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(Stroke. 2008;39:776.)
© 2008 American Heart Association, Inc.

Original Contributions

Trends in Incidence and Outcome of Stroke in Perth, Western Australia During 1989 to 2001

The Perth Community Stroke Study

Md. Shaheenul Islam, MBBS, MPH, MSc; Craig S. Anderson, MBBS, FRACP, PhD; Graeme J. Hankey, MD, FRCP, FRACP; Kate Hardie, BMed, MPH; Kristie Carter, MSc; Robyn Broadhurst, BA, BSc Konrad Jamrozik, MBBS, DPhil, FAFPHM

From the Neurological and Mental Health Division (M.S.I., C.S.A., K.C.), The George Institute for International Health, The Royal Prince Alfred Hospital and University of Sydney, NSW Australia; the Stroke Unit (G.J.H., K.H.), Department of Neurology, Royal Perth Hospital, WA, Australia; the Centre for Health Services Research (R.B.), School of Population Health, University of Western Australia; and the School of Population Health and Clinical Practice (K.J.), University of Adelaide, SA, Australia.

Correspondence to Professor Craig Anderson, Director, Neurological and Mental Health Division, The George Institute for International Health, PO Box M201, Missenden Road, Camperdown NSW 2050. E-mail canderson{at}george.org.au

	Abstract

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Background and Purpose— We studied temporal trends in major stroke outcomes in Perth, Western Australia (WA), comparing 3 12-month periods, roughly 5 years apart, between 1989 and 2001.

Methods— The Perth Community Stroke Study (PCSS) used uniform definitions and procedures in a representative segment (approximately 143 000 people in the year 2000) of Perth, WA. Crude and age-standardized incidence and 28-day case fatality for stroke in the different study periods were compared using Poisson regression. We also undertook temporal comparisons of severity, risk factors, and management of stroke to define the basis for any changes in rates. Data are reported with 95% confidence intervals (CI).

Results— There were 251, 213, and 183 first-ever strokes identified in the first, second, and third study periods, respectively, reflecting significant declines in stroke rates overall, for major age groups, and for both ischemic stroke and intracerebral hemorrhage. The decline in rates was greater in men than women. Compared with the 1989 to 1990 period, sex- and age-adjusted rates declined by 25% (95% CI 10% to 37%) in 1995 to 1996, and by 43% (95% CI 31% to 53%) in 2000 to 2001, corresponding to a 5.5% average annual decrease overall. There were correspondingly significant reductions in the frequencies of key risk factors among cases. However, early case fatality remained stable, both overall and for major pathological subtypes of stroke.

Conclusions— These data confirm significant declines in the incidence of stroke on the western side of Australia, coincident with some improvement in the vascular risk profile of cases in the population. Decreasing risk rather than improving survival appears to be the main driver of falling mortality from stroke in this population.

Key Words: acute stroke • epidemiology • outcome • registry • risk factors • stroke management • case fatality

	Introduction

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Stroke is a major cause of global disease burden.¹ Although advances in approaches to prevention and management of stroke have been made, there is little direct feedback on their success to date and thus uncertainty regarding the potential impact of restraining the projected epidemic of stroke.^2,3 This is especially true in low-to-middle income countries where the populations are undergoing rapid ageing and changes in lifestyle.

Population-based surveillance is the most reliable approach for assessing trends in the burden of stroke.^4,5 However, the considerable efforts and cost required to ensure adherence to optimal methodological criteria have limited the number of such studies. Moreover, the few available data of temporal trends in stroke incidence are conflicting, with rates shown to have increased,^6–12 remained stable,^13–17 and more recently to have declined in predominantly "European" populations.^18–21 Most noteworthy is the remarkably large declines in the rates of stroke overall, and of ischemic stroke (IS) and primary intracerebral hemorrhage (PICH) reported in Oxfordshire, England between 1981–1984 and 2002–2004.²⁰ In addition, there were reductions in key premorbid vascular risk factors (smoking, total cholesterol, and blood pressure) and increased use of preventive therapies (antiplatelet agents, lipid lowering, and blood pressure lowering) among cases. Conversely, a more modest 10% decline in stroke incidence was observed in the large multiethnic population of Auckland, New Zealand over a near similar 20-year calendar period,²¹ whereas a 25% decline occurred in Perth, Western Australia (WA) over 5 years to the mid-1990s.¹⁹ We aimed to provide more robust estimates of trends in the incidence, management, and case fatality of stroke in Perth WA with additional data from a third study undertaken in 2000 to 2001.

	Methods

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Study Population
Details of the Perth Community Stroke Study (PCSS) have been described elsewhere.¹⁹ In brief, sequential studies were undertaken in a geographically-defined segment of the inner metropolitan region of Perth in 1989 to 1990, 1995 to 1996, and 2000 to 2001. The size of the population was approximately 131 000, 136 000, and 143 000, in the respective study periods, according to 5-year census data, and there has been consistency in the range of available health services. As the latest study was undertaken over 12 months from 7 February 2000, but the 2 earlier studies were undertaken over 18 and 13 months, respectively, only incident ("first-ever") strokes registered during 12-month calendar periods (commencing 1 March 1989 for the first study and 3 June 1995 for the second study) were used in our comparative analyses of rates and outcomes across time. Relevant ethics committees approved the protocol for each period of registration.

Ascertainment and Assessment of Cases
Multiple overlapping sources were used to identify all acute episodes of cerebrovascular disease (CeVD), including both stroke and transient cerebral ischemic attack (TIA), affecting residents of the study population. During each study period, all general practitioners (GPs) within and around the study area were requested to notify the PCSS office of any acute CeVD, and the PCSS doctor reviewed neurology requests, inpatient admissions and attendances at emergency departments at all hospitals in Perth, registrations of deaths among residents of the study area, and any events occurring in residential (nursing) care facilities within the study area. Final checks for the completeness of case ascertainment were carried out by scanning electronic records of all inpatient separations and death registrations in WA for various diagnostic codes and key words indicating CeVD. An additional letter was sent to the relevant GPs and physicians to remind them of cases notified from their practices and to ask whether others had been seen.

Once a potential case was identified, the PCSS doctor visited each living case in hospital (or at home) as soon as possible and conducted a structured assessment that covered details of the event, sociodemographic information including a measure of socioeconomic status based on the highest, longest held occupation of the patient or spouse, medical history, and a physical examination. The World Health Organization (WHO) standard definition of stroke was used to categorize each event as a stroke, TIA, or illness other than CeVD. To maximize the accuracy of the diagnosis, efforts were made to obtain a CT scan in cases where it had not been ordered, and treating physicians were encouraged to obtain an autopsy in the event of death of any patient registered with the PCSS. A specialist PCSS neurologist, unaware of the report from a radiologist, reviewed neuroimages using strict criteria for defining cases into major pathological stroke types of IS, PICH, and subarachnoid hemorrhage (SAH). Patients who fulfilled the clinical criteria for stroke but without confirmatory neuroimaging or autopsy, were categorized as having a stroke of "undetermined type" (UND). The same clinician also classified each stroke event according to the Oxfordshire classification of total anterior circulation infarction (TACI), partial anterior circulation infarction (PACI), lacunar infarction (LACI), and posterior circulation infarction (POCI).²²

For these analyses, short term case fatality (expressed in percent) was reflected by vital status at 28 days after the onset of symptoms. Most deaths were discovered through ongoing surveillance of official mortality statistics for new cases. Others were found through contact with caregivers for the follow-up of the patients as part of a related study.

Statistical Analyses
We calculated annual rates per 100 000 with corresponding 95% confidence intervals (CIs) based on the Poisson distribution. Trends in rates and 28-day case fatality obtained from simple Poisson regression models were assessed for statistical significance at the 5% level. Four groupings (64, 65 to 74, 75 to 84, and 85 years) were used for age-adjustment and sex-specific trend analyses. Age-standardized rates were calculated for each pathological stroke subtype using the direct method and the WHO "world" population as the external reference.²³ The ² test and nonparametric tests were used to examine differences in the distribution of baseline characteristics, risk factor profiles, and management across the studies. Analyses were done with STATA (Version 8.0, STATA Corporation) and MS Excel (Microsoft Corporation).

	Results

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Table 1 shows the characteristics of the 251, 213, and 183 cases of first-ever stroke identified during each 12-month study period. Changes are apparent in the sociodemographic profile of the study groups, with a trend for older, more female, and overseas born (particularly from Asia) patients over time. Although level of consciousness, as assessed by the Glasgow Coma Scale (GCS), and the frequency of urinary incontinence were lowest in the 1995 to 1996 study period, physical functioning, as assessed by the Barthel Index within the first few days of stroke onset, was essentially stable. Table 1 also shows that there were significant reductions in the frequencies of certain premorbid vascular risk factors (history of hypertension, use of antihypertensive treatment, smoking, and history of ischemic heart disease) and an increase in the use of anticoagulation.

View this table: [in this window] [in a new window]   Table 1. Characteristics of Cases, by Period of Perth Community Stroke Study

View this table: [in this window] [in a new window]   Table 1. Continued

Table 2 reveals a significant, near linear, decline in stroke rates across the studies, which was consistent across all age groups, and for both men and women. Compared with 1989 to 1990, sex- and age-adjusted rates declined by 25% (95% CI 10% to 37%) in the second study, and by 43% (95% CI 31% to 53%) in the third study, which represents a mean annual decrease of approximately 5.5%. A similar adjusted comparison between the second and third study periods showed a 24% (95% CI 7% to 38%; P=0.01) decrease in rates, or a mean annual decrease of 5.3%, over 5 years. Stroke rates increased by a factor of 4.1 (95% CI 3.8 to 4.3) across the 5 age groups, after adjusting for sex and study period, and the decline in rates varied from 38% in the young (<65 years) to 43% in those aged 75 years or more, over the 10 years (Table 2; Figure).

View this table: [in this window] [in a new window]   Table 2. Annual Age- and Sex-Specific Rates (per 100 000) of First-Ever Stroke in Perth, Western Australia

View larger version (6K): [in this window] [in a new window]   Figure. Age-specific incidence rates in the total population in different follow-up years for all types of stroke combined.

Age-adjusted stroke rates decreased by 49% (95% CI 33% to 61%) in men between the first and third study periods, although age-stratified analyses revealed that these trends were only significant in the 75 to 84 (P=0.002) and 64 (P=0.01) year age groups. Among women, age-adjusted rates decreased by 37% (95% CI 17% to 52%; P=0.001) overall, with age-stratified analyses showing a significant trend only in the 75 to 84 year age group (P=0.03). Across all studies, the age-adjusted rates were 57% (95% CI 34% to 83%; P<0.001) higher in men compared with women.

Age-standardized rates for IS, PICH, and UND all declined significantly, whereas the incidence of SAH was stable. Compared with the first study period, age-standardized rate ratios for IS and PICH in the third study period were 0.62 (95% CI 0.47 to 0.82) and 0.46 (95% CI 0.22 to 0.94), respectively. Sex-stratified analyses showed downwards trends in rates of IS (P=0.001) and PICH (P=0.04), but these were significant only in men (Table 3).

View this table: [in this window] [in a new window]   Table 3. Annual Age-Standardized (to the WHO Population) Rates (per 100 000) With 95 Confidence Intervals (CI) for Major Stroke Types* in Perth, Western Australia

Table 4 shows that 28-day case fatality ratios were stable over the 3 studies, and did not change significantly in either cases managed within (21.4%, 21.8% and 17.8%; P=0.58) or outside (35.3%, 22.2% and 50.0%; P=0.11) hospitals.

View this table: [in this window] [in a new window]   Table 4. 28-Day Case-Fatality (With 95% Confidence Intervals) for First-Ever Strokes* in the Three Study Periods

	Discussion

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Our study has shown consistent declines of about one quarter in stroke rates from 1989 to 1990 to 1995 to 1996, and again to 2000 to 2001, to produce an overall 43% (95% CI 31% to 53%) fall in stroke incidence over 11 years. The decline in rates occurred for both IS and PICH, and was associated with significant reductions in the frequencies of several premorbid vascular risk factors among cases. These trends mirror those reported in Oxfordshire,²⁰ except that the magnitude of decline in incidence was much greater in Perth. Further, our positive findings were similarly counterbalanced by a stable early case fatality for stroke.

Several strengths of this study include: the population-based design with vigorous case ascertainment; high level of verification of stroke subtypes by early neuroimaging or autopsy; consistency of the senior investigators in providing oversight of the PCSS; and conduct of the research in a study population and health care system with high levels of awareness of the aims and procedures of the study. We used multiple overlapping sources of information to identify both hospitalized and nonhospitalized cases of fatal and nonfatal strokes within a well defined and relatively stable population, as recommended for the conduct of "ideal" stroke incidence studies.⁴ We also had access to a computerized record linkage system that covers all inpatient separations (discharges, transfers and deaths) from every hospital in WA.

However, there were some limitations to the study. Although our procedures minimized potential selection and misclassification biases, there were some irregularities in the data. Specifically, there was significant variation in some of the measures of stroke severity (ie, level of consciousness and incontinence) and patterns of ischemic stroke syndromes, as well as an increase in the use of "passive" methods of case ascertainment over the 3 periods. These inconsistencies may raise concerns about the completeness of case ascertainment, especially in the later phases. It was inevitable, though, that there was some misclassification in these measures attributable to changes in research personnel and the timing of clinical assessments over the study periods. The more robust measures, such as physical function according to modified version of the Barthel Index²⁴ and the identification of pathological stroke subtypes, showed comparable patterns across the studies (Table 1). We therefore consider it unlikely that milder cases of stroke, either IS or PICH, were better detected in the most recent study, given the consistency in the downward trends in rates by age and major stroke subtype, and the stable case fatality ratios, both overall and according to whether cases were managed within or outside hospital. The high case fatality ratios for UND stroke reflects an inability to obtain neuroimaging either because of rapid death or because it was considered clinically inappropriate in a premorbidly disabled patient. The assessment of risk factors was complicated by changes in diagnostic criteria (eg, hypertension) and threshold for initiation of treatment (eg, antihypertensive therapy) over time, whereas the greater proportion of missing information on risk factors in the last period, possibly because of a greater reliance on proxy sources of information, further contributes to estimates of trends in these exposures being less precise and more prone to error.

Why was the magnitude of the decline in stroke incidence much greater in Perth than Oxfordshire, whereas both studies had stable early case fatality ratios? A true disparity in trends is difficult to explain on the available data: the 2 populations show comparable baseline rates and age and sex structures. Although there were differences in the relative and absolute frequencies of certain exposures (ie, history of hypertension, smoking) and use of treatments (ie, antihypertensive and antiplatelet agents) among cases, these generally favored Oxfordshire. However, given that the 95% CIs around the estimates of rates were wide and overlapping, alternative explanations include random variation around rates that were not truly different. Inequalities in the magnitude of the decline in rates between Auckland²¹ and Perth can be more easily attributed to the much greater ethnic heterogeneity and disparity in risks of stroke in the former population.

There are very few investigations that have used consistent methods to measure the incidence and outcome of stroke as it affects a whole population over periods of 10 years or more. Surprisingly, the few studies available for populations that are broadly comparable in economic terms have produced conflicting results. Decreasing incidence appears to be the principal force behind the falling mortality from stroke in Perth and Oxfordshire, whereas improving survival has been the dominant factor in Auckland.^15,25 This would appear to leave the former populations better placed to face the ageing of their communities as stroke incidence is a key determinant of both acute caseload and lasting disability. Nevertheless, the size and rapidity of the demographic transition allows no room for complacency, as any faltering in the downward trend in rates and ongoing improvements in survival will quickly translate into a very significant expansion in the burden of stroke in western societies.

	Acknowledgments

 
Sources of Funding

We thank the National Health and Medicine Research Council and National Heart Foundation of Australia for providing funding for various stages of the Perth Community Stroke Study. The study was designed, conducted, analyzed and interpreted by the investigators independent of these funding bodies.

Disclosures

None.

Received May 14, 2007; revision received July 23, 2007; accepted July 25, 2007.

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This Article Abstract Full Text (PDF) All Versions of this Article: 39/3/776    most recent STROKEAHA.107.493643v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Islam, Md. S. Articles by Jamrozik, K. Search for Related Content PubMed PubMed Citation Articles by Islam, Md. S. Articles by Jamrozik, K. Pubmed/NCBI databases Medline Plus Health Information Stroke Related Collections Cerebrovascular disease/stroke Other Treatment CT and MRI Acute Cerebral Hemorrhage Acute Cerebral Infarction Epidemiology