Prognostic utility of serum NT-proBNP (fragments 1-76aa and 13-71aa) and galectin-3 in predicting death and re-hospitalisation due to cardiovascular events in patients with heart failure.

Patients with heart failure (HF) are at a higher risk of rehospitalisation. In this study, we investigated the prognostic utility of galectin-3 (Gal-3) and NT-proBNP fragments (1-76aa and 13-71aa) as biomarkers to predict outcomes for patients with HF. We collected blood samples from patients with HF (n = 101). Gal-3 and NT-proBNP fragments (1-76aa and 13-71aa) concentrations were measured by immunoassay. Survival analysis and Cox proportional regression models were used to determine the prognostic utility of Gal-3 and NT-proBNP fragments. In patients with increased baseline levels of NT-proBNP1-76 the time to primary endpoint (cardiovascular death or re-hospitalisation) was significantly shorter (p = 0.0058), but not in patient with increased baseline levels of Gal-3 or NTproBNP13-71. Patients with increased levels of NT-proBNP13-71aa at 1 month showed reduced time to the primary endpoint (p = 0.0123). Our findings demonstrated that Gal-3 and NT-proBNP can be used as prognostic biomarkers to stratify patients with HF.

Clinical to Population Prevalence of Hypertrophic Cardiomyopathy Phenotype: Insights From the National Echo Database Australia.

BACKGROUND: There is a paucity of data describing the underlying prevalence of hypertrophic cardiomyopathy (HCM), a primary genetic disorder characterised by progressive left ventricular (LV) hypertrophy and sudden death, from both a clinical and a population perspective. METHODS: We screened the echocardiographic reports of 155,668 men and 147,880 women within the multicentre National Echo Database Australia (NEDA) (2001-2019). End-diastolic wall thickness ≥15 mm anywhere in the left ventricle was identified as a characteristic of an HCM phenotype according to current guideline recommendations. Applying a septal-to-posterior wall thickness ratio >1.3 and LV outflow tract obstruction ≥30 mmHg (when documented), we further identified asymmetric septal hypertrophy and obstructive HCM (oHCM), respectively. The observed pattern of phenotypical HCM within the overall NEDA cohort (>650,000 cases) was then extrapolated to the ∼539,000 (5.7% of adult population) and ∼474,000 (4.8%) Australian men and women, respectively, who were investigated with echocardiography in 2021 on an age-specific basis. RESULTS: Overall, 15,380 cases (mean age 71.1±14.6 years, 10,138 men [65.9%]) with the characteristic HCM phenotype within the NEDA cohort were identified. Of these 15,380 cases, 5,552 (36.1%) had asymmetric septal hypertrophy, and 2,276 of the 10,290 cases with LV outflow tract obstruction profiling data (22.1%) had obstructive HCM. A further 3,389 of 13,715 cases (24.7%) had evidence of LV systolic dysfunction (LV ejection fraction <55%). Within the entire NEDA cohort (including those without LV profiling), HCM was found in 10,138 of 342,161 men (2.96%; 95% confidence interval [CI] 2.91%-3.02%) and 5,242 of 308,539 women (1.70%; 95% CI 1.65%-1.75%). When extrapolated to the Australian population, we estimate that a minimum of 15,971 men and 8,057 women presented with echocardiographic features of phenotypical HCM in 2021. This translates into a minimum caseload/prevalence of ∼17 adult men (∼2.5 in those aged ≤50 years) and eight adult women (∼1 in those aged ≤50 years) per 10,000 population meeting phenotypical HCM criteria. CONCLUSIONS: Using contemporary Australian echocardiographic and population data, we estimate that a minimum of 15,971 (17.5 cases/10,000) men and 8,057 women (8.2 cases/10,000) had echocardiographic evidence of phenotypical HCM in 2021. These disease burden data are particularly relevant as new treatment options are emerging.

Optimising Transitional Care Following a Heart Failure Hospitalisation in Australia.

Hospitalisations for heart failure (HF) are associated with high rates of readmission and death, the most vulnerable period being within the first few weeks post-hospital discharge. Effective transition of care from hospital to community settings for patients with HF can help reduce readmission and mortality over the vulnerable period, and improve long-term outcomes for patients, their family or carers, and the healthcare system. Planning and communication underpin a seamless transition of care, by ensuring that the changes to patients' management initiated in hospital continue to be implemented following discharge and in the long term. This evidence-based guide, developed by a multidisciplinary group of Australian experts in HF, discusses best practice for achieving appropriate and effective transition of patients hospitalised with HF to community care in the Australian setting. It provides guidance on key factors to address before and after hospital discharge, as well as practical tools that can be used to facilitate a smooth transition of care.

Consensus statement on the current pharmacological prevention and management of heart failure.

INTRODUCTION: This consensus statement of Australian clinicians provides new recommendations for the pharmacological management of heart failure based on studies reported since the publication of the 2018 Australian heart failure guidelines. MAIN RECOMMENDATIONS: ▪Use of sodium-glucose cotransporter 2 (SGLT2) inhibitors to prevent hospitalisation for heart failure in type 2 diabetes mellitus can be extended to patients with multiple cardiovascular risk factors, albuminuric chronic kidney disease, or atherosclerotic cardiovascular disease. ▪New evidence supports the use of a mineralocorticoid receptor antagonist (finerenone) to prevent heart failure in type 2 diabetes mellitus associated with albuminuric chronic kidney disease. ▪In addition to renin angiotensin system inhibitors (angiotensin receptor neprilysin inhibitor preferred), beta blockers and mineralocorticoid receptor antagonists, an SGLT2 inhibitor (dapagliflozin or empagliflozin) is recommended in all patients with heart failure with reduced left ventricular ejection fraction (LVEF ≤ 40%) (HFrEF). Lower quality evidence supports these therapies in patients with heart failure with mildly reduced LVEF (41-49%) (HFmrEF). ▪A soluble guanylate cyclase stimulator (vericiguat), selective cardiac myosin activator (omecamtiv mecarbil) and, if iron deficient, intravenous iron (ferric carboxymaltose) provide additional benefits in persistent HFrEF. ▪An SGLT2 inhibitor (empagliflozin) should be considered in patients with heart failure with preserved LVEF (≥ 50%) (HFpEF). Key changes in management from this statement: This document broadens the scope of angiotensin receptor neprilysin inhibitor use in patients with HFrEF and HFmrEF. SGLT2 inhibitor use expands to become a cornerstone therapy in HFrEF, with increasing evidence to support its use in HFmrEF and HFpEF.

Urinary sodium concentration predicts time to major adverse coronary events and all-cause mortality in men with heart failure over a 28-33-year period: a prospective cohort study.

BACKGROUND: Lower urinary sodium concentrations (UNa) may be a biomarker for poor prognosis in chronic heart failure (HF). However, no data exist to determine its prognostic association over the long-term. We investigated whether UNa predicted major adverse coronary events (MACE) and all-cause mortality over 28-33 years. METHODS: One hundred and eighty men with chronic HF from the Kuopio Ischaemic Heart Disease Risk Factor Study (KIHD) were included. Baseline data was collected between 1984 and 1989. MACE and all-cause outcomes were obtained using hospital linkage data (1984-2017) with a follow-up of 28-33 years. Cox proportional hazards models were generated using 24-h UNa tertiles at baseline (1 ≤ 173 mmol/day; 2 = 173-229 mmol/day; 3 = 230-491 mmol/day) as a predictor of time-to-MACE outcomes, adjusted for relevant covariates. RESULTS: Overall, 63% and 83% of participants (n = 114 and n = 150) had a MACE event (median 10 years) and all-cause mortality event (median 19 years), respectively. On multivariable Cox Model, relative to the lowest UNa tertile, no significant difference was noted in MACE outcome for individuals in tertiles 2 and 3 with events rates of 28% (HR:0.72; 95% CI: 0.46-1.12) and 21% (HR 0.79; 95% CI: 0.5-1.25) respectively.. Relative to the lowest UNa tertile, those in tertile 2 and 3 were 39% (HR: 0.61; 95% CIs: 0.41, 0.91) and 10% (HR: 0.90; 95% CIs: 0.62, 1.33) less likely to experience to experience all-cause mortality. The multivariable Cox model had acceptable prediction precision (Harrell's C concordance measure 0.72). CONCLUSION: UNa was a significant predictor of all-cause mortality but not MACE outcomes over 28-33 years with 173-229 mmol/day appearing to be the optimal level. UNa may represent an emerging long-term prognostic biomarker that warrants further investigation.

Composite Echocardiographic Score to Predict Long-Term Survival Following Myocardial Infarction.

BACKGROUND: Whilst the left ventricular ejection fraction (LVEF) remains the primary echocardiographic measure widely utilised for risk stratification following myocardial infarction (MI), it has a number of well recognised limitations. The aim of this study was to compare the prognostic utility of a composite echocardiographic score (EchoScore) composed of prognostically validated measures of left-ventricular (LV) size, geometry and function, to the utility of LVEF alone, for predicting survival following MI. METHODS: Retrospective data on 394 consecutive patients with a first-ever MI were included. Comprehensive echocardiography was performed within 24 hours of admission for all patients. EchoScore consisted of LVEF<50%, left atrial volume index>34 mL/m2, average E/e >14, E/A ratio>2, abnormal LV mass index, and abnormal LV end-systolic volume index. A single point was allocated for each measure to derive a score out of 6. The primary outcome measure was all-cause mortality. RESULTS: At a median follow-up of 24 months there were 33 deaths. On Kaplan-Meier analysis, a high EchoScore (>3) displayed significant association with all-cause mortality (log-rank χ2=74.48 p<0.001), and was a better predictor than LVEF<35% (log-rank χ2=17.01 p<0.001). On Cox proportional-hazards multivariate analysis incorporating significant clinical and echocardiographic predictors, a high EchoScore was the strongest independent predictor of all-cause mortality (HR 6.44 95%CI 2.94-14.01 p<0.001), and the addition of EchoScore resulted in greater increment in model power compared to addition of LVEF (model χ2 56.29 vs 44.71 p<0.001, Harrell's C values 0.83 vs 0.79). CONCLUSIONS: A composite echocardiographic score composed of prognostically validated measures of LV size, geometry, and function is superior to LVEF alone for predicting survival following MI.

Sodium-glucose co-transporter 2 inhibitors beyond diabetes.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors lower blood glucose by reducing the reabsorption of glucose in the kidney. They are a second-line therapy for type 2 diabetes. During clinical trials it was noticed that SGLT2 inhibitors had favourable effects on cardiovascular and renal disease. This led to further trials that included patients without diabetes. In studies of heart failure, SGLT2 inhibitors were beneficial in treating patients with a reduced left ventricular ejection fraction. A recent study has also reported benefits in patients with a preserved ejection fraction. In chronic kidney disease, SGLT2 inhibitors may reduce disease progression. However, a decline in the glomerular filtration rate may be seen at the start of treatment. As most experience with SGLT2 inhibitors is in diabetes, patients without diabetes need to be aware of why they are being prescribed these drugs. Some of the potential indications for SGLT2 inhibitors beyond diabetes are not yet approved by regulatory authorities.

Nutraceuticals in Patients With Heart Failure: A Systematic Review.

BACKGROUND: Nutraceuticals are pharmacologically active substances extracted from vegetable or animal food and administered to produce health benefits. We recently reviewed the current evidence for nutraceuticals in patients diagnosed with heart failure as part of the writing of the Australian Guidelines for the prevention, diagnosis, and management of heart failure. METHODS: A systematic search for studies that compared nutraceuticals to standard care in adult patients with heart failure was performed. Studies were included if >50 patients were enrolled, with ≥6 months follow-up. If no studies met criteria then studies <50 patients and <6 months follow-up were included. The primary outcomes included mortality/survival, hospitalization, quality of life, and/or exercise tolerance. Iron was not included in this review as its role in heart failure is already well established. RESULTS: Forty studies met the inclusion criteria. The strongest evidence came from studies of polyunsaturated fatty acids, which modestly decreased mortality and cardiovascular hospitalizations in patients with mostly New York Heart Association class II and III heart failure across a range of left ventricular ejection fraction. Coenzyme Q10 may decrease mortality and hospitalization, but definite conclusions cannot be drawn. Studies that examined nitrate-rich beetroot juice, micronutrient supplementation, hawthorn extract, magnesium, thiamine, vitamin E, vitamin D, L-arginine, L-carnosine, and L-carnitine were too small or underpowered to properly appraise clinical outcomes. CONCLUSION: Only one nutraceutical, omega-3 polyunsaturated fatty acid, received a positive recommendation in the Australian heart failure guidelines. Although occasionally showing some promise, all other nutraceuticals are inadequately studied to allow any conclusion on efficacy. Clinicians should favor other treatments that have been clearly shown to decrease mortality.

The continuous heart failure spectrum: moving beyond an ejection fraction classification.

Randomized clinical trials initially used heart failure (HF) patients with low left ventricular ejection fraction (LVEF) to select study populations with high risk to enhance statistical power. However, this use of LVEF in clinical trials has led to oversimplification of the scientific view of a complex syndrome. Descriptive terms such as 'HFrEF' (HF with reduced LVEF), 'HFpEF' (HF with preserved LVEF), and more recently 'HFmrEF' (HF with mid-range LVEF), assigned on arbitrary LVEF cut-off points, have gradually arisen as separate diseases, implying distinct pathophysiologies. In this article, based on pathophysiological reasoning, we challenge the paradigm of classifying HF according to LVEF. Instead, we propose that HF is a heterogeneous syndrome in which disease progression is associated with a dynamic evolution of functional and structural changes leading to unique disease trajectories creating a spectrum of phenotypes with overlapping and distinct characteristics. Moreover, we argue that by recognizing the spectral nature of the disease a novel stratification will arise from new technologies and scientific insights that will shape the design of future trials based on deeper understanding beyond the LVEF construct alone.

Amyloid Cardiomyopathy.

Amyloid cardiomyopathy is emerging as an important and under-recognised cause of heart failure and cardiac arrhythmias, especially in older adults. This disorder is characterised by extracellular deposition of amyloid fibrils that form due to misfolding of secreted light chains (AL) or transthyretin protein (ATTR). In ATTR, amyloid aggregates typically result from excessive accumulation of wild-type transthyretin (ATTRwt) or from protein structural defects caused by TTR gene variants (ATTRv). Amyloid fibril deposition may predominantly affect the heart or show multi-system involvement. Previously considered to be rare and inexorably progressive with no specific therapy, there has been enormous recent interest in ATTR cardiomyopathy due to upwardly-revised estimates of disease prevalence together with development of disease-modifying interventions. Because of this, there is a clinical imperative to have a high index of suspicion to identify potential cases and to be aware of contemporary diagnostic methods and treatment options. Genetic testing should be offered to all patients with proven ATTR to access the benefits of new therapies specific to ATTRv and allow predictive testing of family members. With heightened awareness of amyloid cardiomyopathy and expanded use of genetic testing, a substantial rise in the numbers of asymptomatic individuals who are carriers of pathogenic variants is expected, and optimal strategies for monitoring and treatment of these individuals at risk need to be determined. Pre-emptive administration of fibril-modifying therapies provides an unprecedented opportunity for disease prevention and promises to change amyloid cardiomyopathy from being a fatal to a treatable disorder.

Hypertrophic Cardiomyopathy: Challenging the Status Quo?

Hypertrophic cardiomyopathy (HCM) is the most common cardiovascular genetic disorder. While our mechanistic understanding has been informed by elegant gene discovery studies that led to the term "disease of the sarcomere", more recent investigations have challenged the single-gene hypothesis. Multimodality imaging has allowed better phenotyping to facilitate early diagnosis, identify treatable phenocopies, and guide management. While HCM remains an important cause of sudden death, recent studies have reported a substantial cumulative burden of heart failure and atrial fibrillation in middle-aged and older individuals. Nonetheless, improvements in risk stratification have allowed early intervention to transition HCM from being a common cause of sudden death in the young to a treatable chronic disease.

Determinants of Diastolic Dysfunction Following Myocardial Infarction: Evidence for Causation Beyond Infarct Size.

BACKGROUND: The determinants of severe diastolic dysfunction (DD) following myocardial infarction (MI) are not well defined. This study sought to define the determinants of severe DD (restrictive mitral inflow pattern on Doppler echocardiography [RFP]) in patients with a first-ever MI, with particular emphasis on the impact of infarct size. METHODS: Retrospective single-centre study including consecutive patients admitted to a tertiary referral centre with a first-ever non-ST-elevation-MI (NSTEMI) or ST-elevation-MI (STEMI) (n=477). Peak troponin-I (Peak-TnI) was used as the principal measure of infarct size, whilst left ventricular ejection fraction (LVEF) and wall motion score index (WMSI) were regarded as surrogate measures. Echocardiography was performed within 24 hours of admission for all patients. RFP was defined as E/A ratio >2.0 or E/A ratio >1.5 and E-wave deceleration time <140 ms. RESULTS: A total of 69 patients (14.5%) had RFP. Peak-TnI levels were higher in the RFP group (32.6±32.7 versus 16.9±25.2 µg/L, p<0.001). In sequential multivariable models incorporating significant clinical, angiographic and left ventricular (LV) size-related variables, Peak-TnI (OR 1.98, p=0.001), WMSI (OR 2.34, p=0.048) and LVEF (OR 0.97, p=0.044) were independent predictors of RFP. Presence of diabetes was also an independent predictor in all the models constructed. When patients were stratified according to an LVEF of 50%, 39% of RFP patients had a preserved LVEF (RFP/preserved EF group), and these patients had lower Peak-TnI levels compared to the RFP/reduced EF group (14.4±18.7 vs 44.5±35.5 µg/L). CONCLUSIONS: Whilst infarct size is a major determinant of severe diastolic dysfunction after MI, a significant subset of patients develop severe diastolic dysfunction despite a small infarct size and preserved LVEF, highlighting that other factors such as pre-existing diastolic dysfunction due to risk factors such as diabetes have an important role in causation.

Accuracy of Cardiac Nurse Acquired and Measured Three-Dimensional Echocardiographic Left Ventricular Ejection Fraction: Comparison to Echosonographer.

BACKGROUND: Three-dimensional echocardiography (3D-Echo) performed by novice health care staff to measure left ventricular ejection fraction (LVEF) could allow cost-effective screening and monitoring for left ventricular systolic dysfunction (LVSD) prior to the development of heart failure. The aim of this study was to determine feasibility and accuracy of cardiac nurses (after completing focussed training) independently acquiring 3D-Echo images, and measuring LVEF using semi-automated software when compared to an echosonographer. METHODS: One echosonographer and three cardiac nurses acquired 3D-Echo images on 73 patients (62 ± 16 years, 62% male) with good image quality, and subsequently measured LVEF using a semi-automated algorithm. RESULTS: Overall feasibility was 89% with the three nurses successfully acquiring 3D-Echo images suitable for LVEF assessment in 65 of the 73 patients. High accuracy (r = 0.82; p < 0.0001) with minimal bias (+0.1, -10.6 to +10.8 limits of agreement; p = 0.91) was observed comparing the nurses to the echosonographer for measuring LVEF. Individual nurses demonstrated high feasibility (86%-92%), accuracy (r = 0.83-0.87; all p < 0.0001) and intra-observer reproducibility (r = 0.96-0.97; all p < 0.0001), with good inter-observer consistency in accuracy compared to the echosonographer (one-way analysis of variance p = 0.559). CONCLUSIONS: We have demonstrated that, following a focussed training protocol, it was feasible for cardiac nurses to acquire 3D-Echo images of sufficient image quality to allow measurement of LVEF using a semi-automated algorithm, with comparable accuracy and intra-observer variability to an expert echosonographer. This could potentially allow the broader application of echocardiography to screen for LVSD in high-risk cohorts.

Patients With Genetic Heart Disease and COVID-19: A Cardiac Society of Australia and New Zealand (CSANZ) Consensus Statement.

In the context of the current global COVID-19 pandemic, this Consensus Statement provides current recommendations for patients with, or at risk of developing, genetic heart disease, and for their health care management and service provision in Australia and New Zealand. Apart from general recommendations, there are specific recommendations for the following conditions: cardiomyopathy, Brugada syndrome (including in children), long QT syndrome (LQTS) and catecholaminergic polymorphic ventricular tachycardia (CPVT). Other recommendations are relevant to patient self-care and primary health care.

COVID-19 and Acute Heart Failure: Screening the Critically Ill - A Position Statement of the Cardiac Society of Australia and New Zealand (CSANZ).

Up to one-third of COVID-19 patients admitted to intensive care develop an acute cardiomyopathy, which may represent myocarditis or stress cardiomyopathy. Further, while mortality in older patients with COVID-19 appears related to multi-organ failure complicating acute respiratory distress syndrome (ARDS), the cause of death in younger patients may be related to acute heart failure. Cardiac involvement needs to be considered early on in critically ill COVID-19 patients, and even after the acute respiratory phase is passing. This Statement presents a screening algorithm to better identify COVID-19 patients at risk for severe heart failure and circulatory collapse, while balancing the need to protect health care workers and preserve personal protective equipment (PPE). The significance of serum troponin levels and the role of telemetry and targeted transthoracic echocardiography (TTE) in patient investigation and management are addressed, as are fundamental considerations in the management of acute heart failure in COVID-19 patients.

New Diastology Guidelines: Evolution, Validation and Impact on Clinical Practice.

The 2016 American Society of Echocardiography/European Association of Echocardiography (ASE/EACVI) guidelines on the assessment of diastolic function sought to simplify the assessment of diastolic function by recommending a streamlined, stepped approach with a focus on four key variables. Haemodynamic validation using simultaneous cardiac catheterisation and echocardiographic assessment of diastolic function have shown robust prediction of left ventricular filling pressure (LVFP) using the streamlined 2016 algorithms, with favourable comparisons to the 2009 guidelines. Similarly, prognostic validation data demonstrates that the 2016 algorithms are easier to implement in clinical practice, have superior inter-observer reliability across a broad range of observer experience, and are better at predicting clinical outcomes. Furthermore, published data show improved classification of clinical heart failure patients. However, increased specificity of the updated 2016 guidelines results in a lower prevalence of diastolic dysfunction compared to the 2009 recommendations. Further refinement of guidelines for the identification and diagnosis of diastolic dysfunction is possible through incorporation of new diastolic parameters.

National Heart Foundation of Australia and Cardiac Society of Australia and New Zealand: Australian clinical guidelines for the management of heart failure 2018.

INTRODUCTION: Heart failure (HF) is a clinical syndrome that is secondary to an abnormality of cardiac structure or function. These clinical practice guidelines focus on the diagnosis and management of HF with recommendations that have been graded on the strength of evidence and the likely absolute benefit versus harm. Additional considerations are presented as practice points. Main recommendations: Blood pressure and lipid lowering decrease the risk of developing HF. Sodium-glucose cotransporter 2 inhibitors decrease the risk of HF hospitalisation in patients with type 2 diabetes and cardiovascular disease. An echocardiogram is recommended if HF is suspected or newly diagnosed. If an echocardiogram cannot be arranged in a timely fashion, measurement of plasma B-type natriuretic peptides improves diagnostic accuracy. Angiotensin-converting enzyme inhibitors, ß-blockers and mineralocorticoid receptor antagonists improve outcomes in patients with HF associated with a reduced left ventricular ejection fraction. Additional treatment options in selected patients with persistent HF associated with reduced left ventricular ejection fraction include switching the angiotensin-converting enzyme inhibitor to an angiotensin receptor neprilysin inhibitor; ivabradine; implantable cardioverter defibrillators; cardiac resynchronisation therapy; and atrial fibrillation ablation. Multidisciplinary HF disease management facilitates the implementation of evidence-based HF therapies. Clinicians should also consider models of care that optimise medication titration (eg, nurse-led titration). Changes in management as a result of the guideline: These guidelines have been designed to facilitate the systematic integration of recommendations into HF care. This should include ongoing audit and feedback systems integrated into work practices in order to improve the quality of care and outcomes of patients with HF.

Differences in management and outcomes for men and women with ST-elevation myocardial infarction.

OBJECTIVE: To examine whether there are sex differences in the characteristics, management, and clinical outcomes of patients with an ST-elevation myocardial infarction (STEMI). Design, setting: Cohort study; analysis of data collected prospectively by the CONCORDANCE acute coronary syndrome registry from 41 Australian hospitals between February 2009 and May 2016. PARTICIPANTS: 2898 patients (2183 men, 715 women) with STEMI. MAIN OUTCOME MEASURES: Rates of revascularisation (percutaneous coronary intervention [PCI], thrombolysis, coronary artery bypass grafting [CABG]), adjusted for GRACE risk score quartile. SECONDARY OUTCOMES: timely vascularisation rates; major adverse cardiac event rates; clinical outcomes and preventive treatments at discharge. RESULTS: The mean age of women with STEMI at presentation was 66.6 years (SD, 14.5 years), of men, 60.5 years (SD, 12.5 years). The proportions of women with hypertension, diabetes, prior stroke, chronic kidney disease, chronic heart failure, or dementia were larger than those of men; fewer women had histories of previous coronary artery disease or myocardial infarction, or of prior PCI or CABG. Women were less likely to have undergone coronary angiography (odds ratio, adjusted for GRACE score quartile [aOR], 0.53; 95% CI, 0.41-0.69) or revascularisation (aOR, 0.42; 95% CI, 0.34-0.52); they were less likely to have received timely revascularisation (aOR, 0.72; 95% CI, 0.63-0.83) or primary PCI (aOR, 0.76; 95% CI, 0.61-0.95). Six months after admission, the rates of major adverse cardiovascular events (aOR, 2.68; 95% CI, 1.76-4.09) and mortality (aOR, 2.17; 95% CI, 1.24-3.80) were higher for women. At discharge, significantly fewer women than men received ß-blockers, statins, and referrals to cardiac rehabilitation. CONCLUSION: Women with STEMI are less likely to receive invasive management, revascularisation, or preventive medication at discharge. The reasons for these persistent differences in care require investigation.