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Background: Recent clinical trials have demonstrated that sodium-glucose cotransporter 2 inhibitors (SGLT2i), which were previously only indicated in treatment of type 2 diabetes mellitus (T2DM), can markedly reduce heart failure hospitalisation (HFH), with less striking potential reductions in acute coronary syndromes and cardiac arrhythmias. To evaluate the impact of SGLT2i on cardiovascular outcomes in real-world practice, we performed a retrospective cohort analysis on South Australian (SA) data., Methods: A total of 842 individuals with T2DM receiving SGLT2i were identified from SA public hospitals between 2011 and 2019. Episodes of care were temporally matched with those of 3,128 individuals with T2DM not receiving SGLT2i (control). Baseline characteristics were adjusted using inverse probability treatment weighting. The incidence of cardiovascular events at 12 and 24 months was evaluated using coded (International Classification of Diseases, Tenth Revision, Australian Modification [ICD-10-AM]) data., Results: The primary outcome of HFH was lower with SGLT2i use at 12 months (adjusted hazard ratio [HR adj ] 0.44; 95% confidence interval [CI] 0.29-0.68; p<0.001) and 24 months. There were also lower hospitalisations due to acute myocardial infarction (HR adj 0.42; 95% CI 0.21-0.85; p=0.015) and atrial or ventricular arrhythmias (HR adj 0.29; 95% CI 0.14-0.59; p=0.001), with no difference observed in hospitalisation due to ischaemic cerebrovascular events. There was no difference in all-cause mortality at 12 months but interestingly a higher rate at 24 months (HR adj 2.08; 95% CI 1.59-2.72; p<0.001). Despite this, similar reductions in cardiovascular outcomes were observed at 24 months., Conclusion: Use of SGLT2i in patients with T2DM in SA was associated with reductions in cardiovascular events even before their recent Pharmaceutical Benefits Scheme (PBS) listing for heart failure. Furthermore, this analysis supports that SGLT2i play a role not only in HFH reduction but also in reducing coronary and tachyarrhythmic events. This real-world evidence supports the use of SGLT2i as broadly protective cardiovascular drugs., Competing Interests: Conflicts of Interest D.P.C. received institutional research funding from AstraZeneca. K.L. is involved in institutional research grants funded by AstraZeneca. E.S.G. was previously involved in institutional research grants funded by Bayer. C.G.D.P. reports research funding from AstraZeneca and Novartis, and consulting fees or speaker honoraria for AstraZeneca, Novartis, CSL Vifor, Boehringer Ingelheim, Bayer, Eli Lilly, and Roche Diagnostics. The remaining authors have no funding sources to report., (Copyright © 2023 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Aims: This study aimed to explore the rapid effects of dapagliflozin in heart failure with reduced ejection fraction (HFrEF)., Methods and Results: We studied the functional, echocardiographic, electrophysiological, lung ultrasound, ambulatory blood pressure (BP), microvascular and macrovascular function, and biochemical effects of 2 week treatment with dapagliflozin in 19 type 2 diabetic HFrEF patients in a double-blind, crossover, placebo-controlled trial. Dapagliflozin had no significant effect on clinical, functional, or quality of life parameters. Dapagliflozin reduced systolic BP [114 (105, 131) vs. 106 (98, 113) mmHg, P < 0.01] and diastolic BP [71 (61, 78) vs. 62 (55, 70) mmHg, P < 0.01]. There was no effect on cardiac chamber size, ventricular systolic function, lung ultrasound, or arterial wave reflection. Dapagliflozin increased creatinine [117 (92, 129) vs. 122 (107, 135) μmol/L, P < 0.05] and haemoglobin [135 (118, 138) vs. 136 (123, 144) g/L, P < 0.05]. There was a reduction in ventricular ectopy [1.4 (0.1, 2.9) vs. 0.2 (0.1, 1.4) %, P < 0.05] and an increase in standard deviation of normal heart beat intervals [70 (58, 90) vs. 74 (62, 103), P < 0.05]. Unexpectedly, dapagliflozin increased high-sensitivity troponin T [25 (19, 37) vs. 28 (20, 42) ng/L, P < 0.01] and reduced reactive hyperaemia index [1.29 (1.21, 1.56) vs. 1.40 (1.23, 1.84), P < 0.05]., Conclusions: After 2 weeks, while multiple parameters supported BP reduction and haemoconcentration with dapagliflozin, reduction in cardiac filling pressure, lung water, and functional improvement was not shown. Reduced ventricular ectopic burden suggests an early antiarrhythmic benefit. The small increase in troponin T and the reduction in the reactive hyperaemia index warrant further mechanistic exploration in this treatment of proven mortality benefit in HFrEF., (© 2021 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

Background: Acute decompensated heart failure (ADHF) carries a high event rate following discharge. The complex interplay between age, frailty and decongestion may lend itself to a functional test., Methods: In the doorbell test the patient simulates answering the doorbell. They are timed rising from a recumbent position, bending over twice and walking 10 metres, this time is added to the change in respiratory rate. We aimed to determine if the doorbell test was associated with post ADHF events (death or readmission). The test was performed at hospital discharge, with follow up at 30-days and 1-year., Results: In 74 patients at 30-days there was a 14% event rate. At 1-year there were 40 (54%) events (9 deaths and 31 readmissions, 28 were cardiovascular of which 14 were [heart failure] HF). Amongst those who had an event at 30-days only doorbell test scores were different (58 [36,72] vs 32 [26,53] p < 0.05). One-year (1-year) events were associated with doorbell test scores (47 [29,62] vs 30 [26,42] p < 0.05), body weight (78 kg [68,94] vs 95 [76,105] (p < 0.05), creatinine (134 mmol/L [114, 173] vs 99 [82, 133] p < 0.01) and age (76 years [61,86] vs 67 [53, 73] p < 0.01). Heart failure readmissions were associated with doorbell test scores (56 [46,68] vs 30 [26,47] p < 0.001). Death was associated with body weight (74 kg [69,81] vs 88 [72,101] p < 0.05) and age (83 years [78,86] vs 69 [55,77] p < 0.01). After age stratification, the hazard ratio for heart failure readmission associated with a high doorbell test score was 11.08 (95%C.I. 2.01-61.17 p = 0.006), while the hazard ratio for 1-year cardiovascular readmission was 4.62 (95%C.I. 1.71-12.51 p = 0.003). There was no association with 1-year mortality., Conclusion: The doorbell test represents a novel test of multiple domains of the ADHF pre-discharge state and demonstrates an association with 30-day and 1-year rehospitalisation., (Copyright © 2019. Published by Elsevier B.V.)

Background: Non-infarct-related artery (non-IRA) disease is prevalent in patients with ST-segment elevation myocardial infarction (STEMI). We aimed to assess the impact of non-IRA disease on infarct size and clinical outcomes in patients with acute STEMI., Methods: The Counterpulsation to Reduce Infarct Size Pre-PCI Acute Myocardial Infarction (CRISP-AMI) trial randomized patients to intra-aortic balloon counterpulsation (IABC) vs no IABC prior to percutaneous coronary intervention in patients with acute STEMI. Infarct size (% left ventricular mass) at 3-5 days post percutaneous coronary intervention and 6-month clinical outcomes were compared between patients with and without non-IRA disease (defined as ≥50% stenosis in at least one non-IRA)., Results: A total of 324 (96.1%) patients had anterior STEMI, of whom 34.9% had non-IRA disease. There was no difference in infarct size (% left ventricular mass) between patients with and without non-IRA disease (median 39% vs 39%; P = .73). At 6 months, there was no difference in rates of recurrent myocardial infarction (0.9% vs 0.9%; P = .78), major Thrombolysis In Myocardial Infarction bleeding (0.9% vs 0.5%; P = .77), or all-cause death (3.5% vs 2.4%; P = .61) in patients with and without non-IRA disease, respectively. Patients with non-IRA disease had a higher rate of new/worsening heart failure with hospitalization (8.8% vs 1.9%; P = .0050)., Conclusions: More than one-third of patients with anterior STEMI in the CRISP-AMI study had non-IRA disease. These patients had similar infarct sizes and rates of recurrent myocardial infarction, major bleeding, and all-cause death. Patients with non-IRA disease did have a higher rate of new/worsening heart failure with hospitalization. Further study is needed to understand the mechanisms of outcomes of patients with non-IRA disease., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Mechanical left ventricular (LV) dyssynchrony, as determined by tissue Doppler imaging (TDI), predicts response to cardiac resynchronization therapy (CRT). However, changes in TDI mechanical dyssynchrony after CRT implantation have only limited investigation. Our objective was to detect changes in the extent and location of TDI mechanical dyssynchrony pre- and post-CRT, and to explore their relationship in response to CRT., Methods: Thirty-nine consecutive patients undergoing CRT implantation for chronic heart failure underwent TDI analysis pre-CRT and up to 12 months post-CRT. Regional dyssynchrony was determined by the time to systolic peak velocity of opposing LV walls. Dyssynchrony was defined as a difference in time to peak contraction of >105 msec. Two patients were excluded, as suitable coronary venous access was not available., Results: Of the 37 patients, 28 (76%) had significant mechanical dyssynchrony pre-CRT. Of those with dyssynchrony, 18 (64%) had septal delay and 10 (36%) had LV free wall delay. Post-CRT, 29 (78%) patients had significant mechanical dyssynchrony, 17 (59%) with septal delay, and 12 (41%) with LV free wall delay. There was no difference in both the amount of dyssynchrony (P=0.8) or the location of the dyssynchrony (P=0.5), before and after CRT, even though 28 (76%) were considered responders based on symptomatic and echocardiographic parameters., Conclusion: The TDI-derived dyssynchrony does not change with CRT despite significant symptomatic and echocardiographic improvement in cardiac function. The TDI is of limited utility for monitoring response to CRT., (© 2011, Wiley Periodicals, Inc.)

Background: The primary determinate for the indication of cardiac resynchronization therapy in symptomatic chronic heart failure currently is a prolonged QRS duration. This is based on the premise that a prolonged QRS duration is a marker of left ventricular (LV) dyssynchrony. Tissue synchronization imaging (TSI) is an emerging technology that uses tissue Doppler velocities to determine the time to peak velocity of regions of the ventricular myocardium., Objectives: Our objectives were to determine the prevalence of dyssynchrony in a cardiomyopathic population referred for echocardiography irrespective of QRS duration, to validate the novel technique of TSI in evaluation of mechanical LV dyssynchrony and to determine the accuracy of QRS duration in predicting significant LV dyssynchrony., Methods: A total of 100 patients with significant LV dysfunction (Simpson's ejection fraction < or = 35%) referred for echocardiography underwent TSI. Dyssynchrony was defined as a difference in time to peak contraction of greater than 105 milliseconds between opposing ventricular segments., Results: Overall, 61 patients (61%) demonstrated significant dyssynchrony, whereas 52% had a QRS duration of greater than 120 milliseconds. Among those with a prolonged QRS duration, significant dyssynchrony was evident in 30 (58%). However, dyssynchrony was also common among those with a narrow QRS duration (<120 milliseconds) (31 patients [65%]). Of the 61 patients with dyssynchrony, 31 (51%) would have been missed if QRS criteria were used alone., Conclusions: A substantial proportion of patients have dyssynchrony by TSI, but do not have a prolonged QRS duration. These patients may benefit from cardiac resynchronization therapy but on traditional criteria would be excluded from the therapy. Expanding the criteria for cardiac resynchronization therapy to include echocardiographic parameters may extend the benefit of this technology to a greater population in need.

Background: In chronic heart failure (CHF), elevated pulmonary microvascular pressure (P(mv)) results in pulmonary edema. Because elevated P(mv) may alter the integrity of the alveolocapillary barrier, allowing leakage of surfactant protein-B (SP-B) from the alveoli into the circulation, we aimed to determine plasma levels of SP-B in CHF and their relation to clinical status., Methods and Results: Fifty-three outpatients with CHF had plasma SP-B and N-terminal proBNP (NT-proBNP) assayed, in addition to a formalized clinical assessment at each clinic review over a period of 18 months. The control group comprised 19 normal volunteers. Plasma SP-B was elevated in CHF (P<0.001), and levels increased with New York Heart Association classification (P<0.001). SP-B correlated with objective clinical status parameters and NT-proBNP. During follow-up, major cardiovascular events occurred in patients with higher plasma SP-B (P<0.01) and NT-proBNP (P<0.05). Furthermore, on conditional logistic regression analysis, only SP-B was independently associated with CHF hospitalization (P=0.005). The 53 patients underwent a total of 210 outpatient visits. When the diuretic dosage was increased on clinical grounds, SP-B had increased 39% (P<0.001) and NT-proBNP had increased 32% (P<0.001). Conversely, at the next visit, SP-B fell 12% (P<0.001), whereas NT-proBNP fell 39% (P<0.001)., Conclusions: Plasma SP-B is increased in CHF, and levels are related to clinical severity. Furthermore, within individual patients, SP-B levels vary with dynamic clinical status and NT-proBNP levels. Because plasma SP-B is independently associated with CHF hospitalization, it may, by virtue of its differing release mechanism to NT-proBNP, be a clinically useful biomarker of the pulmonary consequences of raised P(mv).

Aims: We aimed to investigate the independent associations between growth differentiation factor 15 (GDF‐15) level at admission and cardiovascular (CV) death, thrombotic events, heart failure (HF), and bleeding outcomes in patients with coronary artery disease (CAD). Methods and results: We measured the plasma concentrations of GDF‐15 centrally in patients from the BIomarker‐based Prognostic Assessment for patients with Stable angina and acute coronary Syndrome (BIPass) registry, which consecutively enrolled patients with CAD from November 2017 to September 2019 at five tertiary hospitals in China. The outcomes included CV death, thrombotic events [myocardial infarction (MI) and ischaemic stroke], HF events [acute HF during hospitalization and hospitalization for HF post‐discharge (A/H HF) and cardiogenic shock], and bleeding outcomes [non‐coronary artery bypass grafting‐related major bleeding and clinically significant bleeding (CSB)] during the 12 month follow‐up period after hospitalization. Among 6322 patients with CAD {65.4% male, median age 63.7 [inter‐quartile range (IQR)] 56.0–70.1 years}, the median concentration of plasma GDF‐15 at admission was 1091 (IQR 790.5–1635.0) ng/L. Higher concentrations of GDF‐15 were associated with an increased risk of CV death [hazard ratio (HR) 1.98, 95% confidence interval (CI) 1.35–2.88, P < 0.001], A/H HF (HR 2.69, 95% CI 1.92–3.77, P < 0.001), cardiogenic shock (HR 1.46, 95% CI 1.04–2.05, P = 0.029), and CSB (HR 1.48, 95% CI 1.22–1.79, P < 0.001), but not for MI or stroke, after adjusting for clinical risk factors and prognostic biomarkers. Adding GDF‐15 to the model with risk factors and biomarkers improved the net reclassification for CV death, A/H HF, cardiogenic shock, and CSB. Conclusions: In patients with CAD, admission levels of GDF‐15 were associated with an increased 1 year risk of CV death, HF, and bleeding outcomes, but not with thrombotic events. GDF‐15 may be a prognostic biomarker for CV death, HF, and bleeding outcomes and could be used to refine the risk assessment of these specific clinical outcomes. Trial Registration: ClinicalTrials.gov Identifier: NCT04044066 [ABSTRACT FROM AUTHOR]

Background: Atrial fibrillation (AF) and heart failure (HF) often accompany one another, and each is independently associated with poor outcomes. However, the association between AF burden and outcomes is poorly understood.Objective: The purpose of this study was to describe the association between device-based AF burden and HF clinical outcomes.Methods: We used a nationwide, remote monitoring database of cardiac implantable electronic devices (CIEDs) linked to Medicare claims. We included patients with nonpermanent AF, undergoing new CIED implant, stratified by baseline HF. The outcomes were new-onset HF, HF hospitalization, and all-cause mortality at 1 and 3 years.Results: We identified 39,710 patients who met inclusion criteria (25,054 with HF; 14,656 without HF). Patients with HF were younger (mean age 76.3 vs 78.5 years; P <.001), more often male (65% vs 54%; P <.001), and had higher mean CHA2DS2-VASc scores (5.4 vs 4.1; P <.001). Among those without HF, increasing device-based AF burden was significantly associated with increased risk of new-onset HF (adjusted hazard ratio [HR] 1.09 per 10% AF burden; 95% confidence interval [CI] 1.06-1.12; P <.001) and all-cause mortality (adjusted HR 1.05 per 10% AF burden; 95% CI 1.01-1.10; P = .012). Among patients with HF, increasing AF burden was significantly associated with increased risk of HF hospitalization (adjusted HR 1.05 per 10% AF burden; 95% CI 1.04-1.06; P <.001) and all-cause mortality (adjusted HR 1.06 per 10% AF burden; 95% CI 1.05-1.08; P <.001).Conclusion: Among older patients with AF receiving a CIED, increasing AF burden is significantly associated with increasing risk of adverse HF outcomes and all-cause mortality. [ABSTRACT FROM AUTHOR]

Introduction: The coronavirus 2019 disease (COVID-19) pandemic is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Pre-existing cardiovascular disease (CVD) increases the morbidity and mortality of COVID-19, and COVID-19 itself causes serious cardiac sequelae. Strategies to minimise the risk of viral transmission to health care workers and uninfected cardiac patients while prioritising high quality cardiac care are urgently needed. We conducted a rapid literature appraisal and review of key documents identified by the Cardiac Society of Australia and New Zealand Board and Council members, the Australian and New Zealand Society of Cardiac and Thoracic Surgeons, and key cardiology, surgical and public health opinion leaders.Main Recommendations: Common acute cardiac manifestations of COVID-19 include left ventricular dysfunction, heart failure, arrhythmias and acute coronary syndromes. The presence of underlying CVD confers a five- to tenfold higher case fatality rate with COVID-19 disease. Special precautions are needed to avoid viral transmission to this population at risk. Adaptive health care delivery models and resource allocation are required throughout the health care system to address this need.Changes in Management AsA Result Of This Statement: Cardiovascular health services and cardiovascular health care providers need to recognise the increased risk of COVID-19 among CVD patients, upskill in the management of COVID-19 cardiac manifestations, and reorganise and innovate in service delivery models to meet demands. This consensus statement, endorsed by the Cardiac Society of Australia and New Zealand, the Australian and New Zealand Society of Cardiac and Thoracic Surgeons, the National Heart Foundation of Australia and the High Blood Pressure Research Council of Australia summarises important issues and proposes practical approaches to cardiovascular health care delivery to patients with and without SARS-CoV-2 infection. [ABSTRACT FROM AUTHOR]

Beyond this time, the ongoing risk of mortality and myocardial infarction is determined by coronary artery disease burden, and not residual ischaemia. Keywords: Angina pectoris; Coronary artery disease; Angiography EN Angina pectoris Coronary artery disease Angiography 140 141 2 08/22/23 20230801 NES 230801 In the management of coronary artery disease, trepidation associated with the risk of future myocardial infarction weighs heavily on the minds of patients and physicians alike, given the well recognised and often publicly highlighted association with premature cardiovascular mortality. In contrast, the burden of coronary artery disease (ie, extent of coronary plaque) was strongly associated with future cardiovascular death or myocardial infarction.[5] Although these findings may be considered counterintuitive, they are entirely consistent with the previous subanalysis of the STICH trial. [Extracted from the article]

Evolution of diagnostic testing modalities in cardiovascular medicine has been rapid. Technological advances in cardiac imaging have enabled the assessment of cardiac texture and function with unprecedented resolution, while the assessment of coronary artery disease by non-invasive means has matured to rival coronary angiography. Similarly, developments in the area of serum biomarkers have given further insights into the risk experienced by patients with coronary artery disease, acute coronary syndromes and heart failure. However, the rate of this innovation calls for a moment''s pause to refocus on the goals of the diagnostic and risk refinement process that is to deliver better care and improve clinical outcome. To date many studies in this area have fallen short of demonstrating such benefits and it is our responsibility as a clinical community to demand more of such innovation. [Copyright &y& Elsevier]

Background: Randomized clinical trials have demonstrated that catheter ablation for atrial fibrillation in patients with heart failure with reduced ejection fraction may improve survival and other cardiovascular outcomes.Methods: We constructed a decision-analytic Markov model to estimate the costs and benefits of catheter ablation and medical management in patients with symptomatic heart failure with reduced ejection fraction (left ventricular ejection fraction ≤35%) and atrial fibrillation over a lifetime horizon. Evidence from the published literature informed the model inputs, including clinical effectiveness data from meta-analyses. Probabilistic and deterministic sensitivity analyses were performed. A 3% discount rate was applied to both future costs and benefits. The primary outcome was the incremental cost-effectiveness ratio assessed from the US health care sector perspective.Results: Catheter ablation was associated with 6.47 (95% CI, 5.89-6.93) quality-adjusted life years (QALYs) and a total cost of $105 657 (95% CI, $55 311-$191 934; 2018 US dollars), compared with 5.30 (95% CI, 5.20-5.39) QALYs and $63 040 (95% CI, $37 624-$102 260) for medical management. The incremental cost-effectiveness ratio for catheter ablation compared with medical management was $38 496 (95% CI, $5583-$117 510) per QALY gained. Model inputs with the greatest variation on incremental cost-effectiveness ratio estimates were the cost of ablation and the effect of catheter ablation on mortality reduction. When assuming a more conservative estimate of the treatment effect of catheter ablation on mortality (hazard ratio of 0.86), the estimated incremental cost-effectiveness ratio was $74 403 per QALY gained. At a willingness-to-pay threshold of $100 000 per QALY gained, atrial fibrillation ablation was found to be economically favorable compared with medical management in 95% of simulations.Conclusions: Catheter ablation in patients with heart failure with reduced ejection fraction patients and atrial fibrillation may be considered economically attractive at current benchmarks for societal willingness-to-pay in the United States. [ABSTRACT FROM AUTHOR]

Evidence-based guidelines recommend cardiac rehabilitation(CR) for secondary prevention of recurrent myocardial infarction(re-MI) and risk factor management, but poor referral and completion rates persist. Regular audit can measure the effectiveness of services. A 2011 audit of public CR services, by the South Australian Department of Health CR Clinical Network showed a 12% program attendance rate. Following development of standardised minimum data and uniform electronic data capture, 24 CR services have contributed within 3 audits. We aimed to link referral and attendance with administrative data to assess characteristics and outcomes of eligible patients. Methods: The CR patient database for 2013-2015 was linked to patients discharged alive with a primary cardiac-related diagnosis and/or interventional procedure, identified through public hospital administrative data. Outcomes were defined as readmission for cardiovascular causes and death captured through the Births Deaths and Marriages database. Patient categories were not referred, referred/declined and attended CR. Associations with cardiovascular readmission and composites of death, new/re-MI, heart failure, atrial fibrillation and stroke over the 12-month follow-up duration were reported using inverse probability weighted survival methods among those who attended and those referred/declined. Results: Of 49,909 eligible cardiac separations, referral rate was 15,089/49,909 (30.2%) and attendance 4,286/15,089 (28.4%). Those referred/declined were older (median: 67.3 vs 65.3 years, P< 0.001), more likely to be female (32.3% vs 26.5%, P< 0.001) with more heart failure (17.1% vs 10.9%, P< 0.001) and arrhythmia (6.1% v 2.1%, P< 0.001) admissions, ≥2 comorbidities (35.3% v 23.3%, P< 0.001), with higher socio-economic disadvantage (median IRSAD: 950.1 vs 960.4, p<0.001). Attending patients had lower cardiovascular readmission, (attended vs not referred: 27.3% vs 34.5% and attended vs referred/declined ; 27.3% vs 41.4%, P< 0.001). After clinical and social factors adjustment there was no difference in composite clinical outcomes to 12-months, but attendance was associated with reduced cardiovascular readmission (HR:0.68, 95% IQR: 0.58-0.81, P = 0.001). Conclusions: This analysis highlights the complexity of factors that influence referral, non-attendance and attendance to CR. Conducting clinical audit and reporting to services is vital for measuring program effectiveness and can be a mechanism for service improvement. [ABSTRACT FROM AUTHOR]

Introduction: Troponin (cTn) elevations in the absence of acute coronary events are associated with excess morbidity and mortality. We evaluated the temporal course of excess hazard associated with different cTn patterns. Methods: We drew upon the state wide administrative and pathology reporting systems to assimilate a dataset of all patients presenting to public emergency departments in South Australia between June 2012 – 2016. Episodes of care (EOC) were classified into three groups based on cTn and linked diagnostic codes (ICD10). Patients with an EOC with a rise and/or fall pattern of cTn (>20%) and a primary diagnosis of coronary artery disease were classified as a 'type 1 myocardial infarction (MI).' EOC with a rise and/or fall in cTn with a non-coronary primary diagnosis were classified as 'type 2 MI.' Patients were deemed as having 'cardiac injury' if they had an elevated cTn but without a rise and/or fall. We used multivariable flexible parametric models to characterise the time varying hazard of MI, heart failure (HF) and death. To explore whether cTn rise was simply a measure of systemic risk, we assessed its association with pathologies commonly seen in frailty (pneumonia and neck of femur fracture [NOFF]). Results: In total, 278816 EOC were included with 12345 (4%) patients classified as type 1 MI, 31487 (11%) as type 2 MI, 27728 (10%) as myocardial injury and 207256 (74%) had no cTn rise. At one year, the rate of MI were 9% (769), 3% (553), 2% (428) and 1% (1165); HF were 3% (425), 5% (1528), 5% (1512) and 1% (2470); and death were 12% (1456), 26% (8096), 20% (5675) and 5% (11408) respectively. After adjustment, we observed an early hazard in patients with type 1 MI (30 and 365 day hazard ratio [HR] for MI= 13.4 & 5.4; HF= 2.0 & 1.2; death= 3.1 & 2.4). In contrast, patients with type 2 MI and myocardial injury experienced a constant excess hazard (30 and 365 day HR of death for type 2 MI: 4.2 & 3.9; myocardial injury: 2.5 & 2.4). No excess risk of pneumonia or NOFF was observed. Conclusions: In contrast to the early hazard seen in type 1 MI, cTn elevation in other settings is associated with a persistently elevated cardiovascular risk. These divergent profiles suggest potential limited benefit of treatments targeting acute coronary lesions and benefits of therapies targeting late cardiac risk. [ABSTRACT FROM AUTHOR]