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Background Heart failure with preserved ejection fraction (HFpEF) is an emerging global health problem of which there is limited awareness. HFpEF has a prognosis similar to that of heart failure with reduced ejection fraction (HFrEF) and accounts for approximately half of all patients with heart failure. Objective The aim of this article is to review HFpEF and its consequences and management, including examples of patients with HFpEF. Discussion Patients with HFpEF may present with dyspnoea, fluid retention, lethargy and dizziness, making it difficult to differentiate clinically from HFrEF. The risk factors include increasing age, obesity, hypertension, diabetes, chronic kidney disease and obstructive sleep apnoea. The diagnosis requires good clinical acumen combined with echocardiography and elevated plasma B-type natriuretic peptide concentration Management of HFpEF, especially in later stages, is difficult as there is no evidence-based therapy to date. Prevention is the best strategy. Early recognition and diagnosis are also very important to tackle this global epidemic. [ABSTRACT FROM AUTHOR]

Background: Prosthetic valve thrombosis (PVT) is an uncommon but serious cause of morbidity and mortality after cardiac valve implantation. The most common cause leading to PVT is inadequate anticoagulation. Royal Darwin Hospital is a major referral centre for the Top End of Australia and is unique in having a high burden of rheumatic heart disease (RHD) requiring valve surgery, issues with adherence with oral anticoagulants, and the absence of onsite cardiothoracic facility.Methods: We report clinical characteristics and outcomes of consecutive patients presenting with PVT to a single centre without on-site cardiothoracic surgery.Results: Thirty-two (32) episodes involving 21 patients were retrospectively identified between 2000 and 2017. Our cohort had an average age of 37 years. Nineteen (19) patients were of Aboriginal or Torres Strait Islander descent. All valves were mechanical, except for one bioprosthetic mitral valve, with average time from implantation to initial PVT 5.1 years. The majority of patients were in New York Heart Association (NYHA) class III and IV (6%, and 66%, respectively). Anti-coagulation was sub-therapeutic in 88% of presentations. Eleven (11) (34%) presentations were recurrent PVT involving eight patients. Twenty-six (26) (82%) episodes were treated with thrombolytic therapy which achieved complete success in 65% and partial success in 19%. Five (5) patients received a second dose of the lytic agent. Of the four patients not responding to thrombolytic therapy, two died and two were urgently transferred to a facility with on-site cardiothoracic surgery. Five (5) out of 32 episodes resulted in death (16%) with overall mortality 24% for the cohort over the entire time period. Thrombolytic therapy was associated with five major bleeding episodes (16%) including two fatal bleeds.Conclusions: Prosthetic valve thrombosis is a rare but life-threatening complication of prosthetic valves, with the vast majority of patients found to be inadequately anticoagulated. Despite differences in thrombolytic agents these were successful in the majority of patients. [ABSTRACT FROM AUTHOR]

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: Indigenous Australians experience a greater burden of AF. Whether this is in-part due to differences in arrhythmogenic structures that appear to contribute to AF differences amongst other ethnicities is not known., Methods: We studied forty individuals matched for ethnicity and other AF risk factors. Computed tomography imaging was used to characterise left atrial (LA), pulmonary vein (PV), and left atrial appendage (LAA) anatomy., Results: There were no significant differences in LA diameters or volumes between Indigenous and non-Indigenous Australians. Similarly, we could not detect any consistent differences in PV number, morphology, diameters, or ostial characteristics according to ethnicity. LAA analyses suggested that Indigenous Australians may have a greater proportion of non chickenwing LAA type, and a tendency for eccentric, oval-shaped LAA ostia; however, there were no other differences seen with regards to LAA volume or depth. Indexed values for LA, PV and LAA anatomy corrected for body size were broadly similar., Conclusions: In a cohort of individuals matched for AF risk factors, we could find no strong evidence of ethnic differences in LA, PV, and LAA characteristics that may explain a predisposition of Indigenous Australians for atrial arrhythmogenesis. These findings, in conjunction with our previous data showing highly prevalent cardiometabolic risk factors in Indigenous Australians with AF, suggest that it is these conditions that are more likely responsible for the AF substrate in these individuals. Continued efforts should therefore be directed towards risk factor management in an attempt to prevent and minimise the effects of AF in Indigenous Australians., (© 2021 The Author(s).)