established, clinically evident CVE ranges between 3% and 5% in patients considered at high operative risk to between 1% and 3% in low operative risk patients. Periprocedural CVEs are largely the result of embolization of the thrombus and tissue derived from the valve, vasculature, or myocardium. Cerebral embolic protection devices have been studied in multiple trials, with some evidence supporting a reduction in new cerebral lesion volume, number, and potentially disabling strokes. However, thus far, there is no robust evidence that they reduce the overall stroke rate. The number and severity of comorbidities, in particular, new-onset atrial fibrillation, are associated with CVEs. Valve thrombosis diagnosed using computed tomography as areas of hypoattenuated leaflet thickening has been identified in 10% to 15% of patients. This is a dynamic process associated with an increase in CVEs, but that resolves with anticoagulation or sometimes without it. Routine use of anticoagulation compared with a single antiplatelet agent is associated with an increased risk of bleeding, without any additional alleviation in risk of thromboembolism. Future studies to improve risk stratification could facilitate the tailoring of preventive therapies to patients at high risk of CVE, who stand to gain the most benefit., Competing Interests: Dr Patel reports unrestricted research grant from Edwards Lifesciences. Dr Lansky reports compensation from Emboline for other services; compensation from Boston Scientific Corporation for consultant services; compensation from Cordis for consultant services; employment by Yale School of Medicine; compensation from Abiomed for consultant services; and compensation from ShockWave Medical, Inc, for consultant services. B. Prendergast reports compensation from Edwards Lifesciences for other services; employment by Cleveland Clinic; compensation from Cardiawave for data and safety monitoring services; and compensation from Medtronic for other services. Dr Baumbach reports research support from Abbott Vascular; speaker fees from Abbott Vascular, MicroPort, AstraZeneca, and Sinomed. Dr Rathod reports compensation from the European Heart Journal for consultant services; compensation from the Journal of Cardiovascular Development and Disease for consultant services; compensation from the Journal of the American Heart Association for consultant services; compensation from Cardiovascular Imaging Frontiers in Cardiovascular Medicine for consultant services; employment by Barts and The London School of Medicine and Dentistry; compensation from Coronary Artery Disease Frontiers in Cardiovascular Medicine for consultant services; and compensation from Cardiovascular Pharmacology and Drug Discovery for consultant services. Dr Kharbanda reports grants from Boston Scientific Corporation. The other authors report no conflicts.

Objectives: This study aims to investigate the occurrence, type and correlation of early and late atrial arrhythmias following mitral valve repair in patients with no preoperative history of atrial arrhythmias., Methods: Patients undergoing mitral valve (MV) repair for degenerative disease were included. Early and late postoperative electrocardiograms were evaluated for the incidence and type of atrial arrhythmia (atrial fibrillation [AF] or atrial tachycardia [AT])., Results: The 192 patients were included. Early atrial arrhythmias occurred in 100/192 (52.1%) patients; AF in 61 (31.8%) patients, early AT in 15 (7.8%) and both in 24 (12.5%). In total 89% of patients were discharged in sinus rhythm. During a follow-up time of 7.3 years, 14 patients (7.3%) died and 49 (25.5%) patients developed late atrial arrhythmias. At 10 years, the cumulative incidence of any late atrial arrhythmia, with death as competing risk, was 64% (95% confidence interval [CI] = 55%-72%). On Fine-Gray model analysis, only early postoperative AF lasting >24 h was related to the development of late AF (hazard ratio 5.99, 95% CI = 1.78%-20.10%, p = .004). Early postoperative ATs were related to the development of late tachycardias, independent of their duration (<24 h hazard ratio 4.25, 95% CI = 1.89-9.57, p = .001 and >24 h hazard ratio 3.51, 95% CI = 1.65-7.46, p = .001)., Conclusions: Early and late atrial arrhythmias were common after MV repair surgery. Only early postoperative AF lasting >24 h was a risk factor for the occurrence of late AF. Conversely, any postoperative AT was correlated to the development of late ATs., (© 2024 The Author(s). Journal of Cardiovascular Electrophysiology published by Wiley Periodicals LLC.)

Background: For patients with severe aortic stenosis, transcatheter aortic valve implantation (TAVI) is a less invasive but equally effective treatment option compared with surgical aortic valve replacement (SAVR). In 2019, we reported low rates of TAVI in the UK compared with other countries in western Europe and highlighted profound geographical variation in TAVI care. Here, we provide contemporary data on access to aortic valve replacement by either TAVI or SAVR across clinical commissioning groups in England., Methods: We obtained aggregated data from the UK TAVI registry and the National Adult Cardiac Surgery Audit between 2019 and 2023. Rates of TAVI and SAVR procedures per million population were reported by clinical commissioning groups. The relationship between TAVI and SAVR rates was determined using Pearson correlation coefficients., Results: In 2022/23, the rates of TAVI and SAVR in England were 136 per million population and 60 per million population, respectively. The observed increase in TAVI rates since 2019/20 corresponded with a decline in SAVR rates. There remains substantial variation in access to both procedures, with an over tenfold variation in TAVI rates, and an over fourfold variation in SAVR rates across clinical commissioning groups in England. No relationship was identified between the rates of TAVI and those for SAVR (correlation coefficient 0.06)., Conclusion: Geographical heterogeneity in access to TAVI persists over time, with the low rates of TAVI in many areas not compensated for by higher rates of SAVR, indicating an overall inequality in the treatment of severe aortic stenosis., Competing Interests: Disclosure: SA has received an educational grant from the European Society of Cardiology. NA has received speaker fees from Abbott and Medtronic. NC has received grants from Boston Scientific, Beckman Coulter, Heartflow and Haemonetics, consulting fees from Abbott Vascular, speaker fees from HeartFlow and Abbott Vascular, educational meeting support from Abbott and Edwards and is on the Interventional Cardiology editorial board; this did not influence peer review. ATG is the Clinical Lead of the UK National Adult Cardiac Surgery Audit and a member of the Society for Cardiothoracic Surgeons. DHS is the president of the British Cardiovascular Intervention Society and a proctor/advisory to Medtronic, Abbott, Boston and Edwards. RKK has received institutional grants for trials from Boston Scientific, speaker fees from Boston and Medtronic and is on the advisory board for Boston Scientific and Medtronic. DJB has received institutional research grants from Medtronic and consulting fees from Abbott Vascular and Medtronic and speaker fees from Abbott Vascular and Medtronic. All other authors have no conflicts of interest to declare. Data availability: These data are available as part of the series of annual reports of the National Cardiac Audit Program produced by NICOR. Authors’ contributions: Conceptualisation: DJB, DHS, PFL, RKK, ATG; data curation: SA, PDJ; formal analysis: PDJ, SM, SP; investigation: DJB, SA, NA; methodology: DJB, SA, NA; resources: PFL, RKK; software: PDJ, SM, SP; supervision: DJB; validation: DJB, DHS, PFL, RKK, ATG; writing – original draft preparation: SA, NA; writing – review & editing: DB, SA, NA, PL, NC, AG, DHS, RK, PJ, SM, SP. Ethics: This is an observational study. The NICOR Research Committee has confirmed that no ethical approval is required. Consent: All National Institute for Cardiovascular Outcomes Research (NICOR) audits and registries have approval under Section 251 of the NHS Act 2006 to use patient data, without obtaining patient consent., (Copyright © The Author(s), 2024. Published by Radcliffe Group Ltd.)

Aim: Acute injury and subsequent remodelling responses to ST-segment elevation myocardial infarction (STEMI) are major determinants of clinical outcome. Current imaging and plasma biomarkers provide delayed readouts of myocardial injury and recovery. Here, we sought to systematically characterize all microRNAs (miRs) released during the acute phase of STEMI and relate miR release to magnetic resonance imaging (MRI) findings to predict acute and late responses to STEMI, from a single early blood sample., Methods and Results: miRs were quantified in blood samples obtained from patients after primary PCI (PPCI) for STEMI. Cardiac MRI (cMRI) was performed to quantify myocardial edema, infarct size and salvage index. Regression models were constructed to predict these outcomes measures, which were then tested with a validation cohort. Transcoronary miR release was quantified from paired measurements of coronary artery and coronary sinus samples. A cell culture model was used to identify endothelial cell-derived miRs.A total of 72 patients undergoing PPCI for acute STEMI underwent miR analysis and cMRI. About >200 miRs were detectable in plasma after STEMI, from which 128 miRs were selected for quantification in all patients. Known myocardial miRs demonstrated a linear correlation with troponin release, and these increased across the transcoronary gradient. We identified novel miRs associated with microvascular injury and myocardial salvage. Regression models were constructed using a training cohort, then tested in a validation cohort, and predicted myocardial oedema, infarct size and salvage index., Conclusion: Analysis of miR release after STEMI identifies biomarkers that predict both acute and late outcomes after STEMI. A novel miR-based biomarker score enables the estimation of area at risk, late infarct size and salvage index from a single blood sample 6 hours after PPCI, providing a simple and rapid alternative to serial cMRI characterization of STEMI outcome., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Pain and anxiety are common in patients undergoing cardiac surgery and percutaneous cardiac interventions. Virtual reality (VR) is an emerging non-pharmacological tool for pain and anxiety management. However, its application around cardiac procedures remains relatively unexplored. In this review, we perform a targeted non-systematic literature review to assess the current state-of-the-art of VR for pain and anxiety management in patients undergoing cardiac procedures. Contexts of interest were preprocedural, periprocedural, and postprocedural applications. Existing trials show inconsistent results. The majority of studies in the preprocedural (7 studies, n = 302), periprocedural (1 study, n = 99), and postprocedural stage (4 studies, n = 214) demonstrate significant reduction of pain and anxiety through VR distraction therapy or VR patient education. However, larger-scale trials (2 preprocedural studies [n = 233], 1 periprocedural study [n = 32], 2 postprocedural studies [n = 300]) report no effect. Current literature on effectiveness of VR for pain and anxiety management in cardiac surgery and interventional cardiology remains inconclusive., Competing Interests: The authors have reported that they have no relationships relevant to the contents of this paper to disclose., (© 2024 The Authors.)

Background: Publication of the BRIGHT-4 trial results has restimulated discussion about the optimal periprocedural antithrombotic strategy for patients undergoing percutaneous coronary intervention (PCI) with acute coronary syndromes (ACS). It is possible that variation in the infusion duration, may contribute to observed differences in safety-efficacy profiles of bivalirudin in this clinical setting., Methods: Up to December 2022, randomized controlled trials (RCTs) comparing bivalirudin (either administered peri-procedurally or accompanied by postprocedural infusion) and heparin, both with or without GPI, were searched and entered in a frequentist network meta-analysis. Co-primary endpoints were trial-defined major adverse composite events (MACE) and major bleeding. Incident rate ratios (IRR) and 95 % confidence intervals (CI) were estimated., Results: 10 RCTs (N = 57,137 patients/month) were included. As compared to heparin, prolonged bivalirudin infusion resulted in lower rates of major bleeding (IRR 0.58, 95 % CI 0.36-0.91), but there was no differences in MACE rates between these strategies. With regard to NACE, prolonged bivalirudin infusion yielded lower risk (IRR 0.86, 95 % CI 0.77-0.96), whereas both bivalirudin and heparin increased risk when coupled with GPI (IRR 1.24, 95 % CI 1.01-1.51 and IRR 1.24, 95 % CI 1.06-1.44, respectively). Both these combination strategies also increased minor bleeding rates (IRR 1.49, 95 % CI 1.16-1.93 and IRR 1.58, 95 % CI 1.29-1.95, respectively, for bivalirudin and heparin). Results were consistent across several sensitivity analyses., Conclusion: In patients with ACS undergoing PCI, procedural bivalirudin administration followed by prolonged infusion results in lower major bleeding rates, but there does not appear to be a difference in observed MACE., Competing Interests: Declaration of competing interest None., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Objective: Studies investigating the efficacy of concomitant surgical atrial fibrillation (AF) ablation in hypertrophic obstructive cardiomyopathy (HOCM) patients undergoing myectomy are scarce and limited in terms of sample size. We aim to summarize current outcomes of concomitant surgical AF ablation in HOCM patients undergoing surgical myectomy., Methods: This systematic review and meta-analysis was performed according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We included all studies reporting any of the following outcomes of concomitant surgical AF ablation in HOCM patients: freedom from recurrence of AF, overall survival and complications. Outcomes were evaluated using traditional meta-analysis at given time-points and using pooled Kaplan-Meier curves., Results: A total of 13 studies were included, resulting in a total of 616 individual patients available for analysis. AF was paroxysmal in 68.1% of the patients (95% CI 56.0-78.2%; I 2  = 87.1%; 8 studies, 583 participants). The majority of patients (86.2%) underwent either conventional Cox Maze III or IV (95% CI 39.7-98.3%; I 2  = 92.4%; 8 studies, 616 patients) procedure. The incidence of early post-operative pacemaker implantation was 6.1% (95% CI 3.1-11.8%). Overall survival at 3, 5 and 7 years was 95.6% (95% CI 93.4-97.9%), 93.6% (95% CI 90.8-96.5%) and 90.5% (95% CI 86.5-94.6%), respectively. Freedom from recurrent AF at 3, 5 and 7 years was 77.6% (95% CI 73.7-81.7%), 70.6% (95% CI 65.8-75.7) and 63.2% (95% CI 56.2-73.8%), respectively., Conclusion: This meta-analysis supports concomitant surgical AF ablation at the time of surgical myectomy in HOCM patients, as it seems to be safe and effective in terminating AF., Competing Interests: Declaration of Competing Interest None declared., (Copyright © 2023 The Authors. Published by Elsevier B.V. All rights reserved.)

Background: Low-level vagus nerve stimulation through the tragus (tLLVNS) is increasingly acknowledged as a therapeutic strategy to prevent and treat atrial fibrillation. However, a lack in understanding of the exact antiarrhythmic properties of tLLVNS has hampered clinical implementation., Objectives: In this study, the authors aimed to study the effects of tLLVNS on atrial electrophysiology by performing intraoperative epicardial mapping during acute and chronic tLLVNS., Methods: Epicardial mapping of the superior right atrium was performed before and after arterial graft harvesting in patients undergoing coronary artery bypass grafting without a history of atrial fibrillation. The time needed for arterial graft harvesting was used to perform chronic tLLVNS. Electrophysiological properties were compared before and during chronic tLLVNS., Results: A total of 10 patients (median age 74 years [IQR: 69-78 years]) underwent tLLVNS for a duration of 56 minutes (IQR: 43-73 minutes). During acute and chronic tLLVNS, a shift of the sinoatrial node exit site toward a more cranial direction was observed in 5 (50%) patients. Unipolar potential voltage increased significantly during acute and chronic tLLVNS (3.9 mV [IQR: 3.1-4.8 mV] vs 4.7 mV [IQR: 4.0-5.3 mV] vs 5.2 mV [IQR: 4.8-7.0 mV]; P = 0.027, P = 0.02, respectively). Total activation time, slope of unipolar potentials, amount of fractionation, low-voltage areas and conduction velocity did not differ significantly between baseline measurements and tLLVNS. Two patients showed consistent "improvement" of all electrophysiological properties during tLLVNS, while 1 patient appeared to have no beneficial effect., Conclusions: We demonstrated that tLLVNS resulted in a significant increase in unipolar potential voltage. In addition, we observed the following in selective patients: 1) reduction in total activation time; 2) steeper slope of unipolar potentials; 3) decrease in the amount of fractionation; and 4) change in sinoatrial node exit sites., Competing Interests: Funding Support and Author Disclosures Dr Kharbanda is supported by a grant from the Dutch Heart Foundation (2019T091). Dr de Groot is supported by funding grants from NWO-Vidi (grant number 91717339), Biosense Webster USA (ICD 783454) and Medical Delta. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Transcatheter aortic valve implantation (TAVI) is an established treatment for aortic stenosis. Cerebral embolic protection (CEP) devices may impact periprocedural stroke by capturing debris destined for the brain. However, there is a lack of high-quality randomised trial evidence supporting the use of CEP during TAVI. The British Heart Foundation (BHF) PROTECT-TAVI trial will address whether the routine use of CEP reduces the incidence of stroke in patients undergoing TAVI. BHF PROTECT-TAVI is a prospective, open-label, outcome-adjudicated, multicentre randomised controlled trial. The trial is open to all adult patients scheduled for TAVI at participating specialist cardiac centres across the United Kingdom who are able to receive the CEP device. The trial will recruit 7,730 participants. Participants will be randomised in a 1:1 ratio to undergo TAVI with CEP or TAVI without CEP (standard of care). The primary outcome is the incidence of stroke at 72 hours post-TAVI. Key secondary outcomes include the incidence of stroke and all-cause mortality up to 12 months post-TAVI, disability and cognitive outcomes, stroke severity, access site complications and a health economics analysis. The sample size of 7,730 participants has 80% power to detect a 33% relative risk reduction from a 3% incidence of the primary outcome in the controls. Trial recruitment commenced in October 2020. As of October 2022, 3,068 patients have been enrolled. BHF PROTECT-TAVI is designed to provide definitive evidence on the clinical efficacy and cost-effectiveness of using routine CEP with the SENTINEL device to reduce stroke in TAVI.

Aims: Loss of cell-to-cell communication results in local conduction disorders and directional heterogeneity (LDH) in conduction velocity (CV) vectors, which may be unmasked by premature atrial contractions (PACs). We quantified LDH and examined differences between sinus rhythm (SR) and spontaneous PACs in patients with and without atrial fibrillation (AF)., Methods and Results: Intra-operative epicardial mapping of the right and left atrium (RA, LA), Bachmann's bundle (BB) and pulmonary vein area (PVA) was performed in 228 patients (54 with AF). Conduction velocity vectors were computed at each electrode using discrete velocity vectors. Directions and magnitudes of individual vectors were compared with surrounding vectors to identify LDH. Five hundred and three PACs [2 (1-3) per patient; prematurity index of 45 ± 12%] were included. During SR, most LDH were found at BB and LA [11.9 (8.3-14.9) % and 11.3 (8.0-15.2) %] and CV was lowest at BB [83.5 (72.4-94.3) cm/s, all P < 0.05]. Compared with SR, the largest increase in LDH during PAC was found at BB and PVA [+13.0 (7.7, 18.3) % and +12.5 (10.8, 14.2) %, P < 0.001]; CV decreased particularly at BB, PVA and LA [-10.0 (-13.2, -6.9) cm/s, -9.3 (-12.5, -6.2) cm/s and -9.1 (-11.7, -6.6) cm/s, P < 0.001]. Comparing patients with and without AF, more LDH were found during SR in AF patients at PVA and BB, although the increase in LDH during PACs was similar for all sites., Conclusion: Local directional heterogeneity is a novel methodology to quantify local heterogeneity in CV as a possible indicator of electropathology. Intra-operative high-resolution mapping indeed revealed that LDH increased during PACs particularly at BB and PVA. Also, patients with AF already have more LDH during SR, which becomes more pronounced during PACs., Competing Interests: Conflict of interest: None declared., (© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Nearly half of all patients with angina have non-obstructive coronary artery disease (ANOCA); this is an umbrella term comprising heterogeneous vascular disorders, each with disparate pathophysiology and prognosis. Approximately two-thirds of patients with ANOCA have coronary microvascular disease (CMD). CMD can be secondary to architectural changes within the microcirculation or secondary to vasomotor dysfunction. An inability of the coronary vasculature to augment blood flow in response to heightened myocardial demand is defined as an impaired coronary flow reserve (CFR), which can be measured non-invasively, using imaging, or invasively during cardiac catheterisation. Impaired CFR is associated with myocardial ischaemia and adverse cardiovascular outcomes.The CMD workstream is part of the cardiovascular partnership between the British Heart Foundation and The National Institute for Health Research in the UK and comprises specialist cardiac centres with expertise in coronary physiology assessment. This document outlines the two main modalities (thermodilution and Doppler techniques) for estimation of coronary flow, vasomotor testing using acetylcholine, and outlines a standard operating procedure that could be considered for adoption by national networks. Accurate and timely disease characterisation of patients with ANOCA will enable clinicians to tailor therapy according to their patients' coronary physiology. This has been shown to improve patients' quality of life and may lead to improved cardiovascular outcomes in the long term., Competing Interests: Competing interests: DP has received support for a research grant from Abbott Vascular and Philips Volcano in the past. CB is employed by The University of Glasgow, which holds research and consultancy agreements for work done in the course of his employment with the following companies: AstraZeneca, Abbott Vascular, GSK, Heartflow, Menarini, Novartis, Philips and Siemens Healthcare. PDM has received speaker’s honoraria from Abbott Vascular. RP has received speaker’s honoraria from Philips Volcano., (© Author(s) (or their employer(s)) 2023. Re-use permitted under CC BY. Published by BMJ.)