Journal of the New Zealand Medical Association, 21-April-2006, Vol 119 No 1232
Estimated prevalence of cardiovascular disease and distribution of cardiovascular risk in New Zealanders: data for healthcare planners, funders, and providers
Susan Wells, Joanna Broad, Rod Jackson
Cardiovascular disease (CVD) is the leading cause of death and hospitalisation in New Zealand.1 There are major disparities in CVD between ethnic groups and significant under-treatment of high-risk patients. Age-specific death rates are two to three times higher for Maori compared with non-Maori in those aged less than 75 years.2 CVD prevention and management and the reduction of health inequalities have been targeted as priorities in the New Zealand Health Strategy, He Korowai Oranga (Maori Health Strategy), and Primary Health Care Strategy.
Current New Zealand CVD risk management guidelines recommend targeting CVD risk assessment to all men aged over age 45 years and women aged over 55 years (10 years earlier for people of Maori, Pacific Island, or Indian ethnicity or if they have known CVD risk factors or are at high risk of developing diabetes3 [Appendix 1]).
Treatment recommendations are based primarily on the patient’s estimated absolute risk, with pharmacological treatments recommended for those over 15% 5-year absolute CVD risk.
To inform their health-needs assessments, and to guide healthcare planning and funding decisions, over the previous 2 years we have been asked by district health boards (DHBs) and primary healthcare organisations (PHOs) to provide estimates of the prevalence of CVD and distributions of CVD-risk in the community. As there is limited data on CVD and absolute risk prevalence available in the public domain, we considered that this information would also be useful to other DHBs and PHOs.
Population estimates were provided by Statistics New Zealand for the projected 2005 adult population aged over 35 years (divided according to 5-year age groups and gender) for the whole of New Zealand, and for each DHB separately. Estimates were based on the 2001 Census usually resident populations, assuming medium fertility, medium mortality, and medium migration term projection methods.
To calculate absolute CVD risk, we used data from the Auckland Heart and Health Study (AHAH)4 to estimate the proportion eligible for risk assessment and to derive estimates of the prevalence of existing cardiovascular disease and cardiovascular risk factors.
The AHAH study was a population-based cross-sectional survey conducted between 1993 and 1994. The study population included 2507 men and women aged 35–84 years and resident within the Auckland region of New Zealand.
Age-stratified samples were randomly chosen from central Auckland general electoral rolls with a response rate of 72%. The investigators aimed to include 250 subjects from each 10-year age/sex category. For our purposes, data were reaggregated into 5-year age/sex categories.
Analyses excluded Maori and Pacific Island ethnic groups as the sampling frame did not include the Maori electoral roll and the general electoral rolls significantly under-represented the true proportions of Pacific and Maori peoples within the general population. A detailed account of AHAH study methodology is presented elsewhere.4
The proportion eligible for risk assessment was based as closely as possible to the New Zealand Guideline Criteria (Appendix 1). Data on personal history of gestational diabetes, polycystic ovarian syndrome, known impaired glucose tolerance or impaired fasting glycaemia, and waist circumference were not available. However these omissions are unlikely to add significantly to the number of eligible people.
Previous history of CVD in the AHAH study includes coronary heart disease and previous self-reported stroke—but not transient ischaemic attack, peripheral vascular disease, or previous coronary artery surgery. Coronary heart disease was determined by self-reported myocardial infarction, with hospital admission or angina defined as currently taking nitrate medication. The AHAH study did not collect any data on CVD ‘risk equivalents’ (genetic lipid disorders or diabetes with nephropathy).
The absolute CVD risk over a 5-year period for each individual was estimated using a risk prediction model based on the Framingham Heart Study.5 The model includes gender, age, systolic blood pressure, smoking, total cholesterol:high density lipoprotein (TC:HDL) ratio, diabetes, and interaction terms of age by gender, and diabetes by gender. A cardiovascular event is defined in the risk prediction model as a death related to coronary disease, non-fatal myocardial infarction, new angina, fatal or non-fatal stroke, or transient ischaemic attack—or the development of congestive heart failure or peripheral vascular disease.
Summary measures of risk categories (proportion over 20%, 15–20%, 10–15%, and less than 10% absolute CVD risk) were obtained for each 5-year age-gender group.
For the small number of people (1.5%) missing blood pressure or lipid data we calculated their absolute risk using the age/gender specific median value for that risk factor. Rate smoothing via moving averages was applied to better reflect the naturally occurring patterns within populations and all estimated counts were rounded.
To estimate the numbers of people meeting risk-assessment criteria (as defined in the guideline),3 we used:
Of the projected 2.09 million people aged over 35 years in New Zealand in 2005, approximately 1.5 million (72%) would meet national criteria for formal CVD risk assessment. Table 1 shows the proportion of New Zealanders over 35 years with prior CVD and the distribution of absolute CVD risk in those without prior CVD, by gender and 5-year age group for the estimated 2005 population.
Approximately 151,000 people (7%) have suffered a heart attack or stroke or have angina (or a combination of these). About 272,000 people (13%) are at high (CVD risk 15–20%) or very high (CVD risk over 20%) risk of a new CVD event in the next 5 years. Men are about three times as likely to be at high or very high risk than women (19% vs 7%). A further 10% of the total population over the age of 35 years are at moderate risk (CVD risk 10–15% in 5 years).
For each DHB catchment, aggregated estimates of CVD prevalence and CVD risk distributions are shown (Table 2). The proportion of people aged over 35 years meeting criteria for drug treatment (with prior CVD or an absolute CVD risk over 15% in 5 years) varies from 18.3% to 25.5% according to the demographic structure of the DHB.
Current New Zealand guidelines for the management of CVD risk are based on evidence demonstrating that the magnitude of benefit from treatment for an individual patient is directly proportional to their pre-treatment absolute CVD risk.6 Those who have had a prior CVD event and those at high risk of having a first event have the most to gain from identification and coordinated care. In appropriately targeted patients, the New Zealand guidelines suggest that 55% of future CVD events could be prevented.3 We estimate that 7 out of 10 New Zealanders over 35 years of age should have a baseline risk assessment; and of those risk-assessed people, 1 out of 5 would meet criteria for drug treatment.
Cardiovascular risk prediction based on the Framingham Heart Study5 is integral to the New Zealand cardiovascular risk assessment and management guidelines. The Framingham Heart Study was a cohort of mainly white Americans living in Massachusetts, USA in the 1970s and 1980s. The resultant cardiovascular risk prediction equation has been found to accurately predict on a population basis the 5-year risk of hospitalisation or death from a first cardiovascular event in New Zealand men aged 35 to 74 years and women aged 35 to 69 years.7
Extrapolating data collected over 10 years ago from 2507 Aucklanders to the New Zealand population in 2005 requires caution. However they are the only currently available data and are given as ‘ball park’ estimates only. Our findings may underestimate the true prevalence of CVD in New Zealand as they are based on a study that did not include Maori and Pacific people who have higher risk of CVD. Furthermore, these estimates do not include those who have had a sole diagnosis of other cardiovascular disease including transient ischaemic attack, acute coronary syndrome, percutaneous coronary intervention (PCI), or peripheral vascular disease. However, many people with these diagnoses will have other manifestations of atherosclerotic disease. For example, studies of patients presenting with intermittent claudication indicate that around 50% have evidence of coronary disease on clinical history and ECG,8,9 (and 90% have coronary disease angiographically10).
Nevertheless, the magnitude of the reported CVD risk burden is likely to be reasonable because the effect of excluding Maori and Pacific people, and some CVD diagnoses will be offset by declining secular trends in CVD morbidity and mortality over the previous 10 years.2
Despite the limitations of the data, this aggregate information is much needed by PHOs and DHBs to guide service planning and health care delivery particularly with new funding streams (for example the CarePlus programme) and requirements to fulfil key quality indicators for their population’s health. The major challenge for primary care is to systematically identify those people most at risk and to ensure they are appropriately managed. If this occurs, the potential to reduce this leading cause of mortality and morbidity in New Zealand, while also reducing disparities between ethnic and socioeconomic groups, will be substantial.
Author information: Susan Wells, Senior Lecturer – Clinical Epidemiology; Joanna Broad, Epidemiologist; Rod Jackson, Professor of Epidemiology; Section of Epidemiology and Biostatistics, School of Population Health, University of Auckland, Auckland
Acknowledgements: The Auckland Heart and Health Study was funded by the Health Research Council and the National Heart Foundation while Dr Wells is the recipient of a National Heart Foundation Research Fellowship. We also thank Elizabeth Robinson and Patricia Metcalf for their helpful comments and feedback.
Correspondence: Dr Susan Wells, Section of Epidemiology and Biostatistics, School of Population Health, University of Auckland, Private Bag 92019, Auckland 1. Fax: (09) 373 7494; email: email@example.com
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