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The persisting life‐expectancy ‘gap’ between First Nations and non‐First Nations Australians is fundamentally driven by the social determinants of health. These include income and social protection, access to adequate housing and food security, among others. These factors are particularly prominent in Central Australia. Inadequate housing has led to some of the highest rates of Streptococcus pyogenes infection in the world, which in turn drives an extremely high prevalence of rheumatic heart disease. Food insecurity and inadequate social protection manifesting as energy insecurity result in inadequate nutrition and have resulted in a huge burden of diabetes in Central Australia. These factors, combined with social exclusion, racism and the pervasive effect of colonisation, also drive a high rate of alcohol misuse. Only by prioritising equity in these ‘social determinants’ and emphasising the importance of First Nations leadership in formulating and implementing solutions will health inequity be addressed. [ABSTRACT FROM AUTHOR]

Background: There is a paucity of data on the burden of heart failure (HF) in Central Australia, the most populous Indigenous region in the country. Aims: To characterize Indigenous and non‐Indigenous Australians with HF in Central Australia. Methods: Consecutive patients with HF and reduced ejection fraction <50% were included for the period 2019 to 2021. Clinical, echocardiographic and major adverse cardiovascular events (MACE) data were collected. Results: Four hundred twenty‐four patients with HF were included (70% Indigenous, 59% male; follow‐up 2.2 ± 0.5 years). Indigenous Australians were younger (53 ± 15 vs 68 ± 13 years, P < 0.001) with higher rates of rheumatic heart disease (18% vs 1%, P < 0.001), diabetes (63% vs 33%, P < 0.001) and severe chronic kidney disease (CKD; 32% vs 7%, P < 0.001). HF was more prevalent among Indigenous (138 [95% confidence interval (CI), 123–155] per 10 000) compared with non‐Indigenous Australians (53 [95% CI, 44–63] per 10 000), particularly among younger individuals and females. There were similar HF aetiologies between groups. Guideline‐directed medical therapy (GDMT) was suboptimal and similar between the groups: angiotensin‐converting enzyme inhibitor/angiotensin receptor blocker (64% vs 67%, P = 0.47) and β‐blockers (68% vs 71%, P = 0.47). Indigenous Australians had a significantly higher rate of MACE (54% vs 28%, P < 0.001) and death from any cause (24% vs 13%, P = 0.013). Conclusions: HF is more than two times as prevalent among Indigenous Central Australians, particularly among younger individuals and females. Despite similar HF aetiologies and GDMT, MACE and mortality outcomes are higher in Indigenous individuals with HF. These data have implications for efforts to close the Indigenous gap in morbidity and mortality. [ABSTRACT FROM AUTHOR]

The article reports that In the diagnosis of obstructive coronary artery disease (CAD), computed tomography (CT) is an accurate, noninvasive alternative to invasive coronary angiography (ICA). However, the comparative effectiveness of CT and ICA in the management of CAD to reduce the frequency of major adverse cardiovascular events is uncertain.

Indigenous Australians are known to have a higher prevalence of coronary artery disease (CAD) than non-Indigenous counterparts. Atherogenic lipid profiles, characterised by low serum levels of high-density lipoprotein (HDL) and higher serum triglycerides, have been shown to be more prevalent in Indigenous Australians. The use of computed tomography coronary angiography (CTCA) for risk stratification and diagnosis of CAD has been validated in moderate risk populations, but limited data exists in specific high-risk populations such as Indigenous Australians. Through a retrospective study of patient records, we aimed to confirm if an atherogenic lipid profile occurred in Indigenous Australians undergoing CTCA in the Northern Territory of Australia and if so, whether this correlated with the prevalence or burden of CAD. We demonstrate that Indigenous Australians have similar prevalence (52.6% vs . 50.3%, P=0.80) and burden of CAD (Leaman score 6.03±4.66 vs . 6.96±4.82, P=0.44) on CTCA as non-Indigenous patients, but were 8 years younger (41.9±8.9 vs . 50.0±11.9 years, P<0.001) at the time of examination. We confirmed the presence of an atherogenic lipid profile in Indigenous patients and showed low serum-HDL was associated with very premature (patients aged 18-35 years) CAD in comparison to premature (patients aged 36-55 years) and mature-onset (patients aged 56 years and older) CAD (0.71±0.25 vs . 1.09±0.35 vs . 1.18±0.36 mmol/L, P=0.009). Future clinical guidelines should consider the role of CTCA in Indigenous Australians and whether younger patients may benefit. The causes of premature CAD, including atherogenic lipid profiles, require an ongoing focus in order to achieve equitable cardiovascular outcomes for Indigenous and non-Indigenous Australians., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-23-458/coif). P.J.P. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from July 2022 to June 2024. D.W. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from February 2023 to January 2025. P.J.P. reports that he received speaker honoraria ad hoc from AstraZeneca and Boehringer Ingelheim related to antiplatelet/anticoagulant management of coronary syndromes; received support from Eli Lilly and NovoNordisk; and served as unpaid president of Australian Atherosclerosis Society. The other authors have no conflicts of interest to declare., (2024 Cardiovascular Diagnosis and Therapy. All rights reserved.)

Background: Vascular inflammation plays a crucial role in the development of atherosclerosis and atherosclerotic plaque rupture resulting in acute coronary syndrome (ACS). Pericoronary adipose tissue (PCAT) attenuation quantified from routine coronary computed tomography angiography (CCTA) has emerged as a promising non-invasive imaging biomarker of coronary inflammation. However, a detailed understanding of the natural history of PCAT attenuation is required before it can be used as a surrogate endpoint in trials of novel therapies targeting coronary inflammation. This article aims to explore the natural history of PCAT attenuation and its association with changes in plaque characteristics., Methods: The Australian natuRal hISTOry of periCoronary adipose tissue attenuation, RAdiomics and plaque by computed Tomographic angiography (ARISTOCRAT) registry is a multi-centre observational registry enrolling patients undergoing clinically indicated serial CCTA in 9 centres across Australia. CCTA scan parameters will be matched across serial scans. Quantitative analysis of plaque and PCAT will be performed using semiautomated software., Discussion: The primary endpoint is to explore temporal changes in patient-level and lesion-level PCAT attenuation by CCTA and their associations with changes in plaque characteristics. Secondary endpoints include evaluating: (I) impact of statin therapy on PCAT attenuation and plaque characteristics; and (II) changes in PCAT attenuation and plaque characteristics in specific subgroups according to sex and risk factors. ARISTOCRAT will further our understanding of the natural history of PCAT attenuation and its association with changes in plaque characteristics., Trial Registration: This study has been prospectively registered with the Australia and New Zealand Clinical Trials Registry (ACTRN12621001018808)., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-23-392/coif). P.J.P. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from July 2022 to June 2024. S.J.N. as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from September 2023 to August 2025. D.T.L.W. serves as an unpaid editorial board member of Cardiovascular Diagnosis and Therapy from February 2021 to January 2023. K.C. was supported by the National Health and Medical Research Council postgraduate scholarship (No. APP2002573), which covers a portion of the research-related expenses and stipend to help with living expenses, research-related travel costs and other expenses associated with research project. S.J.N. received consulting fees from Amgen, Akcea, AstraZeneca, Boehringer Ingelheim, CSL Behring, Eli Lilly, Esperion, Kowa, Merck, Takeda, Pfizer, Sanofi- Regeneron, Vaxxinity, CSL Sequiris, and Novo Nordisk; received grants from AstraZeneca, Amgen, Anthera, CSL Behring, Cerenis, Cyclarity, Eli Lilly, Esperion, Resverlogix, New Amsterdam Pharma, Novartis, InfraReDx and Sanofi-Regeneron. D.T.L.W. received honoraria for lectures from Eli-Lilly, Pfizer and Boehringer. The other authors have no conflicts of interest to declare., (2024 Cardiovascular Diagnosis and Therapy. All rights reserved.)

Background: Non-ST elevation myocardial infarction (NSTEMI) has higher post-discharge mortality than ST-elevation myocardial infarction (STEMI). Prognosis worsens in those with multivessel coronary disease (MVD). However, information about the prevalence and extent of MVD in NSTEMI is limited, in turn limiting insights into optimal treatment strategies. This study aimed to define the prevalence and extent of MVD, preferred treatment strategies and the predictors of MVD in a real-world NSTEMI population., Methods: The Coronary Angiogram Database of South Australia (CADOSA) was used to identify consecutive patients presenting to major teaching hospitals with NSTEMI between 2012 and 2016. Obtaining clinical and angiographic details, patients were stratified by the number of significantly diseased vessels (0,1,2,3-VD), defined by a stenosis of ≥70%, or ≥50% in the left main coronary artery. Data was analysed retrospectively., Results: The prevalence of MVD (2- or 3-VD) was 42% amongst 3,722 NSTEMI presentations. Multivariate logistic regression modelling showed age, male gender, diabetes, dyslipidaemia and prior myocardial infarction predicted MVD over 1-VD or 0-VD. Percutaneous coronary intervention (PCI) was performed in 42% of patients with MVD. This comprised 61% of 2-VD patients and only 22% of 3-VD patients, with 24% and 66% of each group referred for coronary bypass grafting, respectively. Among MVD patients treated with PCI, 76% had their culprit lesion treated alone in the index admission., Conclusions: In this NSTEMI cohort, over 40% had MVD. Notably, a minority of patients with MVD undergoing PCI received multivessel revascularisation. This real-world practice emphasises that further evaluation is required to determine whether complete revascularisation is beneficial in NSTEMI, as reported for STEMI., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cdt.amegroups.com/article/view/10.21037/cdt-21-518/coif). PJP has received speaker honoraria ad hoc from Astra Zeneca and Boehringer Ingelheim related to antiplatelet/anticoagulant management of coronary syndromes, and support from Astra Zeneca to attend American Heart Association meeting in 2019. All other grant, advisory committee and honoraria support are not related to the content of this manuscript. The other authors have no conflicts of interest to declare., (2022 Cardiovascular Diagnosis and Therapy. All rights reserved.)