Influenza as a trigger for cardiovascular disease: An investigation of serotype, subtype and geographic location.

BACKGROUND: Seasonal peaks of influenza and cardiovascular disease tend to coincide. Many excess deaths may be triggered by influenza, and the severity of this effect may vary with the virulence of the circulating influenza strain and host susceptibility. We aimed to explore the association between hospital admissions for influenza and/or pneumonia (IP) and acute myocardial infarction (AMI) or ischaemic heart disease (IHD) in Queensland, Australia, taking into account temporal and spatial variation of influenza virus type and subtype in 2007, 2008 and 2009. METHODS: This ecological study at Statistical Subdivision level (SSD, n=38) used linked patient-level data. For each study year, Standardized Morbidity Ratios (SMRs) were calculated for hospital admissions with diagnoses of IP, AMI and IHD. We investigated the associations between IP and AMI or IHD using spatial autoregressive modelling, adjusting for socio-demographic factors. RESULTS: Spatial autocorrelation was detected in SMRs, possibly reflecting underlying social and behavioural risk factors, but consistent with infectious disease spread. SMRs for IP were consistently predictive of SMRs for AMI and IHD when adjusted for socioeconomic status, population density and per cent Indigenous population (coefficient: 0.707, 95% confidence interval (CI): 0.318 - 1.096; 0.553, 0.222 - 0.884; 0.598, 0.307 - 0.888 and 1.017, 0.711 - 1.323; 0.650, 0.342 - 0.958; 1.031, 0.827 - 1.236) in 2007, 2008 and 2009, respectively. CONCLUSIONS: This ecological study provides further evidence that severe respiratory infections may trigger the onset of cardiovascular events, implicating the influenza virus as a contributing factor.

Improvements in the quality of care and health outcomes with new stroke care units following implementation of a clinician-led, health system redesign programme in New South Wales, Australia.

BACKGROUND AND OBJECTIVES: Provision of evidence-based hospital stroke care is limited worldwide. In Australia, about a fifth of public hospitals provide stroke care units (SCUs). In 2001, the New South Wales (NSW) state government funded a clinician-led, health system redesign programme that included inpatient stroke services. Our objective was to determine the effects of this initiative for improving: (i) access to SCUs and care quality and (ii) health outcomes. DESIGN, SETTING AND PARTICIPANTS: Preintervention-postintervention design (12 months prior and a minimum 6-12 months following SCU implementation). Retrospective, public hospital audit of 50 consecutive medical records per time period of stroke admissions (using International Classification of Diseases (ICD)-10 codes). Combined analyses for 15 hospitals presented. OUTCOMES: Process of care indicators and patient independence (proportional odds modelling using modified Rankin scale). RESULTS: Pre-programme cases (n = 703) (mean (SD) age 74 (14) years; female: 51%) and post-programme cases (n = 884) (mean age 74 (14) years; female: 49%) were comparable. Significant post-programme improvements for most process indicators were found, such as more brain imaging within 24 hours. Post-programme, access to SCUs increased 22-fold (95% CI 16.8 to 28.3). Improvement in inpatient independence at post-programme discharge was significant compared with pre-programme outcomes (proportional odds ratio 0.73, 95% CI 0.57 to 0.94; p = 0.013) when adjusted for patient clustering and case mix. CONCLUSIONS: This distinctive SCU initiative was shown as effective for improving clinical practice and significantly reducing disability following stroke.

Is prestroke use of angiotensin-converting enzyme inhibitors associated with better outcome?

BACKGROUND: There is evidence that angiotensin-converting enzyme inhibitors (ACEIs) reduce the risk of stroke. However, it is unclear whether ACEI use before stroke provides a vasoprotective effect resulting in less severe stroke. METHODS: We ascertained all strokes occurring in a defined population in Melbourne, Australia. Prestroke use of ACEIs and concomitant medications was obtained from medical records. Initial neurologic deficit was dichotomized according to a NIH Stroke Scale (NIHSS) score < 8 (less severe deficit) or > or = 8 (severe deficit). Logistic regression was used to assess the association between prestroke use of ACEIs and stroke severity (measured by severity of neurologic deficits and death at 28 days). RESULTS: Seven hundred sixteen first-ever ischemic stroke patients were included. Previous use of ACEIs was independently associated with a reduced risk of severe neurologic deficits (odds ratio [OR] 0.56; 95% CI 0.35 to 0.91) and death within 28 days (OR 0.46; 95% CI 0.24 to 0.87). Diuretics were associated with an increased risk of severe neurologic deficits (OR 1.81; 95% CI 1.13 to 2.90). Factors associated with a greater NIHSS score were older age, atrial fibrillation, heart failure, and use of diuretics. These factors and claudication were associated with an increased risk of 28-day mortality, whereas use of anticoagulants was associated with a reduced risk of severe neurologic deficits and death. CONCLUSION: Within this large community-based cohort, prestroke use of angiotensin-converting enzyme inhibitors was associated with a reduced risk of severe stroke.

Access to stroke care units in Australian public hospitals: facts and temporal progress.

BACKGROUND: There is level I evidence that management of stroke patients in stroke units (SU) improves outcomes (death and institutionalization) by approximately 20%. In Australia, there is uncertainty as to the proportion of incident cases that have access to SU. Recent national and State-based policy initiatives to increase access to SU have been taken. However, objective evidence related to SU implementation progress is lacking. The aims of the study were (i) to determine the number of SU in Australian acute public hospitals in 2004, (ii) to describe hospitals according to national SU policy criteria and (iii) to compare results to the 1999 survey to track progress. METHODS: The method used in the study was a cross-sectional, postal survey technique. The participants were clinical representatives considered appropriate to describe stroke care within survey hospitals. RESULTS: The outcome of the study was presence of a SU according to an accepted definition. Response rate was 261/301 (87%). Sixty-one sites (23%) had either a SU and/or a dedicated stroke team. Fifty sites claimed to have a SU (19%). New South Wales with 23 had the most number of SU. Based on policy criteria, up to 64 sites could have a SU. In 1999, there were 35 public hospitals with a SU. CONCLUSION: Access to SU in Australian public hospitals remains low compared with other countries (Sweden, 70%). Implementation strategies supported by appropriate health policy to improve access are needed.

Hypoxic tissue in ischaemic stroke: persistence and clinical consequences of spontaneous survival.

In ischaemic stroke, expansion of the infarct core occurs at the expense of surrounding hypoxic, metabolically compromised tissue over a period of 24 h or more in a considerable proportion of patients. It is uncertain whether hypoxic tissue observed at later times after stroke onset retains the potential for survival or whether such survival has an impact on functional outcome. These factors may determine the effectiveness of therapeutic strategies aimed at salvaging this tissue. We tested the hypotheses that metabolically compromised hypoxic tissue observed within 48 h after onset of ischaemic stroke retains the potential for spontaneous survival and that the impact of such survival on functional outcome is time dependent. Consecutive patients presenting within 48 h of ischaemic stroke were studied with [(18)F]fluoromisonidazole, a ligand binding to hypoxic but viable tissue, and PET. Subjects were grouped into two time epochs, 12 h, based on the interval from stroke onset to the time of tracer injection, and had infarct volumes measured on CT/MRI at 7 days (n = 60). The total ischaemic volume (TIV) and the proportion of the TIV that spontaneously survived (surviving hypoxic volume ratio, SHVR) were defined from the co-registered CT/MRI images. These volumetric measures were correlated with neurological outcome assessed at day 7-10 by percentage change in the National Institutes of Health Stroke Scale (DeltaNIHSS), and at 3 months by Barthel Index (BI) and modified Rankin Score (mRS). Of 66 patients investigated, hypoxic tissue occurred in 33 and outcome data was available in 27. Hypoxic tissue constituted >20% of the TIV in 60% of studies 12 h. The spontaneously surviving proportion of the TIV (median 6.9%) or hypoxic tissue (median 45.9%) was not significantly different in patient subgroups studied 12 h after stroke onset. Spontaneous survival of hypoxic tissue (surviving hypoxic volume ratio) was associated with improved neurological outcome in both time epochs: 12 h, DeltaNIHSS (r = 0.59, P < 0.01) and day 90 mRS (r = -0.46, P < 0.05). The finding that similar proportions of hypoxic tissue survived spontaneously within each time epoch suggests that its fate is not predetermined. The favourable neurological outcome associated with spontaneous survival of hypoxic tissue, even 12-48 h after stroke onset, suggests that the volume of hypoxic tissue that progressed to infarction may represent a valuable target for therapeutic intervention.

Age-standardised mortality and proportional mortality analyses of aboriginal and non-aboriginal deaths in metropolitan, rural and remote areas.

The study's aim was to assess how much of the variation in disease-specific mortality between metropolitan, rural and remote areas is specific to those diseases or reflects the all-cause mortality pattern. The ranges and variances of disease-specific standardised proportional mortality ratios between geographical areas were compared to those of the corresponding standardised mortality ratios. For most chapters in the International Classification of Diseases, the ranges and variances of the standardised proportional mortality ratios were less than 40% of those of the corresponding standardised mortality ratios. Only a small proportion of the variation in mortality can therefore be attributed to a specific disease component; the remainder must be attributed to an underlying 'force of mortality'. Research, programs and policies addressing the socio-economic disadvantages of living in remote areas may lead to a greater improvement in mortality than those targeting specific diseases.

Helicobacter pylori infection in an Australian regional city: prevalence and risk factors.

OBJECTIVE: To investigate the prevalence of Helicobacter pylori infection and potential risk factors for infection in an adult Australian population. DESIGN: Cross-sectional study. SETTING: Ballarat, a major regional city in Victoria (population, 78,000; 92% bom in Australia), November 1994 to July 1995. PARTICIPANTS: 217 adults randomly selected from the electoral roll. MAIN OUTCOME MEASURES: H. pylori IgG antibody status by enzyme immunoassay; amount of dental plaque; sociodemographic and other potential risk factors; odds ratios for risk factors determined by logistic regression analysis. RESULTS: Age-standardised prevalence of H. pylori infection was 30.6%. After adjustment for age, sex and socioeconomic index, positive H. pylori status was significantly associated with increasing number of tooth surfaces with a high plaque score (odds ratio [OR], 1.7; 95% confidence interval [CI], 1.1-2.7), increasing number of years in a job with public contact (OR, 1.7; 95% CI, 1.3-2.3), blood group B antigen (OR, 3.1; 95% CI, 1.1-9.1), and having lived in a household with more than six members during childhood (OR, 2.5; 95% CI, 1.1-5.5). Negative H. pylori status was significantly associated with increasing education, having ever lived on a farm, and having teeth scaled less than once a year. CONCLUSIONS: H. pylori infection is common. Dental plaque may be a reservoir for H. pylori, which is probably transmitted by person-to-person contact, and blood group B antigen may predispose to infection. Community education about effective oral hygiene and adoption of good hygiene practices by those with regular public contact may be important to prevent acquisition and transmission of H. pylori.

Helicobacter pylori antibody titres in serum, plasma and successively thawed specimens: implications for epidemiological and clinical studies.

Agreement between Helicobacter pylori IgG antibodies measured using the Pylori-set EIA-G kit in serum, plasma and successively thawed specimens was studied and the implications for epidemiological and clinical studies assessed. Plasma titres may differ from serum titres by -6% to +8% and therefore may be substituted for serum. The change in titre around the cut off value was -0.31 (se = 5.7, p = 0.96) per thaw. The estimated maximum drop after three thawings, 34.5, would result in only a small decrease in sensitivity (1.3%). For qualitative epidemiological studies, this additional misclassification rate is relatively small. However, positive titres did reduce over successive thawings, with the estimated maximum drop being 11.4% per thaw. Therefore, thawing does need to be considered as a contributing factor when interpreting titre drops in eradication trials. Baseline and follow up specimens from clinical studies should be thawed once only and tested concurrently.

Subclass restriction of anti-SS-B (La) autoantibodies.

Antibodies to the SS-B (La) nuclear ribonucleoprotein particle are relatively specific for the diagnoses of Sjögren's syndrome or systemic lupus erythematosus. The formation of such autoantibodies is likely, then, to reflect the basic immunopathogenesis of these disorders. We have studied the isotype distribution of anti-SS-B antibodies as a clue to their immunoregulation. Using specific ELISA assays, we found that nearly all anti-SS-B antibodies in 39 patients were IgG, and, of these, only the IgG1 and, to a much lesser extent, IgG3 subclasses were represented. Both kappa and lambda light chain antibodies were found in most sera, and the overall kappa/lambda ratio approximated that of normal serum immunoglobulin. These results suggest that the formation of anti-SS-B antibodies is T-cell dependent and that the response is polyclonal in most patients.