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Whether early young adulthood dietary patterns predict the risk of metabolic syndrome (MetS) and diabetes-related endpoints prior to middle age remains unknown. We examined the prospective associations of dietary patterns in early young adulthood with MetS and diabetes-related endpoints at later young adulthood.We used data of young adults from a long running birth cohort in Australia. The Western dietary pattern rich in meats, refined grains, processed and fried foods and the prudent dietary pattern rich in fruits and vegetables, whole grains and legumes were derived using principal component analysis at the 21-year follow-up from dietary data obtained by a food frequency questionnaire. Fasting blood samples at 30 years were collected from each participant and their blood biomarkers, anthropometric and blood pressure were measured. MetS, insulin resistance, and prediabetes were based on clinical cut-offs; increased β-cell function and insulin resistance were based on upper quartiles. Log-binomial models were used to estimate diet-related risks of each outcome adjusting for potential confounders.Greater adherence to the Western pattern predicted higher risks of MetS (RR: 2.32; 95% CI: 1.34, 4.00), increased insulin resistance (1.69; 1.07, 2.65), high β-cell function (1.60; 1.10, 2.31) and less likelihood of increased insulin sensitivity (0.57; 0.39, 0.84) in adjusted models. Conversely, adhering more to the prudent pattern predicted lower risks of MetS (RR: 0.47; 95% CI: 0.29, 0.75), increased insulin resistance (0.57; 0.39, 0.82), high β-cell function (0.69; 0.50, 0.93) and a greater likelihood of increased insulin sensitivity (1.84; 1.30, 2.60).This prospective study of young adults indicates greater adherence to unhealthy Western diet predicted higher risks of MetS and increased insulin resistance, whereas healthy prudent diet predicted lower risks. Optimizing diets to improve later cardiometabolic health needs to occur in early adulthood.

The extent to which dietary patterns influence the risk of abnormal blood lipids throughout young adulthood remains unclear. The aim was to investigate whether early young adulthood dietary patterns predict the risk of abnormal blood lipids during later young adulthood.We used data from a long running birth cohort study in Australia. Western dietary pattern rich in meats, processed foods and high-fat dairy products and prudent pattern rich in fruit, vegetables, fish, nuts, whole grains and low-fat dairy products were derived using principal component analysis at the 21-year follow-up from dietary data obtained using a food frequency questionnaire. After 9-years, fasting blood samples of all participants were collected and their total, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterols and triglyceride (TG) levels were measured. Abnormal blood lipids were based on clinical cut-offs for total, LDL and HDL cholesterols, and TG and relative distributions for total:HDL and TG:HDL cholesterols ratios. Log-binomial models were used to estimate risk of each outcome in relation to dietary patterns. Greater adherence to the Western pattern predicted increased risks of high LDL (RR: 1.47; 95%CI: 1.06, 2.03) and TG (1.90; 1.25, 2.86), and high ratios of total:HDL (1.48; 1.00, 2.19) and TG:HDL (1.78; 1.18, 2.70) cholesterols in fully adjusted models. Conversely, a prudent pattern predicted reduced risks of low HDL (0.58; 0.42, 0.78) and high TG (0.66; 0.47, 0.92) and high total:HDL (0.71; 0.51, 0.98) and TG:HDL (0.61; 0.45, 0.84) cholesterols ratios.This is the first prospective study to show greater adherence to unhealthy Western diet predicted increased risks of abnormal blood lipids, whereas healthy prudent diet predicted lower such risks in young adults. Addressing diets in early course may improve cardiovascular health of young adults.

Objective:Previous studies of sociodemographic and lifestyle correlates of dietary patterns among young adults have primarily focused on physical activity and smoking, with inconclusive results. This study aims to examine the associations between a broader range of lifestyles of young adults and their patterns of food consumption.Design:Cross-sectional.Setting:Brisbane, Australia.Participants:The data set are from a long running birth cohort study which commenced in 1981. Details of dietary intake and sociodemographic and lifestyle factors were from the 21-year follow-up of the Mater-University of Queensland Study of Pregnancy (MUSP) birth cohort. The effective cohort (n 2665, 57 % women) is of young adult offspring. Usual dietary intake was assessed using a Food Frequency Questionnaire (FFQ). Data on sociodemographic and lifestyle variables were obtained from self-reports.Results:Western and prudent dietary patterns were identified for the combined cohort of women and men using principal components analysis. Multivariable linear regression models were used to examine the associations between lifestyle variables and dietary patterns adjusting for potential confounders. Results from multivariable adjusted models showed that physical activity, watching TV and smoking were strongly associated with each dietary pattern; alcohol consumption and BMI showed weaker associations (P < 0·05 for all).Conclusions:Our study describes a clustering of unhealthy lifestyles in young adults. Young adults with unhealthy lifestyles less often adhere to a healthy prudent dietary pattern and more often an unhealthy Western pattern. Dietary preferences are enmeshed in a lifestyle matrix which includes physical activity, sedentary activity, smoking and alcohol consumption of young adults.

There is little known about whether exposure to family poverty at specific periods of the early life course independently contributes to coronary heart disease risk beyond the contribution of concurrent poverty. Children were recruited in early pregnancy and additional survey data obtained during the pregnancy and at the 5-, 14- and 30-year follow-ups. Fasting blood samples were also obtained at the 30-year follow-up. Analyses are multinominal logistic regressions stratified by gender and with adjustments for confounding. For male offspring, family poverty at different stages of the early life course was not associated with measures of cardio-metabolic risk. For females early life course, poverty predicted obesity, homeostatic model assessment of insulin resistance (HOMA-IR) and total cholesterol/high-density lipoprotein cholesterol (TC/HDL-C), as well as concurrent family poverty associated with obesity, HOMA-IR, TC/HDL-C, HDL-C and increased systolic and diastolic blood pressure. Family poverty in the early life course independently predicts increased levels of cardio-metabolic risk of females. The primary finding, however, is that concurrent poverty is independently and strongly associated with increased cardio-metabolic risk levels in young adulthood.

Background: Patients with cardiac implantable electronic devices (CIEDs) frequently undergo transthoracic echocardiography (TTE). As a result, incidental mobile echodensities (MEDs) attached to device leads are commonly detected. The aim of this study was to estimate the incidence and clinical outcomes of incidental MEDs on CIED leads. Methods: A retrospective analysis performed between 2011 and 2018 identified 3548 TTE studies performed on 1849 patients with CIEDs. Results: MEDs were identified in 30 patients (1.6%) without clinical suspicion of infective endocarditis (IE). Patients with incidental MEDs were apyrexial, and those tested demonstrated low inflammatory markers and negative blood cultures (BC). In this group, the majority (83%) of MEDs were in the right atrium and no MEDs were detected near the tricuspid valve. Transesophageal echocardiography (TEE) did not influence clinical outcomes. No patient required long-term antibiotics or lead extraction and no IE-related deaths were identified from electronic health records during a mean follow-up period of 43 months (1-89). In contrast, nine patients with suspected IE were all pyrexial with elevated inflammatory markers, had positive BC, and had proven IE. In these cases, the majority of MEDs were at the device lead/tricuspid valve interface. MEDs close to the tricuspid valve were strongly associated with IE (P

IntroductionCardiovascular disease (CVD) represents a significant burden of disease for Aboriginal and Torres Strait Islander people, a population that continues to experience a lower life expectancy than other Australians. The aim of the Better Cardiac Care Data Linkage project is to describe patient care pathways and to identify disparities in care and health outcomes between Aboriginal and Torres Strait Islander people and other Queensland residents diagnosed with CVD in the state of Queensland.MethodsThis is a population-based retrospective cohort study using linked regional, state and national health and administrative data collections to describe disparities in CVD healthcare in primary and secondary prevention settings and during hospitalisation. The CVD cohort will be identified from the Queensland Hospital Admitted Patient Data Collection for admissions that occurred between 1 July 2010 and 31 June 2016 and will include relevant International Classification of Disease codes for ischaemic heart disease, congestive heart failure, stroke, acute rheumatic fever and rheumatic heart disease. Person-level data will be linked by Data Linkage Queensland and the Australian Institute of Health and Welfare (AIHW) in accordance with ethical and public health approvals to describe the patient journey prior to, during and post the hospital admission.AnalysisThis project will focus largely on descriptive epidemiological measures and multivariate analysis of clinical care standards and outcomes for Aboriginal and Torres Strait Islander people compared with other Queenslanders, including identification of risk factors for suboptimal care and change over time. Variation in care pathways and patient outcomes will be compared by Indigenous status, sex, age group, remoteness of residence, year of index hospitalisation and socioeconomic status. Cox models for time-to-event data and mixed models or generalised estimating equations for longitudinal data will be used to measure change over time where temporal effects exist.Ethics and disseminationEthical approval has been granted by Human Research Ethics Committees of the Prince Charles Hospital (HREC/15/QPCH/289) and the AIHW (EO2016-1-233). The Northern Territory Department of Health and Menzies School of Health Research have also provided reciprocal ethical approval of the project (HREC 2019–3490). The deidentified results will be summarised in a report and shared with investigators, advisory groups, Queensland Health and key stakeholders. Findings will be disseminated through workshops, conferences and will be published in peer-reviewed journals.

Background Medication harm can lead to hospital admission, prolonged hospital stay and poor patient outcomes. Reducing medication harm is a priority for healthcare organisations worldwide. Recent Australian studies demonstrate cardiovascular (CV) medications are a leading cause of harm. However, they appear to receive less recognition as ‘high risk’ medications compared with those classified by the medication safety acronym, ‘APINCH’ (antimicrobials, potassium, insulin, narcotics, chemotherapeutics, heparin). Our aim was to determine the scale and type of medication harm caused by CV medications in healthcare. Methods A narrative review of adult (>16 years) medication harm literature identified from PubMed and CINAHL databases was undertaken. Studies with the primary outcome of measuring the incidence of medication harm were included. Harm caused by CV medications was described and ranked against other medication classes at four key stages of a patient’s healthcare journey. Where specified, the implicated medications and type of harm were investigated. Results A total of 75 studies were identified, including seven systematic reviews and three meta-analyses, with most focussing on harm causing hospital admission. CV medications were responsible for approximately 20% of medication harm; however, this proportion increased to 50% in older populations. CV medications were consistently ranked in the top five medication categories causing harm and were often listed as the leading cause. Conclusion CV medications are a leading cause of medication harm, particularly in older adults, and should be the focus of harm mitigation strategies. A practical approach to generate awareness among health professionals is to incorporate ‘C’ (for CV medications) into the ‘APINCH’ acronym. Plain language summary Patient harm from cardiovascular medications Background • Harm from medications can cause poor patient outcomes. • Certain medications have been identified as ‘high risk’ and are known to cause high rates of harm. • ‘High risk’ medications are included in medication guidelines used by health professionals. • Cardiovascular medications (e.g. blood pressure and cholesterol medications) are important and have many benefits. • Recent studies have found cardiovascular medications to cause high rates of harm. • Cardiovascular medication harm is often under-recognised in clinical practice. • Some guidelines do not consider cardiovascular medications to be ‘high risk’. Method • This review investigated the extent of harm caused by cardiovascular medications in adults across four healthcare settings: (1) at the time of hospital admission; (2) during hospital admission; (3) after hospital; and (4) readmission to hospital. • Harm caused by cardiovascular medications was ranked against other medication classes. • We investigated the type of cardiovascular medications to cause harm and the type of harm caused. Results • Seventy-five studies were reviewed across 41 countries. • Cardiovascular medications were ranked within the top five medications to cause harm. • Cardiovascular medications were a leading cause of harm in each healthcare setting investigated. • Harm caused by cardiovascular medications was common in older adults (>65 years). • Cardiovascular medications often caused preventable harm. • Medications to treat high blood pressure and abnormal heart rhythms were the most common causes of harm. • We reported kidney injury, electrolyte changes and low blood pressure as common types of harm. Conclusion • Increased focus on cardiovascular medications in clinical practice is needed. • Health professionals need to carefully prescribe and frequently review cardiovascular medications, especially in older adults. • Patient and health professional discussions should be based on both the benefits and harms of cardiovascular medications. • Cardiovascular medications should be included in all ‘high risk’ medication guidelines.

The Challenges Rural and remote Australians and New Zealanders have a higher rate of adverse outcomes due to acute myocardial infarction, driven by many factors. The prevalence of cardiovascular disease (CVD) is also higher in regional and remote populations, and people with known CVD have increased morbidity and mortality from coronavirus disease 2019 (COVID-19). In addition, COVID-19 is associated with serious cardiac manifestations, potentially placing additional demand on limited regional services at a time of diminished visiting metropolitan support with restricted travel. Inter-hospital transfer is currently challenging as receiving centres enact pandemic protocols, creating potential delays, and cardiovascular resources are diverted to increasing intensive care unit (ICU) and emergency department (ED) capacity. Regional and rural centres have limited staff resources, placing cardiac services at risk in the event of staff infection or quarantine during the pandemic. Main Recommendations Health districts, cardiologists and government agencies need to minimise impacts on the already vulnerable cardiovascular health of regional and remote Australians and New Zealanders throughout the COVID-19 pandemic. Changes in management should include: • Improved access to telehealth consultation for regional and rural outpatients. Specialist-led 24/7 electrocardiograph (ECG) reading and acute cardiology services, uniformly covering all rural inpatients, to minimise potential impacts on acute care. • Transfer models incorporating discussion between clinicians and ambulance, balancing urgency with considerations of ambulance capacity in rural locations. • Protection of the role of specialist cardiovascular nurses, avoiding COVID-19 redeployment to maintain rural cardiac service capacity. • An urgent shift to regional models for pacing services, utilising remote monitoring supported by local device implantation and local technicians.

Bicuspid aortic valve (BAV) is the most common cardiac congenital abnormality and can be associated with significant valvulopathy or aortopathy. Current active areas of BAV research include prediction of development of valve dysfunction and aortopathy, and the various surgical valvular strategies with or without ascending aortic replacement. There is also increasing interest in the emerging role of transcatheter aortic valve replacement (TAVR) even though it is listed as a relative contraindication in current TAVR recommendations. Although there are clearly established guidelines in the clinical management and surgical techniques for the management of BAV with or without aortopathy, many of these newer surgical techniques have shown excellent post-surgical results but need to be directly compared against “standard” guidelines recommended treatment. As such, this creates new controversies regarding the clinical and surgical management of BAV. In this review, we have summarized the current understan...

Our aim was to determine the feasibility of 18F-florbetaben PET in diagnosing cardiac amyloidosis. Methods: 18F-florbetaben PET was performed on 14 patients: 5 amyloid light chain, 5 amyloid transthyretin, and 4 control with hypertensive heart disease. Qualitative and quantitative assessments of 18F-florbetaben activity were performed using the SUVmean of the left ventricular myocardium and blood pool and calculation of target-to-background SUV ratio. Myocardial 18F-forbetaben retention was also calculated as the percentage mean myocardial SUV change between 0 and 5 min and 15 and 20 min after radiotracer injection. Global left ventricular longitudinal and right ventricular free wall longitudinal strain were calculated using 2-dimensional speckle-tracking echocardiography. Results: Target-to-background SUV ratio and percentage myocardial 18F-forbetaben retention were higher in amyloid patients than in hypertensive controls. A cutoff of 40% was able to differentiate between cardiac amyloid patients and hypertensive controls. Percentage myocardial 18F-forbetaben retention was an independent determinant of both global left ventricular longitudinal and right ventricular free wall longitudinal strain via an inverse curve relationship. Conclusion: 18F-florbetaben PET imaging can accurately identify and differentiate between cardiac amyloidosis and hypertensive heart disease. Percentage myocardial 18F-florbetaben retention was an independent determinant of myocardial dysfunction in cardiac amyloidosis.

This case study describes the development, implementation and review of a sustainable and culturally sensitive procedure for a hospital-funded discharge medicine subsidy for Aboriginal and Torres Strait Islander patients registered with the Closing the Gap (CTG) program discharging from a public hospital. A 7-day fully subsidised medication supply was approved to be offered to Aboriginal and Torres Strait Islander patients admitted under cardiac care teams, including cardiology and cardiothoracic surgery patients. Patients were offered the option of a 7-day supply free of cost to them or a full Pharmaceutical Benefits Scheme (PBS) supply if preferred. A general practitioner (GP) appointment was organised within 7 days of discharge to ensure patients received ongoing supply of their medications as well as timely clinical review after discharge. Over a 34-month period from September 2015 to June 2018, 535 Aboriginal and Torres Strait Islander patients were admitted to the hospital under cardiac care teams. Of these patients, 296 received a subsidised discharge medication supply with a total cost of A$6314.56 to the hospital over the trial period, with a mean cost of A$21.26 per discharge. The provision of subsidised medications through the CTG program has improved the continuity of care for Aboriginal and Torres Strait Islander patients. The culturally sensitive approach is well received and has allowed smooth transition back to the community. This site-specific and state-based funding model was found to be financially sustainable at a public hospital. What is known about the topic?The CTG PBS program is not applicable to discharge prescriptions from public hospitals. As such, patients are required to either leave the hospital with no medicines or leave the hospital with medicines for which they have to pay full PBS price. This creates a huge financial barrier to the care for CTG-registered patients in the acute care setting. What does this paper add?A sustainable solution to the problem was found via a state-funded model while providing a supportive team to ensure GP follow-up and continuity of care after discharge. What are the implications for practitioners?If similar approvals are granted and supported at other public hospital sites, practitioners will be afforded one less barrier to provide patient-centred care for Aboriginal and Torres Strait Islander patients.

Background Current understanding of metabolic heart disease consists of a myriad of different pathophysiological mechanisms. Epicardial adipose tissue (EAT) is increasingly recognized as metabolically active and associated with adverse cardiovascular outcomes. The present study aimed to investigate the effect of increased EAT volume index on left ventricular (LV) myocardial fat content and burden of interstitial myocardial fibrosis and their subsequent effects on LV myocardial contractile function. Methods and Results A total of 40 volunteers (mean age, 35±10 years; 26 males) of varying body mass index (25.0±4.1 kg/m 2 ; range, 19.3–36.3 kg/m 2 ) and without diabetes mellitus or hypertension were prospectively recruited. EAT volume index, LV myocardial fat content, and extracellular volume were quantified by magnetic resonance imaging. LV myocardial contractile function was quantified by speckle tracking echocardiography global longitudinal strain on the same day as magnetic resonance imaging examination. Mean total EAT volume index, LV myocardial fat content, and extracellular volume were 30.0±19.6 cm 3 /m 2 , 5.06%±1.18%, and 27.5%±0.5%, respectively. On multivariable analyses, increased EAT volume index and insulin resistance were independently associated with both increased LV myocardial fat content content and higher burden of interstitial myocardial fibrosis. Furthermore, increased EAT volume index was independently associated with LV global longitudinal strain. Conclusions Increased EAT volume index and insulin resistance were independently associated with increased myocardial fat accumulation and interstitial myocardial fibrosis. Increased EAT volume index was associated with detrimental effects on myocardial contractile function as evidenced by a reduction in LV global longitudinal strain.

Heart failure (HF) and atrial fibrillation (AF) frequently coexist, and they can beget one another due to similar factors and shared pathophysiology. These pathophysiologic changes promote the episodes of AF, while they in turn predispose to the exacerbation of HF. In this review, we will discuss pathophysiological mechanisms shared by AF and HF. Patients with concomitant HF and AF are at a particularly high risk of thromboembolism, which contribute to even worse symptoms and poorer prognosis. Vitamin K antagonists (VKA) (warfarin) were the traditional medication in AF patients for the prevention of stroke, whereas the advance of novel non-VKA oral anticoagulants (NOACs) (dabigatran, apixaban, rivaroxaban, and edoxaban) is challenging these standard prescriptions. NOACs' potential advantages over warfarin, including fixed dosing regimens, wide therapeutic window, and more sustained anticoagulant response, promote clinicians to consider these novel agents in the first place. However, some data suggested patients with AF and HF may receive different therapeutic response than those with AF alone in anticoagulant treatment. Accordingly, we aim to assess the potential role of oral anticoagulants, especially NOACs, in the management of patients with concomitant AF and HF.

Epicardial adipose tissue (EAT) is a metabolically active visceral fat depot. Although EAT volume is associated with the incidence and burden of atrial fibrillation (AF), its role in subclinical left atrial (LA) dysfunction is unclear. This study aims to evaluate the relationships between EAT volumes, LA function, and LA global longitudinal strain.One hundred and thirty people without obstructive coronary artery disease or AF were prospectively recruited into the study in Australia and underwent cardiac computed tomography and echocardiography. EAT volume was quantified from cardiac computed tomography. Echocardiographic 3-dimensional (3D) volumetric measurements and 2D speckle-tracking analysis were performed.Using the overall median body surface area-indexed total EAT volume (EATi), the study cohort was divided into 2 groups of larger and smaller EATi volume. Subjects with larger EATi volume had significantly impaired LA reservoir function (3D LA ejection fraction, 46.1% ± 8.9% vs 49.0% ± 7.0%, P = 0.044) and reduced LA global longitudinal strain (37.6% ± 10.2% vs 44.1% ± 10.7%, P0.001). Total EATi volume was a predictor of impaired 2D LA global longitudinal strain (standardized β = -0.204, P = 0.034), reduced 3D LA ejection fraction (standardized β = -0.208, P = 0.036), and reduced 3D active LA ejection fraction (standardized β = -0.211, P = 0.017). Total EATi volume, rather than LA EATi volume, was the more important predictor of LA dysfunction.Indexed EAT volume is independently associated with subclinical LA dysfunction and impaired global longitudinal strain in people without obstructive coronary artery disease or a history of AF.

Right ventricular (RV) function assumes prognostic significance in various disease states, but RV geometry is not amenable to volumetric assessment by two-dimensional echocardiography. Intra-ventricular pressure rate of rise (dP/dt) predicts myocardial contractility and adjusting for the maximal regurgitant velocity (Vmax) corrects for preload. We examined the relationship of noninvasive tricuspid dP/dt and dP/dt/Vmax with RV ejection fraction (RVEF) by cardiac magnetic resonance imaging (CMR) as a measure of RV function.Fifty CMRs and echocardiograms performed within 30 days were included. Tricuspid regurgitation (TR) spectral Doppler trace was analyzed offline. TR dP/dt was calculated using simplified Bernoulli equation (dP/dt between 1 and 2 m/sec). dP/dt/Vmax was calculated as a ratio of dP/dt and TR Vmax . RV end-diastolic (EDV) and end-systolic volumes (ESV) were obtained from contouring of steady-state-free precession axial stack CMR images; RVEF was calculated as [(RVEDV - RVESV)/RVEDV] × 100. RVEF42% was considered normal.Majority of studies were suitable for analysis. Median age was 48 years (IQR = 36-63); 56.4% were female (n = 22/39). There was correlation between dP/dt and RVEF (r(2) = 0.51, P0.01) which improved with dP/dt/Vmax (r(2) = 0.59, P0.01). dP/dt400 mmHg/sec had a positive predictive value of 91%, sensitivity and specificity of 74% and 84% respectively for normal RVEF. Inter-observer agreement and repeatability analysis showed no significant difference.Tricuspid dP/dt correlates well with CMR RVEF. A dP/dt of more than 400 mmHg/sec strongly predicts normal RVEF. Adjusting for preload (dP/dt/Vmax) further improves this correlation.

Background Although epicardial adipose tissue (EAT) volume is associated with increased incidence of coronary artery disease (CAD), its role in myocardial systolic dysfunction is unclear. The present study aimed to identify independent determinants of EAT volume in patients without obstructive CAD, and to evaluate the association between EAT volume (vs other measures of obesity) and myocardial systolic strain analysis. Methods We prospectively recruited 130 patients without obstructive CAD on contrast-enhanced cardiac computed tomography imaging and normal left ventricular ejection fraction on 3-dimensional (3D) echocardiography. EAT volume was quantified from cardiac computed tomography imaging, and 3D multidirectional (longitudinal, circumferential, radial, and area) strain were measured. Results The mean EAT volume was 97.5 ± 43.7 cm 3 . In multivariable analysis, measures of obesity (body mass index [ P = 0.007] and waist/hip ratio [ P = 0.001]) were independently associated with larger EAT volume. EAT volume was correlated with 3D global longitudinal ( r = 0.601; P r = 0.375; P r = −0.546; P r = 0.558; P P P = 0.006), radial (standardized β = −0.422; P P P > 0.05). Conclusions EAT volume is independently associated with impaired myocardial systolic function despite preserved 3D left ventricular ejection fraction and absence of obstructive CAD, and might play a significant role in the pathophysiology of diabetic, obesity, and metabolic heart disease.

ObjectivePrevious studies in cardiac patients noted that early patient follow-up with general practitioners (GPs) after hospital discharge was associated with reduced rates of hospital readmissions. We aimed to identify patient, clinical and hospital factors that may influence GP follow-up of patients discharged from a tertiary cardiology unit.DesignSingle centre retrospective cohort study.SettingAustralian metropolitan tertiary hospital cardiology unit.Participants1079 patients discharged from the hospital cardiology unit within 3 months from May to July 2016.Outcome measuresGP follow-up rates (assessed by telephone communication with patients’ nominated GP practices), demographic, clinical and hospital factors predicting GP follow-up.ResultsWe obtained GP follow-up data on 983 out of 1079 (91.1%) discharges in the study period. Overall, 7, 14 and 30-day GP follow rates were 50.3%, 66.5% and 79.1%, respectively. A number of patient, clinical and hospital factors were associated with early GP follow-up, including pacemaker and defibrillator implantation, older age and having never smoked. Documented recommendation for follow-up in discharge summary was the strongest predictor for 7-day follow-up (pConclusionAfter discharge from a cardiology admission, half of the patients followed up with their GP within 7 days and most patients followed up within 30 days. Patient and hospital factors were associated with GP follow-up rates. Identification of these factors may facilitate prospective interventions to improve early GP follow-up rates.

Aortic valve stenosis (AS) is a frequent and potentially severe disease of the heart. Accurate assessment of AS is a critical factor in determining prognosis and treatment. This paper describes the advantages and limitations of AS assessment from a biomechanical engineering perspective, by contrasting the non-invasive AS diagnostic methods of echocardiography (Echo), computed tomography (CT), magnetic resonance imaging (MRI), computational analysis (CA) including the invasive technique of cardiac catheterization. The findings illustrated that current methods of AS evaluation, with assumptions of an ideal fluid, geometry and governing equations may not apply well to the aortic valve pathology and could increase the uncertainty of the degree of stenosis and valve area. This review suggests an alternative method using CA, which could potentially overcome the pitfalls of other AS assessments that incorporate geometry, pressure recovery and aorta wall compliance, based on the accurate conversion of AS imaging to the numerical modelling. Further, this review highlights the importance of CA boundary conditions, and the role of verification and validation to produce reliable computational results.

Background: The CHA2DS2-VASc score is the standard of care in thromboembolic risk assessment for patients with non-valvular atrial fibrillation (AF). Most patients will undergo transthoracic echocardiography (TTE) for further evaluation, and many also having transesophageal echocardiography (TEE) performed prior to cardioversion or ablation. We sought to evaluate the relationship between left atrial (LA) abnormalities detected on TEE and TTE parameters, to determine if imaging may be additive in risk assessment.Methods: Clinical, TEE and TTE data for patients in AF at the time of their study were included in this retrospective analysis. LA/LA appendage (LAA) abnormalities on TEE included the presence of spontaneous echo contrast, sludge, thrombus and LAA emptying velocity 90% in both groups. Median LAVI, septal e’ and E wave velocity in the ≤ 1 vs ≥2 groups were 46ml/m2vs 48ml/m2, 8cm/s vs 6cm/s and 0.8m/s vs 0.8m/s, respectively. Overall, increased LAVI and reduced septal e’ on TTE was associated with TEE LA/LAA abnormalities (p=0.02, p=0.005 respectively). In subgroup analysis, it was found that LAVI and septal e’ was statistically significant in the low CHA2DS2-VASc group (p=0.03, p =0.01), but not in the higher CHA2DS2-VASc group (p=0.21, p=0.30).Conclusion: TEE LA/LAA abnormalities were not infrequently noted in those patients traditionally deemed low risk (CHA2DS2-VASc ≤ 1). LAVI and septal e’ on TTE appear to be associated with LA/LAA abnormalities detected on TEE, which was particularly relevant in lower CHA2DS2-VASc patients and may be additive to conventional clinical risk assessment. Further study is needed to evaluate the role of imaging in AF thromboembolic risk stratification, and whether this translates to prognostic and clinical endpoints.

Coronary vasospasm is an uncommon, but perhaps under-recognised, cause of cardiac arrest. We present a novel case of an exercise-induced out-of-hospital cardiac arrest due to coronary vasospasm, captured on a heartrate monitor, and discuss the management options for this condition.

The renin-angiotensin system is involved in control of blood pressure and salt and fluid homeostasis. Genes for components of this system have been of major focus in research on the causation of the common, complex, polygenic trait, essential hypertension (HT). Association of an A-->C variant at nucleotide 1166 of the angiotensin II type 1 receptor (AT(1)R) gene with HT, but an absence of linkage of this locus with this disease, has been reported recently. Since cofirmation in a different setting is imperative, we performed a cross-sectional case-control study of the Al166C variant in a well-characterized group of 108 Caucasian HT subjects with a strong family history (two affected parents) and early onset disease. Genotyping was by mismatch polymerase chain reaction/BfrI restriction fragment length polymorphism analysis. Frequency of the C-1166 allele was 0.40 in HTs and 0.29 in normotensives. The difference in genotype (chi(2) = 13, P = 0.0015) and allele (chi(2) = 5.3, P = 0.02) frequencies between the two groups was significant (odds ratio for CC vs AA + AC = 7.3 [95% CI, 1.9-31.9). The present results implicate the AT(1)R gene, or a locus in linkage disequilibrium with the variant tested, in the causation of essential HT.

Purpose To define intramyocardial triglyceride (TG), creatine (Cr), and choline (Cho) in healthy volunteers, and determine the feasibilities, scan durations and agreements between cardiac proton magnetic resonance spectroscopy ([1H]-MRS) performed with fewer signal averages versus a reference standard with 128 signal averages. Materials and methods Thirty-one participants underwent [1H]-MRS using 16, 32, 64, and 128 signal averages. Intramyocardial TG, Cr, or Cho contents relative to water were calculated and expressed as a percentage. Results Mean intramyocardial TG, Cr, and Cho were 1.30 ± 1.13, 0.19 ± 0.18, and 0.24 ± 0.28%, respectively. The feasibilities for quantifying intramyocardial TG, Cr, and Cho using fewer signal averages ranged from 93.5 to 100, 90.3 to 93.5, and 90.3 to 96.8%, respectively. Scan durations for 16, 32, 64, and 128 signal averages were 1.1 ± 0.5, 2.6 ± 0.9, 5.9 ± 2.0, and 13.2 ± 4.5 min, respectively (p

Susceptibility to the autoimmune disease type 1 diabetes has been linked to human chromosome 6q27 and, moreover, recently associated with one of the genes in the region, TATA box-binding protein (TBP). Using a much larger sample of T1D families than those studied by others, and by extensive re-sequencing of nine other genes in the proximity, in which we identified 279 polymorphisms, 83 of which were genotyped in up to 725 T1D multiplex and simplex families, we obtained no evidence for association of the TBP CAG/CAA (glutamine) microsatellite repeat sequence with disease, or for nine other genes, PDCD2, PSMB1, KIAA1838, DLL1, dJ894D12.4, FLJ25454, FLJ13162, FLJ11152, PHF10 and CCR6. This study also provides an exon-based tag single nucleotide polymorphism map for these 10 genes that can be used for analysis of other diseases.

We report here the results of the GENIHUSS study (GENetic Investigation of Hypertension Undertaken in Sydney Sibships)-a genome-wide scan to identify loci linked to essential hypertension (HT). Subjects were Anglo-Celtic Australian sibpairs resident in or near Sydney, Australia, with onset of HT before age 60 years (mean, 44 +/- 13 SD years). A 10-cM scan involving 400 microsatellite markers and 252 HT sibpairs was followed by fine mapping of the most promising locus using 296 HT sibpairs (481 individuals from 200 families). Multipoint and two-point nonparametric linkage analyses were performed using MAPMAKER/SIBS, GENEHUNTER II, and SPLINK. Suggestive loci were found on chromosomes 1 (4 cM) and 4 (129 cM). The chromosome 4 locus coincided with a QTL for systolic blood pressure (BP) in the Australian Victorian Family Heart Study, and the locus on chromosome 1 contains the chloride channel gene CLCNKB and tumor necrosis factor receptor 2 gene TNFRSF1B, which have each shown association with HT. Our study adds to findings of HT loci emanating from genome scans.

To fully understand the allelic variation that underlies common diseases, complete genome sequencing for many individuals with and without disease is required. This is still not technically feasible. However, recently it has become possible to carry out partial surveys of the genome by genotyping large numbers of common SNPs in genome-wide association studies. Here, we outline the main factors - including models of the allelic architecture of common diseases, sample size, map density and sample-collection biases - that need to be taken into account in order to optimize the cost efficiency of identifying genuine disease-susceptibility loci.

β 2 -Adrenergic receptor gene and neuropeptide Y gene may potentially influence lipid metabolism and overall energy balance. Therefore, we examined associations of these genes with lipid fractions and obesity-related phenotypes in hypertensive subjects. A total of 638 white individuals from 212 Polish families with clustering of essential hypertension were phenotyped for cardiovascular risk determinants. Each subject was genotyped for functional polymorphisms of β 2 -adrenergic receptor gene (Arg16Gly and Gln27Glu) and neuropeptide Y (Leu7Pro). Of 3 common haplotypes of β 2 -adrenergic receptor gene, Arg16Gln27 was overtransmitted to offspring with elevated levels of total cholesterol ( Z =2.2; P =0.026) and LDL-cholesterol ( Z =3.2; P =0.002). Individually, Leu7Pro was not associated with any of the metabolic phenotypes in family-based tests or case-control analyses. However, in the presence of Arg allele of Arg16Gly and Gln allele of Gln27Glu, homozygosity for Leu variant of the Leu7Pro polymorphism was associated with 2.1-increased odds ratio (confidence interval, 1.10 to 3.81; P =0.024) of elevated LDL in hypertensive subjects, independent of age, gender, body mass index, adjusted blood pressures, antihypertensive therapy, and use of nonselective β-blockers and diuretics. Consistently, there was a significant multilocus association among variants of Arg16Gly, Gln27Glu, and Leu7Pro in hypertensive probands with elevated LDL (cases; P =0.028) but not in hypertensive subjects with normal LDL (controls). This study revealed an association of LDL-cholesterol with β 2 -adrenergic receptor gene haplotype and provided evidence for epistatic interaction between β 2 -adrenergic receptor gene and neuropeptide Y gene in determination of LDL-cholesterol in patients with essential hypertension.

Recent intriguing findings from genetic linkage, knockout, and physiologic studies in mice and rats led us to conduct the first investigation of the novel angiotensin-converting enzyme 2 gene (ACE2) in human hypertension (HT). We genotyped four single nucleotide polymorphisms (SNP) (A-->G at nucleotide 1075 in intron 1, G-->A at nucleotide 8790 in intron 3, C-->G at nucleotide 28330 in intron 11, and G-->C at nucleotide 36787 in intron 16) in HT (n = 152) and normotensive (NT, n = 193) groups having inherently high biological power (>80%) due to our inclusion only of subjects whose parents had the same BP status as themselves. The SNPs were in linkage disequilibrium (D' = 54% to 100%, P =.05 to 0.0001). Because ACE2 is on the X chromosome, data for each sex were analyzed separately. Minor allele frequencies in HT versus NT were as follows: for the intron 1 variant 0.21 versus 0.17 in female subjects (P =.31) and 0.25 versus 0.29 in male subjects (P =.60); intron 3 variant 0.22 versus 0.18 in female subjects (P =.35) and 0.15 versus 0.20 in male subjects (P =.47); intron 11 variant 0.39 versus 0.46 in male subjects (P = 0.17) and 0.31 versus 0.30 in male subjects (P =.96); intron 16 variant 0.20 versus 0.19 in female subjects (P =.72) and 0.17 versus 0.17 in male subjects (P =.95). Haplotype analysis was also negative. These data provide little support for ACE2 in genetic predisposition to HT.

To perform association studies of polymorphisms of the potential candidate essential hypertension (HT) genes GRK4, PTP1B and HSD3B1.Subjects consisted of 168 unrelated, Caucasian essential hypertensive (HT) patients and 312 normotensive (NT) controls. Biological power was increased by ensuring subjects in each group had parents with the same blood pressure (BP) status as theirs. Three GRK4gamma variants (R65L, A142V and A486V), one HSD3B1 variant (T---C Leu) and one PTP1B variant (1484insG) were genotyped by polymerase chain reaction and restriction enzyme digestion or by homogenous MassEXTEND Assay.The V allele of the A486V variant of GRK4gamma, but not the R65L or A142V variants, showed an association with HT (P = 0.02). The V allele was also associated with an elevation in systolic blood pressure (SBP) (P = 0.002). Although the L65 and the V142 alleles tracked with elevation in diastolic (DBP), this was seen only in male HTs (P = 0.009; P = 0.002, respectively). Haplotype frequencies differed between the HT and NT groups, particularly for the R, V, V haplotype combination of R65L, A142V and A486V, respectively. Neither of the HSD3B1 or PTP1B variants were associated with HT.Genetic variation in GRK4gamma was associated with HT in the subjects studied.

Large-scale discovery and validation of single-nucleotide polymorphisms (SNPs) facilitates indirect association mapping. It has recently been estimated that, in Europeans, 77% of all SNPs with frequency of 10% or more could be ascertained through linkage disequilibrium (LD) by genotyping variants in the database dbSNP. Using a sampling approach from 73 genes with near complete SNP maps, we show here the usefulness of SNP maps at different densities and the large variability of SNP coverage in different genomic regions. While even sparse SNP maps are of some value to genetic mapping, in order to undertake disease association studies providing at least 80% of SNPs in 90% of genes, much denser maps need to be constructed, at more than one SNP per kb in some regions.

The CYP11B2 locus is an important candidate region in essential hypertension (HT). We therefore investigated CYP11B2 polymorphisms T-344C, T4986C and A6547G for association with essential HT. This included haplotype analysis and measurement of plasma aldosterone levels.The three single nucleotide polymorphisms were genotyped by polymerase chain reaction-restriction fragment length polymorphism analysis of genomic DNA from 146 HT and 291 normotensive (NT) white subjects of Anglo-Celtic descent, in whom parental blood pressure status was the same as the subjects'. Genotype and allele frequencies in HTs and NTs were compared by chi2 analysis. Linkage disequilibrium and haplotype frequencies were estimated by the program 'snphap'. Phenotype-genotype relationships were tested using one-way analysis of variance.The T-344C variant was associated with HT (chi2 = 7.4, P = 0.0064). This association was confined to female HTs (P = 0.0061 for genotypes, P = 0.0013 for alleles). A strong association with HT was also seen for the A6547G variant (P = 0.0015), being greatest in females (P0.0001). No association was seen for the T4986C variant. Haplotype analysis of the three single nucleotide polymorphisms across eight different haplotype combinations showed a significant association with HT (chi2 = 24, seven degrees of freedom, P0.001). No significant tracking of plasma aldosterone with genotype was observed.The T-344C and A6547G, but not the T4986C, variants of the aldosterone synthase gene are associated with HT in females of the Anglo-Celtic population studied. This was reinforced by haplotype analysis.

Patterns of linkage disequilibrium (LD) in the human genome are beginning to be characterized, with a paucity of haplotype diversity in “LD blocks,” interspersed by apparent “hot spots” of recombination. Previously, we cloned and physically characterized thelow-density lipoprotein-receptor-related protein 5(LRP5) gene. Here, we have extensively analysed bothLRP5 and its flanking three genes, spanning 269 kb, for single nucleotide polymorphisms (SNPs), and we present a comprehensive SNP map comprising 95 polymorphisms. Analysis revealed high levels of recombination across LRP5, including a hot-spot region from intron 1 to intron 7 of LRP5, where there are 109 recombinants/Mb (4882 meioses), in contrast to flanking regions of 14.6 recombinants/Mb. This region of high recombination could be delineated into three to four hot spots, one within a 601-bp interval. ForLRP5, three haplotype blocks were identified, flanked by the hot spots. Each LD block comprised over 80% common haplotypes, concurring with a previous study of 14 genes that showed that common haplotypes account for at least 80% of all haplotypes. The identification of hot spots in between these LD blocks provides additional evidence that LD blocks are separated by areas of higher recombination.[Supplementary material: primers are available from our Web site:http://www-gene.cimr.cam.ac.uk/todd/human_data.shtml.]

Bactrocera tryoni (Froggatt) and B. neohumeralis (Hardy) (Diptera: Tephritidae) are sympatric species which hybridise readily in the laboratory yet remain distinct in the field. B. tryoni mates only at dusk and B. neohumeralis mates only during the day, but hybrids can mate at both times. We investigated the inheritance of mating time in successively backcrossed hybrid stocks to establish whether mating with either species is more likely. The progeny of all backcrosses to B. tryoni mated only at dusk. The majority of the progeny of the first and a minority of the progeny of the second backcross to B. neohumeralis also mated at dusk, but the third successive B. neohumeralis backcross produced flies that mated only during the day. This trend towards dominance of the B. tryoni trait was also reflected in a diagnostic morphological character. We discuss the possible genetic background for these phenomena and propose that unidirectional gene flow might explain how the two species remain distinct in the face of natural hybridisation.