Journal of the New Zealand Medical Association, 07-November-2008, Vol 121 No 1285
Ethnic and socioeconomic disparities in the prevalence of cardiovascular disease in New Zealand
Wing Cheuk Chan, Craig Wright, Tania Riddell, Susan Wells, Andrew J Kerr, Geeta Gala, Rod Jackson
Cardiovascular disease (CVD) remains the leading cause of death in New Zealand despite the age standardised mortality rate having fallen by more than 40% between 1997 and 2003.1 Coronary heart disease and cerebrovascular disease combined accounted for 8889 deaths in New Zealand in 2003 compared to 7932 deaths related to cancer.1 In New Zealand, longstanding ethnic and socioeconomic disparities have been well documented for CVD mortality.2,3
Patients with prevalent CVD are at the highest risk of developing future CVD events,4,5 and would benefit the most from aggressive cardiovascular risk factors management. This study aims to identify specific subgroups with the highest prevalence of a broad range of cardiovascular disease in New Zealand.
As far as we are aware, this is the first published New Zealand study to estimate national CVD prevalence by ethnicity and socioeconomic status using multiple datasets linked by the National Health Index (NHI) number, a unique national personal identifier for all New Zealanders which is attached to major routinely collected health datasets.
This study is based on data extracted from the National Minimum Dataset (NMDS) (for hospital events), the New Zealand Health Information Service national mortality collection (1988–2007), and the National Pharmaceutical collection (July 2001 to June 2007).
The following hospital discharge codes and procedural codes were used to identify patients with known CVD (including codes for coronary heart disease, ischaemic stroke, peripheral vascular disease, congestive heart failure, hypertensive heart disease, atrial fibrillation, and ventricular fibrillation):
In addition, the National Pharmaceutical data collection from July 2001 to June 2007 was used to identify people with two or more prescriptions for glyceryl trinitrate, isosorbide dinitrate, isosorbide mononitrate, nicorandil, and perhexiline, which are used almost exclusively to manage angina. To exclude those patients for whom nitrate prescribing formed part of a diagnostic test, only patients with two or more prescriptions were selected.
The CVD prevalence estimates exclude all the deaths identified by the mortality collection via encrypted NHI linkage. The NHI number is a unique identifier that is assigned to each health services user in New Zealand and it allows linkage between different data collections.
In keeping with the New Zealand CVD risk management guidelines,4 CVD prevalence estimates were stratified by ethnicity according to the following groups: Māori (ethnic code 21), Pacific people (30–37), Indian (43), and ‘Other’ New Zealanders. However, since NHI only records Statistics New Zealand level 2 ethnic codes, the Indian group of this study includes Indian and Fijian Indian but not some of the other Indian subcontinent groups such as Sri Lankan and Pakistani. The standard New Zealand prioritised definition of ethnicity (Māori, then Pacific peoples, then Indian peoples) was used. The most recently available ethnicity codes from all national collections were used for each NHI.
Socioeconomic status was measured using the NZDep2001 index of deprivation by quintile at the census area unit (CAU) level. NZDep2001 is an index of deprivation for small areas, accounting for nine variables covering income, employment, access to transport, education, and home ownership.6
Age-specific prevalence was calculated using a 2006/07 population derived from the national collections and NHI. The study population required a person to:
The prevalence proportions were separated into 5-year age groups from 0 to >85 for direct age standardisation using the World Health Organization (WHO) World population as the standard.7
Standard errors (SE) and 95% confidence intervals for age standardisation are calculated from the following formula:
w = weights of the WHO population within the age bracket.
p = prevalence proportions within the age bracket.
n = number of people in the denominator within the age bracket.
The study population included 4,191,388 people in New Zealand, which is a 0.87% undercount compared to Statistics New Zealand estimates of the resident population at June 2007 of 4,228,000.8
In 2007, a total of 281,333 people in New Zealand were estimated to have CVD as defined by this study (Table 1). About 9.7%, 4.1%, and 1.4% of people with CVD in New Zealand were of Māori, Pacific, and Indian ethnicities respectively. The remainder (84.8%) of people with CVD were mainly of European descent and are referred to here as ‘Other’ New Zealanders.
Māori had the highest age-standardised prevalence of CVD, which was 67% higher than among ‘Other’ New Zealanders.
Table 1. Estimated number of people in New Zealand with prevalent cardiovascular disease (CVD) by ethnicity in 2007
*Mostly of Samoan, Tongan, Niuean, or Cook Islands origin.
Age specific prevalence—As expected and illustrated in Figure 1, the prevalence of CVD in New Zealand increases rapidly from 35 years of age and is higher in all age groups in males compared to females.
As shown in Figures 2 and 3, Māori males and females had the highest age-specific prevalence of CVD compared to all other ethnic groups after age 35 years. Although not readily apparent in Figures 2 and 3, CVD prevalence among Māori females was 184% higher than females in the ‘Other’ New Zealanders group in the 45-49 year age group. Similarly, CVD prevalence in Māori males was 98% higher than ‘Other’ New Zealand males in the 35–39 year age group.
Prevalence among Indian and Pacific males was intermediate between Māori and ‘Other’ New Zealanders up to the age of 64 years. However, CVD prevalence among Pacific females is higher than Indian females from age 45 years onwards. The CVD prevalence among both Pacific and Indian peoples is lower than ‘Other’ New Zealanders after age 70 years for males and after age 75 years for females.
NZDep2001 was available for 91% (n=256,277) of people with CVD and for the remaining 9% NZDep has not been estimated due to the small size of the population living in those CAU.
There was a clear socioeconomic gradient in prevalence of CVD. People living in most deprived areas had consistently higher age-specific prevalence than people living in less deprived areas (Figure 4). For example, in the 55–59 years age group, the prevalence among the most deprived group was 123% higher than their least deprived counterparts.
Figure 2. Age-specific prevalence of cardiovascular disease in New Zealand by ethnicity (males) in 2007
Figure 3. Age specific prevalence of cardiovascular disease in New Zealand by ethnicity (females) in 2007
Figure 4. Age-specific prevalence of cardiovascular disease in New Zealand in 2007 by quintiles of socioeconomic deprivation
As illustrated in Figure 5, the corresponding age-specific prevalence among the least deprived quintile of Māori and the most deprived quintile of ‘Other New Zealanders’ were almost identical up to 79 years of age.
Between ages 40–59 years, the most deprived quintile of Māori had consistently at least a 240% higher CVD prevalence than the least deprived quintile of ‘Other New Zealanders.’
Inequalities in health status between different groups within a given population are found internationally. These include inequalities by age, sex, ethnicity, and socioeconomic group.
This study has demonstrated major disparities in the prevalence of CVD in New Zealand by ethnicity and socioeconomic deprivation, based on national hospitalisations and mortality datasets between 1998 and 2007 and the National Pharmaceutical data collection from 2001–2007.
The relative burden of CVD falls most heavily on Māori, middle-aged Pacific, and Indian peoples and those who live in the most deprived areas of New Zealand. It has also demonstrated that the most consistent and compelling disparity in CVD prevalence is that for the indigenous Māori population.
Figure 5. Comparison of age-specific cardiovascular disease prevalence between the most and least socioeconomically deprived quintiles of Māori and ‘Other’ New Zealanders
Ethnic and socioeconomic disparities in CVD mortality have been previously described in the New Zealand census mortality study.9–12 The study also demonstrated that disparities in cardiovascular mortality between Māori and non-Māori persisted after adjusting for socioeconomic status.11 Consistent with the mortality findings,2 our study demonstrated that age-specific prevalence of the least deprived Māori were similar to the prevalence of CVD among the most deprived ‘Other’ New Zealanders group up to 79 years of age.
It is important to note the marked differences in population demography when comparing health outcomes between ethnic groups. Māori have a much younger age structure than the total New Zealand population. According to the 2006 New Zealand census, the median age of Māori was 22.7 years compared to 36 years for the total population.13,14 Proportionally, the crude CVD prevalence among Māori is in fact lower than for ‘Other’ New Zealanders (Table 1). However, after adjusting for the effect of age, prevalence among Māori was 66% higher than among ’Other’ New Zealanders.
Consistent with national CVD risk management guidelines,4 this study also demonstrated Pacific and Indian populations had higher age-standardised prevalence of CVD than ‘Other’ New Zealanders. It is interesting to note, however, that CVD prevalence among both Pacific and Indian populations were lower than ‘Other’ New Zealanders in the older age groups. The “healthy migrant effect” may in part account for this observation15 or perhaps these older people are more likely to have persisted with the traditional healthier diets they had in their countries of birth.
This study did not examine temporal trends in prevalence. Since prevalence of CVD depends on the dynamic interactions between incidence and mortality, it is uncertain if the disparities demonstrated in this study have narrowed or widened over time. Nevertheless, we have identified a significant opportunity to reduce future CVD morbidity and mortality disparities in New Zealand.
Targeting patients with prevalent CVD is likely to be a cost-effective strategy to reduce the morbidity and mortality burden of CVD since patients with known disease are at the highest risk and would benefit most from interventions. NHI-linked National Pharmaceutical usage data routinely collected in New Zealand could become a convenient source of information to identify the potential gaps in management of CVD. Further research with linkage to pharmaceutical data is likely to be very relevant in shaping and evaluating ongoing policy and interventions in addressing disparities of CVD outcomes in New Zealand.
A major strength of the study is that the findings are derived from national data collections and are therefore not subjected to the response rate biases common in many prevalence surveys. Moreover, as this study is based on data for the entire New Zealand population, the large numbers have made it possible to estimate prevalence for multiple population subgroups with a high degree of precision.
A weakness is that the findings are dependent on the electronic recording of CVD events of the publicly funded health system. Moreover, these analyses used census area units rather than meshblocks for classifying people by socioeconomic status as these were the data most readily available. We have since done some preliminary analyses using meshblocks, which not surprisingly show a wider disparity in prevalence than using census area units, since it is a better measure of socioeconomic status. In future studies we plan to use meshblock-based measures of socio-economic status where possible. Furthermore, an extended range of CVD was selected for the study to demonstrate disparities in prevalence, which made comparison to results of similar studies more difficult. A new 2007/08 extract for diabetes prevalence and a more specifically defined CVD prevalence are now underway.
Private hospital admissions and diagnoses from general practice were not included. Therefore, these estimates are conservative since some patients with CVD such as peripheral vascular disease, transient ischaemic attack (stroke), or heart failure may not present to public hospital services. However, few acute CVD events result in admission to private hospitals in New Zealand and given the relatively long timeframe of the study, the completeness of routinely collected health statistics, and the availability of a unique national health identifier, the study is likely to provide reasonably accurate prevalence estimates of significant CVD.
It is known that the national collections suffer from an undercount in non-European ethnic groups (normally causing a numerator/denominator bias)9,16 but in this analysis both numerators and denominators came from the same NHI-derived population frame and hence do not suffer from this bias.
The potential benefits of a comprehensive national secondary prevention strategy is highlighted by the recent observation that more than 60% of coronary heart disease hospitalisations in New Zealand in 2005 were accounted for by patients who had coronary heart disease admissions in the previous 5 years.17 Therefore, even a small improvement in adherence to secondary prevention is likely to have a significant impact on future total hospitalisations.
The high-risk patient groups highlighted by this study are easily identifiable as they have all had previous contacts with health services. These groups should be prioritised for secondary prevention, to help reduce the major disparities in cardiovascular health in New Zealand. Therefore, in order to effectively and efficiently remove CVD inequities in New Zealand, future health policies and interventions should aim to realign the inequitable distribution of resources, including healthcare, and prioritise Māori health gain within the health sector.
Disclaimer: This report is published with the permission of the Deputy Director-General of Health (Public Health), New Zealand Ministry of Health. Opinions expressed are those of the authors and do not necessarily reflect policy advice provided by the Ministry of Health.
Competing interests: None known.
Author information: Wing Cheuk Chan, Honorary Research Fellow/Public Health Medicine Registrar, School of Population Health, University of Auckland, Auckland; Craig Wright, Senior Advisor (Statistics and Epidemiology), Public Health Intelligence, Ministry of Health, Wellington; Tania Riddell, Senior Lecturer, Section of Epidemiology and Biostatistics, School of Population Health, University of Auckland, Auckland; Susan Wells, Senior Lecturer, Section of Epidemiology and Biostatistics, School of Population Health, University of Auckland, Auckland; Andrew J Kerr, Cardiologist, Cardiology Department, Middlemore Hospital, South Auckland; Geeta Gala, Public Health Medicine Registrar, Public Health Operations, Ministry of Health, Auckland; Rod Jackson, Professor of Epidemiology, Section of Epidemiology and Biostatistics, School of Population Health, University of Auckland, Auckland
Correspondence: Dr Wing Cheuk Chan, Section of Epidemiology and Biostatistics, School of Population Health, Tamaki Campus, University of Auckland.
PO Box 92-019, Auckland, New Zealand. Email: firstname.lastname@example.org
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