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| Journal of the New Zealand Medical Association,
07-November-2008, Vol 121 No 1285
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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.
MethodsThis 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.
ResultsThe 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.’
DiscussionInequalities 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: wc.chan@auckland.ac.nz References:
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