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Aortic stenosis (AS) is the most common valvular heart disorder in the elderly population. As a result of the shared pathophysiological processes, AS frequently coexists with coronary artery disease (CAD). These patients have traditionally been managed through surgical aortic valve replacement (SAVR) and coronary artery bypass grafting. However, increasing body of evidence supports transcatheter aortic valve implantation (TAVI) as an alternative treatment for severe AS across the spectrum of operative risk. This has created the potential for treating AS and concurrent CAD completely percutaneously. In this review we consider the evidence guiding the optimal management of patients with severe AS and CAD. While invasive coronary angiography plays a central role in detecting CAD in patients with AS undergoing surgery or TAVI, the benefits of complementary functional assessment of coronary stenosis in the context of AS have not been fully established. Although the indications for revascularisation of significant proximal CAD in SAVR patients have not recently changed, routine revascularisation of all significant CAD before TAVI in patients with minimal angina is not supported by the latest evidence. Several ongoing trials will provide new insights into physiology-guided revascularisation in TAVI recipients. The role of the heart team remains essential in this complex patient group, and if revascularisation is being considered careful evaluation of clinical, anatomical and procedural factors is essential for individualised decision-making.

Secondary mitral regurgitation (SMR) occurs as a result of multifactorial left atrioventricular dysfunction and maleficent remodelling. It is the most common and undertreated form of mitral regurgitation (MR) and is associated with a very poor prognosis. Whether SMR is a bystander reflecting the severity of the cardiomyopathy disease process has long been the subject of debate. Studies suggest that SMR is an independent driver of prognosis in patients with an intermediate heart failure (HF) phenotype and not those with advanced HF. There is also no universal agreement regarding the quantitative thresholds defining severe SMR and indeed there are challenges with echocardiographic quantification. Until recently, no surgical or transcatheter intervention for SMR had demonstrated prognostic benefit, in contrast with HF medical therapy and cardiac resynchronisation therapy. In 2018, the first two randomised controlled trials (RCTs) of edge-to-edge transcatheter mitral valve repair versus guideline-directed medical therapy in HF (Percutaneous Repair with the MitraClip Device for Severe (MITRA-FR), Transcather mitral valve repair in patients with heart failure (COAPT)) reported contrasting yet complimentary results. Unlike in MITRA-FR, COAPT demonstrated significant prognostic benefit, largely attributed to the selection of patients with disproportionately severe MR relative to their HF phenotype. Consequently, quantifying the degree of SMR in relation to left ventricular volume may be a useful discriminator in predicting the success of transcatheter intervention. The challenge going forward is the identification and validation of such parameters while in parallel maintaining a heart-team guided holistic approach.

The International Liaison Committee on Resuscitation has called for a randomised trial of delivery to a cardiac arrest centre. We aimed to assess whether expedited delivery to a cardiac arrest centre compared with current standard of care following resuscitated cardiac arrest reduces deaths. ARREST is a prospective, parallel, multicentre, open-label, randomised superiority trial. Patients (aged ≥18 years) with return of spontaneous circulation following out-of-hospital cardiac arrest without ST elevation were randomly assigned (1:1) at the scene of their cardiac arrest by London Ambulance Service staff using a secure online randomisation system to expedited delivery to the cardiac catheter laboratory at one of seven cardiac arrest centres or standard of care with delivery to the geographically closest emergency department at one of 32 hospitals in London, UK. Masking of the ambulance staff who delivered the interventions and those reporting treatment outcomes in hospital was not possible. The primary outcome was all-cause mortality at 30 days, analysed in the intention-to-treat (ITT) population excluding those with unknown mortality status. Safety outcomes were analysed in the ITT population. The trial was prospectively registered with the International Standard Randomised Controlled Trials Registry, 96585404. Between Jan 15, 2018, and Dec 1, 2022, 862 patients were enrolled, of whom 431 (50%) were randomly assigned to a cardiac arrest centre and 431 (50%) to standard care. 20 participants withdrew from the cardiac arrest centre group and 19 from the standard care group, due to lack of consent or unknown mortality status, leaving 411 participants in the cardiac arrest centre group and 412 in the standard care group for the primary analysis. Of 822 participants for whom data were available, 560 (68%) were male and 262 (32%) were female. The primary endpoint of 30-day mortality occurred in 258 (63%) of 411 participants in the cardiac arrest centre group and in 258 (63%) of 412 in the standard care group (unadjusted risk ratio for survival 1·00, 95% CI 0·90–1·11; p=0·96). Eight (2%) of 414 patients in the cardiac arrest centre group and three (1%) of 413 in the standard care group had serious adverse events, none of which were deemed related to the trial intervention. In adult patients without ST elevation, transfer to a cardiac arrest centre following resuscitated cardiac arrest in the community did not reduce deaths. British Heart Foundation.

Infective endocarditis complicating transcatheter aortic valve implantation (TAVI-IE) is a relatively rare condition with an incidence of 0.2%–3.1% at 1 year post implant. It is frequently caused by Enterococci, Staphylococcus aureus and c oagulase negative staphylococci. While the incidence currently appears to be falling, the absolute number of cases is likely to rise substantially as TAVI expands into low risk populations following the publication of the PARTNER 3 and Evolut Low Risk trials. Important risk factors for the development of TAVI-IE include a younger age at implant and significant residual aortic regurgitation. The echocardiographic diagnosis of TAVI-IE can be challenging, and the role of supplementary imaging techniques including multislice computed tomography (MSCT) and positron emission tomography (18FDG PET) is still emerging. Treatment largely parallels that of conventional prosthetic valve endocarditis (PVE), with prolonged intravenous antibiotic therapy and consideration of surgical intervention forming the cornerstones of management. The precise role and timing of cardiac surgery in TAVI-IE is yet to be defined, with a lack of clear evidence to help identify which patients should be offered surgical intervention. Minimising unnecessary healthcare interventions (both during and after TAVI) and utilising appropriate antibiotic prophylaxis may have a role in preventing TAVI-IE, but robust evidence for specific preventative strategies is lacking. Further research is required to better select patients for advanced hybrid imaging, to guide surgical management and to inform prevention in this challenging patient cohort.

ObjectiveTo define the incidence and risk factors for infective endocarditis (IE) following surgical aortic valve replacement (SAVR) and transcatheter aortic valve implantation (TAVI).MethodsAll patients who underwent first SAVR or TAVI in England between 2007 and 2016 were identified from the NICOR databases. Hospital admissions with a primary diagnosis of IE were identified by linkage with the NHS Hospital Episode Statistics database. Approval was obtained from the NHS Research Ethics Committee.Results2057 of 91 962 patients undergoing SAVR developed IE over a median follow-up of 53.9 months—an overall incidence of 4.81 [95% CI 4.61 to 5.03] per 1000 person-years. Correspondingly, 140 of 14 195 patients undergoing TAVI developed IE over a median follow-up of 24.5 months—an overall incidence of 3.57 [95% CI 3.00 to 4.21] per 1000 person-years. The cumulative incidence of IE at 60 months was higher after SAVR than after TAVI (2.4% [95% CI 2.3 to 2.5] vs 1.5% [95% CI 1.3 to 1.8], HR 1.60, p<0.001). Across the entire cohort, SAVR remained an independent predictor of IE after multivariable adjustment. Risk factors for IE included younger age, male sex, atrial fibrillation, and dialysis.ConclusionsIE is a rare complication of SAVR and TAVI. In our population, the incidence of IE was higher after SAVR than after TAVI.

BackgroundCurrent risk scores inadequately predict long-term mortality after transcatheter aortic valve replacement (TAVR), limiting their ability to guide decisions around procedural futility. We aimed to develop and externally validate a machine learning (ML) model using only preprocedural variables to predict 1-year all-cause mortality.MethodsAn ML model was trained on a retrospective cohort of 1025 TAVR patients using 52 clinical and echocardiographic variables. Feature selection and model tuning were performed via a multiobjective evolutionary algorithm to optimise predictive performance and model simplicity. The final model used 13 preprocedural variables and was externally validated in an independent cohort of 270 patients. Performance was compared with European System for Cardiac Operative Risk Evaluation II (EuroSCORE II), FRANCE-2 and TAVI2-SCORE using the area under the curve (AUC), calibration and net reclassification improvement (NRI).ResultsThe ML model demonstrated excellent discrimination, with AUCs of 0.81 in the discovery cohort and 0.84 in the external validation cohort. This exceeded the performance of EuroSCORE II (AUC: 0.61 and 0.70), FRANCE-2 (0.52 and 0.58) and TAVI2-SCORE (0.56 and 0.64). Calibration plots showed strong agreement between predicted and observed risks. NRI in the test set compared with FRANCE-2 was 0.62 (95% CI: 0.49 to 0.75); compared with TAVI2-SCORE, it was 0.36 (95% CI: 0.14 to 0.61). The final model incorporated age, atrial fibrillation, creatinine, haemoglobin, pulmonary function, frailty markers (Katz Index, poor mobility) and tricuspid regurgitation. Misclassification analysis revealed that most errors were clustered near the decision threshold, with no evidence of systematic bias. Performance was consistent across subgroups and robust to temporal and institutional variation.ConclusionThis externally validated ML model, using 13 routinely available variables, significantly outperforms existing risk scores in predicting 1-year mortality post-TAVR. Its simplicity and generalisability support its potential use in real-world clinical decision-making to identify patients at high risk of procedural futility.

ObjectiveExisting clinical prediction models (CPM) for short-term mortality after transcatheter aortic valve implantation (TAVI) have limited applicability in the UK due to moderate predictive performance and inconsistent recording practices across registries. The aim of this study was to derive a UK-TAVI CPM to predict 30-day mortality risk for benchmarking purposes.MethodsA two-step modelling strategy was undertaken: first, data from the UK-TAVI Registry between 2009 and 2014 were used to develop a multivariable logistic regression CPM using backwards stepwise regression. Second, model-updating techniques were applied using the 2013–2014 data, thereby leveraging new approaches to include frailty and to ensure the model was reflective of contemporary practice. Internal validation was performed by bootstrapping to estimate in-sample optimism-corrected performance.ResultsBetween 2009 and 2014, up to 6339 patients were included across 34 centres in the UK-TAVI Registry (mean age, 81.3; 2927 female (46.2%)). The observed 30-day mortality rate was 5.14%. The final UK-TAVI CPM included 15 risk factors, which included two variables associated with frailty. After correction for in-sample optimism, the model was well calibrated, with a calibration intercept of 0.02 (95% CI −0.17 to 0.20) and calibration slope of 0.79 (95% CI 0.55 to 1.03). The area under the receiver operating characteristic curve, after adjustment for in-sample optimism, was 0.66.ConclusionThe UK-TAVI CPM demonstrated strong calibration and moderate discrimination in UK-TAVI patients. This model shows potential for benchmarking, but even the inclusion of frailty did not overcome the need for more wide-ranging data and other outcomes might usefully be explored.

13 In the presence of a stenosis, CBF increases by smaller increments than would be elicited without a stenosis because of progressive exhaustion of the vasodilator reserve of the resistance vessels. 13 At higher MVO2, myocardial oxygen supply may no longer be able to match myocardial oxygen demand, resulting in ischaemia. 13 Effects of cold stress on the cardiovascular system Cold leads to a range of physiological responses to prevent a fall in core temperature, which can have important consequences for subjects with CAD ( figure 3 ). The cold pressor test was initially criticised as demonstrating the effects of a painful stimulus rather than a cold stimulus; 20 however, the cardiovascular effects have since been shown to persist after thoracic anaesthesia, suggesting that primarily adaptation to cold was occurring. 21 In healthy subjects Myocardial oxygen demand Cold typically produces an increase in heart rate (HR) of 5-10 bpm and an increase in systolic blood pressure (SBP) of 15-20 mm Hg. 22-25 Studies in which cold air inhalation was used showed a blunted HR response 26 27 compared with the cold pressor test, 22 likely because trigeminal nerve activation resulted in vagal opposition to the sympathetic response to cold. 27 Skin surface cooling causes peripheral vasoconstriction, 28 increasing systemic vascular resistance (SVR) 29 and diastolic blood pressure (DBP).

Cardiac troponins are released and cleared slowly after myocardial injury, complicating the diagnosis of early, and recurrent, acute myocardial infarction. Cardiac myosin-binding protein C (cMyC) is a similarly cardiac-restricted protein that may have different release/clearance kinetics. Using novel antibodies raised against the cardiac-specific N-terminus of cMyC, we used confocal microscopy, immunoblotting and immunoassay to document its location and release. In rodents, we demonstrate rapid release of cMyC using in vitro and in vivo models of acute myocardial infarction. In patients, with ST elevation myocardial infarction (STEMI, n  = 20), undergoing therapeutic ablation of septal hypertrophy (TASH, n  = 20) or having coronary artery bypass surgery (CABG, n  = 20), serum was collected prospectively and frequently. cMyC appears in the serum as full-length and fragmented protein. Compared to cTnT measured using a contemporary high-sensitivity commercial assay, cMyC peaks earlier (STEMI, 9.3 ± 3.1 vs 11.8 ± 3.4 h, P  < 0.007; TASH, 9.7 ± 1.4 vs 21.6 ± 1.4 h, P  < 0.0001), accumulates more rapidly (during first 4 h after TASH, 25.8 ± 1.9 vs 4.0 ± 0.4 ng/L/min, P  < 0.0001) and disappears more rapidly (post-CABG, decay half-time 5.5 ± 0.8 vs 22 ± 5 h, P  < 0.0001). Our results demonstrate that following defined myocardial injury, the rise and fall in the serum of cMyC is more rapid than that of cTnT. We speculate that these characteristics could enable earlier diagnosis of myocardial infarction and reinfarction in suspected non-STEMI, a population not included in this early translational study.

Acute ST-segment elevation myocardial infarction (STEMI) is a dynamic, thrombus-driven event. As understanding of its pathophysiology has improved, the central role of platelets in initiation and orchestration of this process has become clear. Key components of STEMI include formation of occlusive thrombus, mediation and ultimately amplification of the local vascular inflammatory response resulting in increased vasoreactivity, oedema formation, and microvascular obstruction. Activation, degranulation, and aggregation of platelets are the platforms from which these components develop. Therefore, prompt, potent, and predictable antithrombotic therapy is needed to optimise clinical outcomes after primary percutaneous coronary intervention. We review present pharmacological and mechanical adjunctive therapies for reperfusion and ask what is the optimum combination when primary percutaneous coronary intervention is used as the mode of revascularisation in patients with STEMI.