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ObjectiveTo assess the frequency and predictors of unplanned readmissions after hospitalisation for incident atrial fibrillation (AF) and the association of readmissions with mortality over 2 years.MethodsWe performed a retrospective cohort study using Western Australian morbidity and mortality data to identify all patients, aged 25–94 years, who survived incident (first-ever) hospitalisation for AF (principal diagnosis), between 2001 and 2015. Ordinal logistic models determined the covariates independently associated with unplanned readmission(s), and Cox proportional hazards models with time-varying exposures determined the hazard ratios (HR) of one or more readmissions for mortality over 2 years after incident AF.ResultsOf 22 956 patients, 57.7% male, mean age 67.9 (SD 13.8) years, 44.0% experienced 22 053 unplanned readmissions within 2 years, 50.6% being cardiovascular-related. All-cause death occurred in 8.0% of the cohort, and the multivariable-adjusted mortality HR of 1 (vs 0) readmission was 2.9 (95% CI 2.6 to 3.3), increasing to 5.6 (95% CI 5.0 to 6.5) for 3+ readmissions. First emergent readmission for AF, stroke, heart failure or myocardial infarction was independently associated with an increased hazard for mortality. Coexistent cardiovascular and other comorbidities were independently associated with increased readmission and mortality risk, whereas AF ablation was associated with reduced risk.ConclusionThis study highlights the large burden of unplanned all-cause and cardiovascular-specific readmissions within 2 years after being hospitalised for incident AF and their associated adverse impact on mortality. Concomitant comorbidities are independently associated with unplanned hospitalisations and mortality, which supports integrated multidisciplinary management of comorbidities, along with AF-targeted treatments, to improve long-term outcomes in patients with AF.

ObjectivesTo generate contemporary age-specific mortality rates for Indigenous and non-Indigenous Australians aged <65 years who died from rheumatic heart disease (RHD) between 2013 and 2017, and to ascertain the underlying causes of death (COD) of a prevalent RHD cohort aged <65 years who died during the same period.MethodsFor this retrospective, cross-sectional epidemiological study, Australian RHD deaths for 2013–2017 were investigated by first, mortality rates generated using Australian Bureau of Statistics death registrations where RHD was a coded COD, and second COD analyses of death records for a prevalent RHD cohort identified from RHD register and hospitalisations. All analyses were undertaken by Indigenous status and age group (0–24, 25–44, 45–64 years).ResultsAge-specific RHD mortality rates per 100 000 were 0.32, 2.63 and 7.41 among Indigenous 0–24, 25–44 and 45–64 year olds, respectively, and the age-standardised mortality ratio (Indigenous vs non-Indigenous 0–64 year olds) was 14.0. Within the prevalent cohort who died (n=726), RHD was the underlying COD in 15.0% of all deaths, increasing to 24.6% when RHD was included as associated COD. However, other cardiovascular and non-cardiovascular conditions were the underlying COD in 34% and 43% respectively.ConclusionPremature mortality in people with RHD aged <65 years has approximately halved in Australia since 1997–2005, most notably among younger Indigenous people. Mortality rates based solely on underlying COD potentially underestimates true RHD mortality burden. Further strategies are required to reduce the high Indigenous to non-Indigenous mortality rate disparity, in addition to optimising major comorbidities that contribute to non-RHD mortality.

The healthcare burden of atrial fibrillation (AF) is dominated by hospitalizations, but data on 30-day unplanned readmissions after AF hospitalization and impact on mortality are limited.

A study shows that antiplatelet therapy, mainly with aspirin is effective in reducing the risk of non-fatal myocardial infarction, non-fatal stroke or vascular death among patients with established arterial disease. The definite and possible indications for aspirin prophylaxis based on the clinical trial evidence, when used for secondary prevention, primary prevention and in heart disease are discussed.

Abstract Objective To test the hypothesis that the incidence of fatal coronary heart disease and cardiovascular disease in a general population is related to serum and red cell folate and [...]

Byline: Marcus K. Ilton, Paul E. Langton, Marcia L. Taylor, Neil L.A. Misso, Mark Newman, Philip J. Thompson, Joseph Hung Abstract: Background: Activation of neutrophil adhesion molecules and subsequent neutrophil adhesion to vascular endothelium are key events initiating inflammatory organ dysfunction after cardiopulmonary bypass and ischemic reperfusion. Objectives: We sought to characterize neutrophil integrin CD11b and L-selectin activation associated with coronary artery bypass graft surgery and to determine whether neutrophil activation contributes to their sequestration on postbypass reperfusion. Methods: Twenty patients undergoing routine coronary artery bypass were studied. Heparinized whole blood was simultaneously sampled from a central venous line, aorta, coronary sinus, and right and left atrium before, during, and up to 20 minutes after cardiopulmonary bypass. Neutrophil counts were obtained, and neutrophil CD11b and L-selectin expression was determined by flow cytometric analysis in whole blood. Results: CD11b expression on circulating neutrophils increased during cardiopulmonary bypass, peaking at 145% of baseline level after release of the aortic clamp and then declined by 20 minutes after bypass (analysis of variance, P = .003). No change in neutrophil L-selectin expression was observed during cardiopulmonary bypass. Neutrophils responded to ex vivo stimulation by C5a and leukotriene B.sub.4 during cardiopulmonary bypass but not at 24 hours after the operation. After reperfusion, neutrophil loss, but not local activation, was demonstrated in the coronary and pulmonary circulations. Conclusions: Upregulated CD11b expression on neutrophils is likely to contribute to neutrophil sequestration in the heart and lungs after bypass, but neutrophil activation may be limited by their reduced responsiveness to agonist stimulation. CD11b represents a potential therapeutic target for diminishing inflammation after cardiac operations. (J Thorac Cardiovasc Surg 1999;118: 930-7) Author Affiliation: From the Department of Medicine,.sup.a University of Western Australia, the Department of Cardiovascular Medicine,.sup.b Sir Charles Gairdner Hospital (M.K.I., P.E.L., J.H.), and the Department of Cardiothoracic Surgery,.sup.c Sir Charles Gairdner Hospital, Perth, Western Australia Article History: Received 19 April 1999; Revised 12 July 1999; Revised 4 August 1999; Accepted 11 August 1999 Article Note: (footnote) [star] Supported by grants from the R. F. Shaw Foundation; Sir Charles Gairdner Hospital, Perth, Western Australia; and the Raine Medical Research Foundation, the University of Western Australia., [star][star] Address for reprints: Joseph Hung, FRACP, Associate Professor, University Department of Medicine, Sir Charles Gairdner Hospital, Nedlands, WA 6009 Australia., a 0022-5223/99 $8.00 + 0 12/1/102088

ObjectiveTo determine the incidence, risk predictors and relative mortality risk of incident heart failure (HF) in patients following atrial fibrillation (AF) hospitalisation.MethodsThe Western Australian Hospitalisation Morbidity Data Collection was used to identify patients aged 25–94 years with index (first-in-period) AF hospitalisation, but without a prior HF admission, between 2000 and 2013. We evaluated the risk of incident HF hospitalisation within 3 years after AF admission, and the impact of HF hospitalisation on all-cause mortality.ResultsThe cohort comprised 52 447 patients, 57.5% men, with a median age of 73.1 (IQR 63.2-80.8) years. At 3 years after AF discharge, the cumulative incidence of HF (n=6153) was 11.7% (95% CI 11.5% to 12.0%) and all-cause death (n=9702) was 18.5% (95% CI 18.2% to 18.8%). Independent predictors of incident HF included advancing age, any history of myocardial infarction (MI), peripheral vascular disease, valvular heart disease, chronic kidney disease, chronic obstructive pulmonary disease, hypertension, diabetes, obesity and excessive alcohol use (all p<0.001). Patients hospitalised for first-ever HF compared with those without HF hospitalisation had an adjusted HR of 3.3 (95% CI 3.1 to 3.4) for all-cause mortality (p<0.001). Independent predictors of HF were also shared with those for mortality, with the exception of hypertension.ConclusionHospitalisation for new HF is common in patients with AF and independently associated with a 3-fold hazard for death. The clinical predictors of incident HF emphasise the importance of integrated management of common comorbid conditions and lifestyle risk factors in patients with AF to reduce their morbidity and mortality.

CVD is the leading cause of death worldwide, and genetic investigations into the human lipidome may provide insight into CVD risk. The aim of this study was to estimate the heritability of circulating lipid species and their genetic correlation with CVD traits. Targeted lipidomic profiling was performed on 4,492 participants from the Busselton Family Heart Study to quantify the major fatty acids of 596 lipid species from 33 classes. We estimated narrow-sense heritabilities of lipid species/classes and their genetic correlations with eight CVD traits: BMI, HDL-C, LDL-C, triglycerides, total cholesterol, waist-hip ratio, systolic blood pressure, and diastolic blood pressure. We report heritabilities and genetic correlations of new lipid species/subclasses, including acylcarnitine (AC), ubiquinone, sulfatide, and oxidized cholesteryl esters. Over 99% of lipid species were significantly heritable (h2: 0.06–0.50) and all lipid classes were significantly heritable (h2: 0.14–0.50). The monohexosylceramide and AC classes had the highest median heritabilities (h2= 0.43). The largest genetic correlation was between clinical triglycerides and total diacylglycerol (rg= 0.88). We observed novel positive genetic correlations between clinical triglycerides and phosphatidylglycerol species (rg: 0.64–0.82), and HDL-C and alkenylphosphatidylcholine species (rg: 0.45–0.74). Overall, 51% of the 4,768 lipid species-CVD trait genetic correlations were statistically significant after correction for multiple comparisons. This is the largest lipidomic study to address the heritability of lipids and their genetic correlation with CVD traits. Future work includes identifying putative causal genetic variants for lipid species and CVD using genome-wide SNP and whole-genome sequencing data.

To assess the risks of stroke and cardiovascular mortality for Aboriginal and non‐Aboriginal Australians with atrial fibrillation. Retrospective data linkage cohort study. All people aged 20–84 years hospitalised with atrial fibrillation in Western Australia during 2000–2012. Stroke incidence rates and mortality after hospitalisation for atrial fibrillation, and 10‐year risks of stroke and of cardiovascular and all‐cause mortality. Among 55 482 index admissions with atrial fibrillation, 7.7% of 20–59‐year‐old patients and 1.3% of 60–84‐year‐old patients were Aboriginal Australians. A larger proportion of Aboriginal patients aged 20–59 years had CHA2DS2‐VASc scores of 2 or more (59.8% v21.8%). In 20–59‐year‐old Aboriginal patients, the incidence during follow‐up (maximum, 10 years; median, 7.1 years) of stroke (incidence rate ratio [IRR], 3.2; 95% CI, 2.5–4.1) and fatal stroke (IRR, 5.7; 95% CI, 3.9–8.9) were markedly higher than for non‐Aboriginal patients. Stroke incidence was higher for 60–84‐year‐old patients, but the difference between Aboriginal and non‐Aboriginal patients was smaller (IRR, 1.6; 95% CI, 1.3–2.0). Cardiovascular mortality during follow‐up was also higher for 20–59‐year‐old Aboriginal patients (IRR, 4.4; 95% CI, 4.3–5.9). The hazards of stroke (adjusted HR[aHR], 1.67; 95% CI, 1.22–2.28) and cardiovascular mortality (aHR, 1.47; 95% CI, 1.18–1.83) in younger Aboriginal patients remained significantly higher after multivariable adjustment; age/sex, principal diagnosis of atrial fibrillation, and CHA2DS2‐VASc score were the most influential factors. Stroke risk and cardiovascular mortality are markedly higher for Aboriginal than non‐Aboriginal patients with atrial fibrillation, particularly for patients under 60. Strategies for providing evidence‐based therapies and cardiovascular prevention to Aboriginal people with atrial fibrillation must be improved.

A study was conducted to assess if a collaborative interdepartmental pathway involving emergency department (ED) physicians activating the cardiac catheterisation laboratory (CCL) with immediate patient transfer to the CCL reduces door-to-balloon (DTB) times for patients with suspected ST-elevation myocardial infarction (STEMI). ED physician activation of CCL with immediate patient transfer was observed to be associated with highly significant improvements in DTB time without increased false positive rates.

A retrospective study investigates the effect of evidence-based medication use on long-term survival in patients hospitalized for heart failure (HF) in Western Australia. Results indicate that evidence-based medication such as angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers (ARBs) and beta-blockers prescribed on discharge after the first hospitalization for HF improve long-term survival of patients.

A study uses data from the Acute Coronary Syndrome Prospective Audit (ACACIA) registry to investigate treatment disparities and effect on late mortality outcomes in patients with and without diabetes presenting with acute myocardial infarction (MI). Analysis reveals that patients with diabetes presenting with acute myocardial infarction have a higher risk of late mortality following an acute MI than non-diabetic patients, but receive fewer evidence-based pharmacological and early invasive treatments.

To examine the effectiveness of different strategies for recruiting participants for a large Australian randomised controlled trial (RCT), the Australian Study for the Prevention through Immunisation of Cardiovascular Events (AUSPICE). Men and women aged 55–60 years with at least two cardiovascular risk factors (hypertension, hypercholesterolaemia, overweight/obesity) were recruited for a multicentre placebo‐controlled RCTassessing the effectiveness of 23‐valent pneumococcal polysaccharide vaccine (23vPPV) for preventing cardiovascular events. Invitations were mailed by the Australian Department of Human Services to people in the Medicare database aged 55–60 years; reminders were sent 2 weeks later. Invitees could respond in hard copy or electronically. Direct recruitment was supplemented by asking invitees to extend the invitation to friends and family (snowball sampling) and by Facebook advertising. Proportions of invitees completing screening questionnaire and recruited for participation in the RCT. 21 526 of 154 992 invited people (14%) responded by completing the screening questionnaire, of whom 4725 people were eligible and recruited for the study. Despite the minimal study burden (one questionnaire, one clinic visit), the overall participation rate was 3%, or an estimated 10% of eligible persons. Only 16% of eventual participants had responded within 2 weeks of the initial invitation letter (early responders); early and late responders did not differ in their demographic or medical characteristics. Socio‐economic disadvantage did not markedly influence response rates. Facebook advertising and snowball sampling did not increase recruitment. Trial participation rates are low, and multiple concurrent methods are needed to maximise recruitment. Social media strategies may not be successful in older age groups. Australian New Zealand Clinical Trials Registry, ACTRN12615000536561.

Introduction:Atrial fibrillation (AF) is increasing in prevalence and is associated with significant morbidity and mortality. The optimal diagnostic and treatment strategies for AF are continually evolving and care for patients requires confidence in integrating these new developments into practice. These clinical practice guidelines will assist Australian practitioners in the diagnosis and management of adult patients with AF. Main recommendations:These guidelines provide advice on the standardised assessment and management of patients with atrial fibrillation regarding: screening, prevention and diagnostic work-up;acute and chronic arrhythmia management with antiarrhythmic therapy and percutaneous and surgical ablative therapies;stroke prevention and optimal use of anticoagulants; andintegrated multidisciplinary care. Changes in management as a result of the guideline: Opportunistic screening in the clinic or community is recommended for patients over 65 years of age.The importance of deciding between a rate and rhythm control strategy at the time of diagnosis and periodically thereafter is highlighted. ß-Blockers or non-dihydropyridine calcium channel antagonists remain the first line choice for acute and chronic rate control. Cardioversion remains first line choice for acute rhythm control when clinically indicated. Flecainide is preferable to amiodarone for acute and chronic rhythm control. Failure of rate or rhythm control should prompt consideration of percutaneous or surgical ablation.The sexless CHA2DS2-VA score is recommended to assess stroke risk, which standardises thresholds across men and women; anticoagulation is not recommended for a score of 0, and is recommended for a score of = 2. If anticoagulation is indicated, non-vitamin K oral anticoagulants are recommended in preference to warfarin.An integrated care approach should be adopted, delivered by multidisciplinary teams, including patient education and the use of eHealth tools and resources where available. Regular monitoring and feedback of risk factor control, treatment adherence and persistence should occur.

Background Temporal trends in incidence and mortality of cardiovascular disease (CVD) have been well described, with recent data suggesting declining improvements in those aged under 55 years. However, little is known about the combined impact of incidence and mortality trends on disease prevalence, an important indicator of disease burden and cost. We analysed changes in age-specific and age-standardised temporal trends in prevalence and incidence of CVD subtypes.Methods Annual prevalence and incidence rates of coronary heart disease, cerebrovascular disease and peripheral arterial disease for the Western Australian population for 1995–2010 were calculated using data from the Western Australian Data Linkage System. Joinpoint regression analyses were used to identify joinpoints in trends in age-specific and age-standardised annual prevalence and incidence rates for each CVD subtype.Results Between 1995 and 2010, age- and sex-specific incidence and prevalence of the CVD subtypes generally decreased among middle-aged and older adults, but were stable or increased among younger adults. In < 55 year olds, increases in incidence tended to occur from 2003, while increases in prevalence were from 2007/2008. Declines in age-standardised incidence were greater than those in crude incidence, with changes in population structure having a greater impact among men than women.Conclusions The majority of CVDs occurs in older adults. Our findings of generally worsening trends in prevalence in younger adults across most CVD subtypes were in contrast to generally declining trends in older age groups. These data highlight the importance of monitoring prevalence and incidence, particularly in younger adults.

ObjectiveHigh-sensitivity cardiac troponin I (hs-cTnI) is an emerging biomarker for cardiovascular risk. We examined hs-cTnI as a predictor of mortality and cardiovascular outcomes in an Australian population-based cohort and evaluated if a sex difference exists.MethodsSerum hs-cTnI was measured in the Busselton Health Study 1994/1995 Cohort (n=3939). Outcome measures were total and cardiovascular mortality, cardiovascular disease (CVD) and coronary heart disease (CHD) events, heart failure and stroke.ResultsHs-cTnI was detectable (>1.2 ng/L) in 66.1% of participants (males 81.8%, females 54.4%) at baseline. There were 886 deaths (including 361 from CVD) and 940 CVD events during 20-year follow-up. Adjusting for Framingham Risk Score variables, hs-cTnI was a significant predictor of total mortality (HR (95% CI): 1.16 (1.09 to 1.24)), CVD mortality (1.33 (1.23 to 1.44)), CVD events (1.18 (1.11 to 1.25)), CHD events (1.11 (1.03 to 1.20)), heart failure (1.44 (1.31 to 1.58)) and stroke (1.13 (1.03 to 1.24)) per doubling of hs-cTnI at baseline. HRs remained significant in CVD-free individuals at baseline (n=3215), except for CHD events. There were no significant interactions between sex and hs-cTnI as a predictor of outcomes. Compared with individuals with hs-cTnI ≤1.2 ng/L, men with hs-cTnI ≥6.0 ng/L and women with hs-cTnI ≥4.0 ng/L had an HR of 2.18 (1.42 to 3.37) and 1.84 (1.30 to 2.62), respectively, for any CVD event, which persisted in the CVD-free subgroup.ConclusionsCardiac troponin I, measured with a high-sensitive assay, is an independent predictor of fatal and non-fatal CVD events and may help identify at-risk individuals in a general population.

The Women's Health Study carried out a study confined to healthy women aged 45 years or older where aspirin prophylaxis did not lower the risk of a first major cardiovascular event the primary endpoint. However, it did significantly reduce the risk of all strokes by 17%, and ischaemic stroke by 24%, without affecting the risk of myocardial infarction or cardiovascular death.

Rheumatic heart disease (RHD) comprises heart-valve damage caused by acute rheumatic fever (ARF). The Australian Government Rheumatic Fever Strategy funds RHD Control Programs to support detection and management of ARF and RHD. We assessed epidemiological changes during the years of RHD Control Program operation.

Describe the dispensing patterns for guideline‐recommended medications during 2008 in people with acute coronary syndrome (ACS) and how dispensing varies by gender and time since last ACS hospitalization. A descriptive cohort spanning 20 years of people alive post‐ACS in 2008. We extracted all ACS hospitalizations and deaths in Western Australia (1989–2008), and all person‐linked Pharmaceutical Benefits Scheme claims nationally for 2008. Participants were 23 642 men and women (36.8%), alive and aged 65–89 years in mid‐2008 who were hospitalized for ACS between 1989 and 2008. Main outcome was the proportion of the study cohort (in 2008) dispensed guideline‐recommended cardiovascular medications in that year. Adjusted odds ratios estimating the association between type (and number) of guideline‐recommended medications and time since last ACS hospitalization. Medications most commonly dispensed in 2008 were statins (79.6% of study cohort) and then angiotensin‐converting enzyme inhibitors or angiotensin‐receptor blockers (ACEi/ARBs) (71.1%), aspirin or clopidogrel (59.4%), and β‐blockers (54.6%). Only 51.8% of the cohort was dispensed three or more of these drug types in 2008. Women with ACS were 18% less likely to be dispensed statins (adjusted odds ratio (OR)=0.82; 95% CI 0.76–0.88). Overall, for each incremental year since last ACS admission, there was an 8% increased odds (adjusted OR=1.08; 95% CI 1.07–1.08) of being dispensed fewer of the recommended drug regimen in 2008. Longer time since last ACS admission was associated with dispensing fewer medications types and combinations in 2008. Interventions are warranted to improve dispensing long term and any apparent gender inequality in the drug class filled.

Background Long-term mortality following myocardial infarction is higher in diabetic than non-diabetic individuals. Early case-fatality after myocardial infarction has improved but it is unclear whether trends extend to long-term mortality. We aimed to determine whether the disparity in long-term all-cause and cardiovascular disease mortality by diabetes status has decreased.Methods All incident myocardial infarction cases were identified from Western Australian whole-population linked data for 1998–2009. Mortality follow-up was available until 30 June 2011. Unadjusted survival was estimated using Kaplan–Meier survival curves. Hazard ratios comparing five-year mortality in diabetic versus non-diabetic people across three periods (1998–2001, 2002–2005, 2006–2009) were estimated from multivariable Cox regression models, and adjusted trends calculated from interaction (diabetes status × period) models.Results There were 22,594 30-day survivors of incident MI. There was little change across the three periods in all-cause mortality in diabetic men (27.1%, 28.2%, 25.5%) and women (34.9%, 36.8%, 36.1%), but small declines from first to last periods in non-diabetic men (14.5% to 12.1%, p= 0.03) and women (21.0% to 19.4%, p= 0.08). There was no temporal change in the increased all-cause mortality hazard ratios in diabetic versus non-diabetic men and women. Multivariable-adjusted relative risk for cardiovascular disease mortality remained elevated in diabetic women (2006–2009 hazard ratio 1.73, 95% confidence interval 1.29, 2.32) but not in men (2006–2009 hazard ratio 1.08, 95% confidence interval 0.85, 1.37).Conclusions The excess long-term mortality associated with diabetes and excess cardiovascular disease mortality in diabetic women indicates a need for improved secondary prevention in diabetic patients, especially women.

Context:Advancing age is accompanied by an accumulation of ill health and shortening of chromosomal telomeres signifying biological aging. T is metabolized to DHT by 5α-reductase (SRD5A2) and to estradiol (E2) by aromatase (CYP19A1). Telomerase preserves telomeres, and T and E2 regulate telomerase expression and activity in vitro.Objective:The objective of the study was to establish whether circulating T or its metabolites, DHT or E2, and single-nucleotide polymorphisms in SRD5A2 or CYP19A1 associate with leucocyte telomere length (LTL) in men.Participants and Methods:Early-morning serum T, DHT, and E2 were assayed using mass spectrometry, and SRD5A2 and CYP19A1 single-nucleotide polymorphisms and LTL analyzed by PCR in 980 men from the Western Australian Busselton Health Survey who participated in the study. LTL was expressed as the T/S ratio.Results:Men were aged (mean ± SD) 53.7 ± 15.6 years. LTL decreased linearly with age, from the T/S ratio of 1.89 ± 0.41 at younger than 30 years to 1.50 ± 0.49 at 70 to younger than 80 years (r = −0.225, P< .0001). After adjustment for age, DHT and E2 were positively correlated with LTL (DHT, r = 0.069, P= .030; E2, r = 0.068, P= .034). The SRD5A2 rs9282858 polymorphism was associated with serum DHT but not with LTL. Three dominant alleles of CYP19A1 were each associated with lower serum E2 and shorter LTL: rs2899470 T (E2, 59.3 vs 68.6 pmol/L, P< .0001; T/S ratio, 1.54 vs 1.62, P= .045), rs10046 C (60.5 vs 68.1 pmol/L, P= .0005, 1.54 vs 1.62, P= .035), and rs700518 A (59.9 vs 68.9 pmol/L, P< .0001, 1.54 vs 1.63, P= .020). A single-copy haplotype C/T/I/A/T rs10046/rs2899470/rs11575899/rs700518/rs17703883 (52% prevalence) was associated with both lower E2 and shorter LTL.Conclusions:In men, serum DHT and E2 correlate with LTL independently of age. Aromatase gene polymorphisms include three dominant alleles that are associated with both lower serum E2 and shorter LTL. E2 influences telomere length in vivo, thus warranting further studies to examine whether hormonal interventions might slow biological aging in men.

OSA is a common condition that has been associated with atrial fibrillation (AF), but there is a paucity of data from large longitudinal cohorts to establish whether OSA is a risk factor for AF independent of obesity and other established risk factors.

The risk of myocardial infarction (MI) is elevated in people with diabetes mellitus (DM) compared with non-DM counterparts. The aim of this study was to compare population trends in the incidence of hospitalized MI and coronary heart disease (CHD) in adults with and without DM.

To examine protocol adherence to structured intensive management in the Valsartan Intensified Primary carE Reduction of Blood Pressure (VIPER-BP) study involving 119 primary care clinics and 1562 randomized participants.

The incidence of myocardial infarction has declined during the past 4 decades in many populations. However, there are limited population data measuring trends in acute coronary syndromes (ACS). We therefore examined temporal trends in the incidence of hospitalized ACS by age and sex in a population-based cohort.

We examined trends in incidence of first-ever (index) hospitalization for heart failure (HF), hospitalization rates, and 30-day and 1-year all-cause mortality subsequent to index hospitalization for HF.

BackgroundTo investigate the prognostic importance of the metabolic syndrome (MetS) on incident cardiovascular disease (CVD).DesignProspective cohort study.MethodsThe study was based on 10-year follow-up of 3041 men and women aged 25-84 years without CVD or diabetes who participated in the 1994/1995 Busselton Health Survey. Hazards ratio (HRs) from Cox regression models were used to describe the effect of the MetS as a dichotomous classification and as the number of risk components on incident coronary heart disease (CHD), stroke and all CVD events.ResultsAll cardiovascular and metabolic risk factors studied showed a strong association with the number of MetS risk components. The age-adjusted and sex-adjusted HR for the MetS was 1.70 (95% confidence interval: 1.15-2.51) for incident CHD but this was reduced to almost unity after adjustment for cardiovascular risk factors or the homoeostasis model assessment measure of insulin resistance. However, the number of MetS risk components remained significant (P < 0.01) with those having 3+ risk components with a three-fold increase in risk compared with those with no risk components (adjusted HR: 3.59, 95% confidence interval: 1.43-8.99).ConclusionConsideration of the number of MetS risk components seems to be more informative than the (dichotomous) MetS classification when determining risk in clinical practice. Identification of people without any MetS risk components is clinically valuable, as these people seem to have a substantially reduced risk of developing CHD. Eur J Cardiovasc Prev Rehabil 16:235-241 © 2009 The European Society of Cardiology

To test the effectiveness of a minimal nutrition intervention to increase dietary intake of folate.

To discuss various issues related to the in-process 20-minute endotoxin “limit test” (20-minute bacterial endotoxin test [BET]) per the United Stated Pharmacopeia(USP) general chapter <823>, “Radiopharmaceuticals for Positron Emission Tomography—Compounding.”

In chemical quality control tests for 2-18Ffluoro-2-deoxy-D-glucose (18F-FDG), gel time is inversely related to endotoxin concentration. Solutions for positive product control (PPC) and positive water control (PWC) should contain a highly concentrated endotoxin level. The aims of our study were to derive an endotoxin concentration that causes PPC and PWC to gel and to evaluate inhibitory effects caused by FDG on gel formation in PPC and PWC test solutions.

To modify a commercial xenon gas dispenser so that two xenon unit-dose vials could be combined with a modified dispenser to deliver a recommended dose.

Arterial remodelling contributes to the development of hypertension. Stromelysin-1 (MMP-3), a member of the matrix metalloproteinase family may contribute to this process. Stromelysin-1 gene expression is partly regulated by a common polymorphism in the promoter region of either five or six consecutive adenosine bases (5A/6A).

Objective. To determine the impact of a hospital-coordinated discharge care plan, involving a multidisciplinary team of primary health care providers, on hospital length of stay, quality of life, and both patient and general practitioner inclusion in, and satisfaction with, discharge procedures.Design. This investigation comprised a prospective, randomized, controlled, clinical trial.Setting. This multicentre and cross-jurisdictional study focused on areas of tertiary and primary health care as well as community allied health in Western Australia.Participants. Patients (n = 189) with chronic cardiorespiratory diagnoses were recruited from respiratory, cardiovascular, and general medical wards at two tertiary hospitals.Intervention. Subjects were randomly assigned to one of two groups. Intervention group patients received a discharge care plan in accordance with that outlined in the Australian Enhanced Primary Care Package, completed before discharge and sent to the patient’s general practitioner and other community service providers for review. Control patients were discharged under existing hospital processes.Outcome measures. Patients and general practitioners were surveyed pre-discharge and 7 days post-discharge for quality of life and opinion of discharge procedures. Hospital length of stay was also determined.Results. Significant improvements in discharge planning involvement, health service access, confidence with discharge procedures, and opinion of discharge based on previous experience were seen for patients who received the discharge care plan. Further, improved perceptions of mental quality of life were observed within the first week post-discharge for intervention patients. Length of stay showed no difference between groups. Extent and speed of hospital–general practitioner communication were significantly improved via the intervention.Conclusions. Our results indicate that a multidisciplinary discharge care plan, initiated before separation, improves quality of life, involvement, and satisfaction with discharge care, and hospital–general practitioner integration. As such, it possesses benefits over current Western Australian hospital discharge procedures for the care of chronically ill populations.

Folic acid supplementation lowers total plasma homocysteine (tHcy) and improves endothelial function in individuals with coronary artery disease (CAD) and in those with additional CAD risk factors. In the present study, we assessed whether endothelial function is impaired in healthy subjects with hyperhomocysteinaemia but without other CAD risk factors and whether folic acid supplementation improves endothelial function in these subjects. Flow-mediated dilatation (FMD) of the brachial artery was performed on 26 healthy subjects, age 49±2 years (mean±S.E.M.), with high tHcy (15.6±1.5 µmol/l) and 16 healthy age-matched subjects with low tHcy (7.9±0.6 µmol/l; P<0.001). Subjects with high tHcy were then randomized to receive 5 mg/day of folic acid or placebo for 8 weeks in a double-blind cross-over trial with a 4-week washout. FMD was not associated with tHcy and was not different between high and low tHcy groups (7.0±0.6% compared with 6.6±1.2%, P=0.76). Treatment with folic acid decreased tHcy by 34% in hyperhomocysteinaemic subjects (P=0.02 compared with placebo), but had no effect on FMD (+0.5±0.6% compared with -0.7±0.5%; P=0.17 compared with placebo). In healthy subjects with hyperhomocysteinaemia, but without additional cardiovascular risk, endothelial function is unimpaired and folic acid supplementation has no additional effect.

To identify potential deficiencies in product labeling (package insert) instructions for the preparation of radiopharmaceuticals.

To provide background information related to the development of the Nuclear Pharmacy Compounding Guidelines,to discuss regulatory complexities related to radiopharmaceutical compounding practice, and to summarize the gaps in the current compounding regulations for radiopharmaceuticals.

To develop an in-house preparation method for technetium 99m-labeled human serum albumin (99mTc-HSA) to meet the clinical need for gastrointestinal (GI) protein loss evaluation in our institution.

OBJECTIVES

There is concern over the safety of calcium channel blockers (CCBs) in acute coronary disease. We sought to determine if patients taking calcium channel blockers (CCBs) at the time of admission with acute myocardial infarction (AMI) had a higher case-fatality compared with those taking beta-blockers or neither medication. Clinical and drug treatment variables at the time of hospital admission predictive of survival at 28 days were examined in a community-based registry of patients aged under 65 years admitted to hospital for suspected AMI in Perth, Australia, between 1984 and 1993. Among 7766 patients, 1291 (16.6%) were taking a CCB and 1259 (16.2%) a betablocker alone at hospital admission. Patients taking CCBs had a worse clinical profile than those taking a beta-blocker alone or neither drug (control group), and a higher unadjusted 28-day mortality (17.6% versus 9.3% and 11.1% respectively, both P< 0.001). There was no significant heterogeneity with respect to mortality between nifedipine, diltiazem, or verapamil when used alone, or with a beta-blocker. After adjustment for factors predictive of death at 28 days, patients taking a CCB were found not to have an excess chance of death compared with the control group (odds ratio [OR] 1.06, 95% confidence interval [CI]; 0.87, 1.30), whereas those taking a beta-blocker alone had a lower odds of death (OR 0.75, 95% CI; 0.59, 0.94). These results indicate that established calcium channel blockade is not associated with an excess risk of death following AMI once other differences between patients are taken into account, but neither does it have the survival advantage seen with prior beta-blocker therapy.

To assess commercial macroaggregated albumin (MAA) reagent kits for compliance with particle-size parameters needed for proper clinical evaluation of pulmonary shunts (right-to-left).

To determine whether adenosine could be safely administered to patients with chronic obstructive pulmonary disease (COPD) for coronary vasodilatation during perfusion scintigraphy without causing bronchospasm.

The purpose of this study was to measure the changes and rates of adaptation of left ventricular volumes at the onset of exercise. Eight asymptomatic subjects, in whom intramyocardial markers had been implanted 3–6 years previously during aortocoronary bypass surgery, exercised in the supine position at a constant workload of 73.6 W for 5 min. Six also exercised first at 16.4 W, and then against a workload which progressively increased by 8.2 W every 15s. Cardiac volumes were measured by computer assisted analysis of the motion of the implanted markers. In the constant workload test, cardiac output increased rapidly from 5.7±1 min-1 to 10.3±1.9 1 min-1 by 2 min and then increased more slowly to 10.8±2.0 1 min-1 by 5 min. The cardiac output increase was mainly due to an increase in heart rate from 68±12 beats min-1 to 120±16 beats min-1 with minimal changes in stroke volume. The time constant for the early increase in cardiac output was 45 s and for heart rate, 35 s. With progressively increasing workloads, there was an almost linear increase of heart rate and cardiac output, but these increased at a slower rate than during the early phase of the constant load exercise test. In conclusion: (i) rapid changes in cardiac output during supine exercise were produced by changes in heart rate; (ii) changes in stroke volume provided minor adjustments to cardiac output; (iii) the end-diastolic volume was almost constant.

1. Close contact between platelets and neutrophils modulates their cellular interactions in thrombotic and inflammatory states, with stimulation of P-selectin expression on platelets by agonists such as thrombin and neutrophil-derived cathepsin G being critical in mediating platelet—neutrophil adhesion. This study compared the effects of thrombin and cathepsin G on platelet P-selectin expression and on P-selectin-mediated platelet—neutrophil adhesion. 2. Washed platelets and platelet—neutrophil mixed cell suspensions (platelet/neutrophil ratio, 10:1) were incubated with either the supernatant of activated neutrophils, purified cathepsin G or thrombin. Platelet P-selectin expression and platelet adhesion to neutrophils was quantified by flow fluorocytometric analysis. 3. The supernatant from activated neutrophils stimulated platelet P-selectin expression comparable to that produced by purified cathepsin G or thrombin. P-selectin expression induced by both activated neutrophil supernatant and purified cathepsin G was completely inhibited by α1-antichymotrypsin, a specific inhibitor of cathepsin G. Unlike thrombin, which induced maximum platelet P-selectin expression by 10 min, sustained to 120 min, cathepsin G induced an initial large increase in platelet P-selectin expression, followed by a progressive reduction over 30–60 min to baseline levels. 4. Co-incubation of neutrophils with thrombin-stimulated platelets resulted in a significant increase in P-selectin-mediated platelet—neutrophil adhesion, which was completely inhibited by preincubation of neutrophils with anti-sialyl Lewisx monoclonal antibody. Thrombin produced maximum platelet—neutrophil adhesion by 10 min which remained stable over 120 min. In contrast, cathepsin G-stimulated platelets did not adhere to neutrophils over 120 min of co-incubation. Addition of cathepsin G to thrombin-stimulated platelets caused a progressive reduction over 30–60 min to baseline levels of platelet—neutrophil adhesion. 5. Neutrophil-derived cathepsin G is a potent platelet activator, but unlike thrombin it causes a time-dependent loss of platelet P-selectin expression and inhibits P-selectin-mediated platelet—neutrophil adhesion. Therefore, cathepsin G may modulate thrombin-mediated platelet—neutrophil adhesive interactions in inflammation and thrombosis.

A previous method for determination of the radiochemical purity (RCP) value of [ 125 I]sodium iothalamate uses two paper strips and solvents (total developing time is ∼2.5 h ). To simplify and shorten the RCP testing procedure, our laboratory has developed a single-strip chromatography method that not only distributes free 125 I and [ 125 I]sodium iothalamate to different relative front (R f ) locations, but is also faster and easier to perform. RCP of [ 125 I]sodium iothalamate was determined with the use of a 10-cm instant thin-layer chromatography strip impregnated with polysilicic acid gel (ITLC-SA) as the solid phase, and a mobile phase of 2-butanol:acetic acid:water (140:2.5:70, v/v). By using autoradiography and counting the strip segments in a gamma counter, our results indicated that free 125 I migrated to R f = 0.89-1.00 while the [ 125 I]sodium iothalamate moved to R f = 0.44-0.67 . The total developing time for the single-strip ITLC-SA system was ∼ 1 h .

Indium-111 (111In)—labeled leukocyte scanning has been used frequently in patients suspected of having infections. Recently, technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) has been used to label leukocytes. This study was undertaken to determine the distribution and dosimetry of 99mTc-HMPAO leukocytes in healthy subjects.

The development of single photon emission computed tomography (SPECT) has lead to increased interest in brain nuclear medicine imaging for a variety of neurologic diseases. The principal tracers (Tc-99m HMPAO and Tc-99m ECD) map cerebral perfusion and have either shown efficacy or promise in cerebrovascular disease, the evaluation of stroke, transient ischemic attack, vasospasm following subarachnoid hemorrhage, and arteriovenous malformation.

Twenty-five patients with severe left ventricular (LV) dysfunction (radiologic cardiomegaly, ejection fraction of ≤ 0.35) were operated upon for severe coronary artery disease (CAD). The long-term survivors were reviewed to see if LV function improved. Preoperatively all patients had angina pectoris, 72% had congestive heart failure (CHF), and 92% had had one or more myocardial infarctions. Critical stenoses in two or three major coronary vessels were present in all patients, and six in addition were found to have left main coronary artery stenosis. An average of 3.5 grafts per patient were inserted. The surgical mortality rate was 12% (three patients). Twenty (80%) patients were alive at an average interval of 21 months (range 8 to 42) postoperatively. All had partial or complete relief of angina and 85% had no heart failure. LV ejection fraction was measured by radionuclide angiography at a mean time of 19 months postoperatively in 18 survivors. It was unchanged in 12 who had two- and 3-vessel disease (0.23 ± 0.06 [mean ± SD] preoperatively versus 0.25 ± 0.09 postoperatively, p > 0.05) but improved in six with main left coronary disease (0.24 ± 0.06 preoperatively versus 0.40 ± 0.14 postoperatively, p < 0.01). The actuarial 18 month survival rate for the entire group was 82%. Aorta-coronary artery bypass grafting (ACBG) can be performed in patients with CAD and severe LV dysfunction with good relief of angina and a favorable long-term survival rate. Heart failure is usually improved clinically but, except in the case of main left coronary disease, the measured LV function at rest is unchanged.