Changing Patterns of Mortality in Australia

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Analysing mortality patterns from 1968 to 2017, focusing on the role played by cardiovascular diseases in the large reduction in mortality rates

Reference period
1968 - 2017
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Changing patterns of mortality in Australia

The release of the 2017 Causes of Death report marked half a century since 1968, the year that the heart disease epidemic in Australia reached its peak. In 1968, Ischaemic heart disease (IHD) accounted for almost one third of all deaths and half of those deaths were among people under 70 years of age.

After 1968 the death rate from IHD began to decline. Studies undertaken in response to the rapidly increasing mortality rates in the 1940s and 1950s began to highlight key risk factors and the earliest of interventions began to slow and reverse decades of increasing cardiovascular death rates.

Reductions in mortality over the past 50 years have seen life expectancy at birth increase by more than 10 years (increasing from 67.6 to 80.5 years for males, and from 74.2 to 84.6 years for females, when comparing 1965-67 with 2015-17 (ABS, 2014; ABS, 2018)). Over this period our understanding of diseases and ability to prevent and treat them has steadily grown.

This report examines changes in death rates over the past 50 years, focussing on cardiovascular diseases. It also provides information on advancements in understanding and treatment of cardiovascular diseases which have contributed to reductions in mortality and corresponding increases in life expectancy. Other key changes in patterns of mortality will be covered in subsequent releases.

Changes in leading causes of death

One of the simplest and most commonly used measures of mortality is the leading cause of death tabulation. The ABS bases leading cause tabulations on the Bulletin of the World Health Organization, Volume 84, Number 4, April 2006, 297-304. While there have been classification changes since 1968, correspondences have been used to construct a tabulation of leading causes for 1968 based on the same groups of conditions used in the present day. This is shown in the table below.

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The leading causes of death in 1968 were characterised by high numbers of IHD and cerebrovascular disease deaths. In 1968 these conditions accounted for nearly 49,000 deaths and 44.5% of all deaths. In 2017 these conditions accounted for only 17.9% of all deaths. IHD accounted for almost 10 times the number of deaths as the 3rd ranked condition (Chronic lower respiratory diseases), highlighting an order of magnitude difference between deaths from IHD and other common causes of death.

Aside from IHD and stroke, two other key differences in leading causes between 1968 and 2017 were the ranking of Land transport accidents (4th in 1968 compared with 28th in 2017) and Certain conditions originating in the perinatal period (9th in 1968 compared with 42nd in 2017). These changes highlight the long term and cumulative effects of progressive road safety policies and mechanical/manufacturing advancements, as well as the wide ranging educational, medical and scientific advances which have reduced perinatal mortality rates.

The below table shows the leading causes ranked according to their order in 2017. Seven of the top ten leading causes remain the same conditions as those in 1968, but despite this, differences are quite profound.

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In 2017, the decreased number and proportional contributions of IHD and stroke compared to 1968 are significant. However, as the remainder of this report will highlight, they provide only a small indication of the magnitude of change over time.

Another key difference between mortality in 2017 and 1968 is the emergence of Dementia, including Alzheimer disease, now the second leading cause. While increased life expectancy is the main reason for this increase, there are also death certification changes and classification changes which have contributed to the emergence of dementia as a leading cause.

Other changes in leading causes include the increased rank of Diabetes (7th in 2017 compared with 10th in 1968) and Malignant neoplasms of lymphoid, haematopoietic and related tissue (ranked 8th in 2017 compared with 14th in 1968).

While leading cause rankings give some indication of changes in patterns of mortality, other measures, such as standardised death rates, age-specific death rates, and years of potential life lost (as a measure of premature mortality), provide a more in-depth view of how changes have occurred across different population cohorts. The initial analysis in this report focuses on these measures for cardiovascular diseases, with other key changes in patterns of mortality to be covered in subsequent releases.

The graph below presents standardised death rates for the top 5 leading causes in 1968 alongside rates for 2017. It provides a further insight into the magnitude of the decrease in death rates for IHD and strokes by taking account of the change in the population size and structure over the 50-year period.

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While the magnitude of changes in cardiovascular disease mortality are the focus of this report, these changes do not indicate that IHD is less of a concern for individuals now than it was in 1968. Cardiovascular health is critically important for individuals, and while medical advances may have helped reduce mortality rates, especially among younger people, the maintenance of cardiovascular health can have a huge impact on both length and quality of life.

The Heart Foundation website ( provides a wealth of information and resources about cardiovascular diseases in Australia.



Fifty years of cardiovascular mortality

Cardiovascular diseases

Cardiovascular diseases are those which affect the heart and blood vessels. The most common form of heart disease is termed “ischaemic”, referring to reduced blood (and therefore oxygen) supply via the coronary arteries to the heart muscles themselves. Acute or sudden ischaemic heart disease (IHD) may lead to death of some heart muscle (myocardial infarction), commonly known as heart attack. Longer term IHD can result in poor pumping capacity (heart failure) or irregular heart actions. Other less common forms of heart disease result from inflammation in heart muscle, damage to the valves which direct the flow of blood, or the effects of high blood pressure.

The underlying cause of IHD is atherosclerosis, a build-up of fatty plaques in the walls of the coronary arteries that, over time, cause blood vessels to become narrowed or blocked. The factors which predispose to atherosclerosis are numerous, but include smoking, high blood pressure, high cholesterol, diabetes, poor diet and lack of exercise.

Another form of cardiovascular disease, cerebrovascular disease, describes the effects of interrupted circulation to the brain. Sudden changes due to blockage of blood vessels or leaking from damaged vessels (haemorrhage) cause strokes; long-term reduced circulation to the brain is also a recognised causative factor for dementia.

Collectively, all cardiovascular diseases (predominantly IHD and stroke) were the stated cause of 43,477 deaths (27.0% of total) in 2017. This was in contrast to the 60,930 deaths (55.6% of total) from these causes in 1968. The reduction in absolute and proportional numbers of cardiovascular deaths in persons aged under 75 years represents the single strongest driver of increased life expectancy between 1968 and 2017.

Changes in cardiovascular mortality

Ischaemic heart disease

IHD has been the leading cause of death in Australia for the past 50 years, and accounts for the majority of cardiovascular deaths. Although still remaining the leading of cause of death in 2017, the picture of IHD mortality in Australia has changed significantly over this time. Mortality from IHD was at its peak in Australia in 1968 with 33,411 deaths recorded, equating to a rate of 428.3 deaths per 100,000 population. This compares to 18,590 deaths from IHD in 2017, a mortality rate of 59.3 per 100,000 people (see graph below). The 86.2% decrease in the rate of death due to IHD highlights the success of medical interventions and medications to manage risk factors (e.g. cholesterol and hypertension), as well as public health campaigns aimed at promoting the importance of heart health.

Should the all-cause mortality rates for 1968 have persisted in 2017, there would have been 408,400 deaths from all causes, this being 254 per cent of the actual total. Over 247,500 additional Australians would have died, with IHD alone contributing approximately 109,000 (44.1%) of these additional deaths

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Acute and chronic heart diseases

Deaths from IHD are classified into sub types based on the duration, complications and consequences of the disease progression. Five major sub types of IHD are included in the International Classification of Diseases, Version 10 (ICD-10), with deaths specified using a single code from I20-I25. In general, these sub types help designate whether the IHD was acute or chronic in nature.

Acute manifestations of IHD are assigned to ICD-10 codes between I20-I24. When acute IHD occurs, there is sudden deterioration of blood flow in the coronary arteries which supply the heart muscles. If sufficiently severe or prolonged then death of heart muscle (myocardial infarction, or a “heart attack”) occurs. ICD-10 codes I21, I22 and I23 are used for these conditions. Less severe though still dangerous, obstructions in the coronary arteries may result in new or increased episodes of chest pain (unstable angina) together with other symptoms of compromised heart function. ICD codes I20 and I24 capture these conditions. When acute IHD is certified as being due to chronic IHD, the acute disease is assigned as the underlying cause of death for statistical purposes.

When chronic IHD is certified on a death certificate it is coded to I25 Chronic Ischaemic Heart Disease. A diagnosis of chronic IHD is based upon laboratory or clinical evidence of coronary atherosclerosis sufficient to reduce oxygen supply to heart muscle, without rapid progression to an acute coronary event. Stress tests, coronary angiograms, echo-cardiograms or a history of classical symptoms are the usual diagnostic measures. Stable angina, being episodes of typical chest pain on consistent levels of exertion and responsive to treatment, is the most common initial clinical feature. Chronic IHD can develop slowly or may follow an acute IHD episode which leaves heart damage. In the Australian setting, chronic IHD is a common cause of heart failure or irregular heart rhythms.

At the height of IHD mortality in Australia in 1968 approximately three quarters of IHD deaths were due to acute disease. Rapid reductions in mortality rates from acute IHD have resulted in chronic IHD deaths assuming increasing proportions of the total IHD deaths. From the late 2000s, chronic IHD such as coronary atherosclerosis accounted for the majority of total IHD deaths. In the last 5 years, 55.5% of IHD deaths have been certified as being due to chronic IHD. The graph below shows the proportional composition of IHD deaths over time and highlights the rapid decline of acute disease. The accompanying article, "Preventing Cardiovascular Deaths" details the success of primary, secondary and tertiary interventions in contributing to the reduction of acute IHD deaths in Australia over the last half century.

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Although the proportion of deaths due to chronic IHD have increased within the IHD group, the age-standardised mortality rates for both acute and chronic IHD have been falling progressively since 1968 (see graph below). The decline in mortality due to acute IHD has been particularly significant over the last 50 years falling 91.5% from a rate of 308.2 deaths per 100,000 people in 1968 to 26.2 in 2017. The decline in the mortality rate from acute IHD or heart attacks accounted for just over three-quarters (76.4%) of the decline in deaths from IHD and a third (33.1%) of the reduced mortality from all causes. With the majority of this decline occurring in persons aged under 75 years, the major contribution of these changes to increased life expectancy is evident.

Should the IHD mortality rates for 1968 have persisted in 2017, there would have been over 109,000 additional IHD deaths, with approximately 82,900 from acute IHD and 26,200 from chronic IHD.

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Age-profile of deaths due to IHD

In addition to the decreasing rate of mortality due to IHD, the median age of death for those who die from IHD has increased. In 2017, the median age at death for those who died of IHD was 85.0 years compared with 72.2 years in 1968. When looking at a cumulative frequency of deaths due to IHD in 2017 and 1968 the shift in age structure is significant (see graph below). The decline in premature mortality due to IHD is also evidenced by the decrease in number of years of life lost over time. Although the proportion of people who have died prematurely from IHD has reduced significantly over time, the average number of years of life lost is still high at 11.2 years in 2017 compared with 15.9 years in 1968 for those who died prematurely.

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Age specific mortality

The significant decrease in mortality due to IHD over the last fifty years has occurred across all age groups for both chronic and acute manifestations of the disease (see tables below). Declines for people aged under 75 years of age show the largest proportional decreases in mortality due to IHD. In 1968, approximately 59% of deaths occurred within age groups under 75. This is in contrast to 2017 where only one quarter of IHD deaths occur within these younger age groups.

Age-specific mortality for all cardiovascular diseases is presented in five year groupings. Age-specific death rates reflect deaths per 100,000 of the estimated resident population

Acute IHD age-specific mortality

Declines in mortality are most pronounced for acute IHD, and especially deaths due to myocardial infarction. Advancements in treatments of modifiable risk factors such as statins for cholesterol and anti-hypertensive medications, as well as reductions in adverse health behaviours such as cigarette smoking have all contributed to the declining rate of mortality due to IHD.

As well as greatly reduced numbers, deaths from acute IHD have involved progressively older Australians. In the period 1968-1972, 63.6% of all persons who died from acute IHD were under 75 years of age. The corresponding proportion in 2013-2017 was 22.4%. The table below shows the rates of acute IHD deaths are now up to 25 times lower within some age groups than rates recorded fifty years ago. The rates for those aged between 55-74 have significantly decreased compared with other age groups, with both recording rates over twenty times lower than half a century ago. Although those aged 85 years and over only recorded a rate 3.5 times lower than in 1968-1972, the rate difference is significant, at 2,472.2.

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Chronic IHD age-specific mortality

Death rates due to chronic IHD have also decreased across all age groups since 1968. Fifty years ago premature deaths were a substantial burden with 47.4% of chronic IHD mortality occurring before age 75. In comparison, only 28.2% of deaths occurred before age 75 in 2013-2017. While the scale of the reductions in these rates (rate ratios between 2.7 and 4.3) is much less than that for acute IHD, these represent very substantial changes.

The table below shows a decrease in age-specific rates across middle and older ages over the past half century. The rate decrease is stable across age groups with rate ratios ranging from 4.3 for those aged 65-74 years and 2.3 for those 85 years and over. Similar to acute IHD, the largest rate difference was in the 85 years and over age group at 1,432.9.

In addition to deaths coded directly as chronic IHD, an unknown but substantial proportion of deaths due to cardiac failure (ICD-10 code I50) or irregular rhythms (ICD-10 codes I44-I49) would be due to chronic IHD in the Australian population. Between 2013-2017 there were just over 5,000 deaths annually coded as cardiac failure or irregularity of heart rhythm.

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IHD mortality by sex

In 2017 males had a mortality rate from IHD at 1.8 times higher than that of females, with 78.7 deaths per 100,000 (for males) and 42.6 (for females) being recorded respectively. Although mortality rates for females are approaching half that of males, the proportional declines in death rates for IHD have been similar as shown in the graph below. The median age of males who die from IHD is 81.0 compared with 88.6 years for females.

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IHD mortality by state and territory

Decreases in mortality due to IHD have been mostly comparable across all states and territories across Australia, with death rates generally being around 5-6 times lower than half a century ago (excluding Northern Territory, see table below). The Australian Capital Territory (ACT) recorded the lowest IHD mortality over the last five years at an average of 53.9 deaths per 100,000 people, followed by Victoria at 61.7. Between 2015-2017 the ACT recorded the highest average life expectancy at birth for females at 85.2 years and Victoria the highest average for males at 81.3 years.

The Northern Territory (NT) had the lowest rate of IHD mortality in the early 1970s when compared to other Australian states and territories at 212.7 deaths per 100,000 people, but now has the highest rate at 90.3. The NT recorded the lowest average life expectancy at birth for both males and females between 2015-2017 (75.9 years and 79.4 years respectively) (ABS, 2018). 

The table below shows state and territory standardised death rates from 1973-2017. Due to the absence of state population estimates for 1970 (the mid-point year), rates are provided for the period 1973-1977 onwards.

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International trends in IHD

The change in IHD mortality and associated public health and medical improvements is a phenomenon which has been seen globally. When compared against other selected high income countries Australia has recorded the largest decrease in deaths due to IHD, with a reduction of almost 80%, and has the lowest rate of death, as seen in the graph below. Canada and the United Kingdom have both seen decreases of 75% in mortality rates due to IHD. Of the countries presented in the graph, the United States of America has the highest rate of IHD mortality and saw the lowest level of rate reduction over time. With the large decreases in IHD mortality in high income countries, over 80% of IHD deaths now occur in low and middle income countries, where trends are flat or even increasing in some regions (Finegold, Asaria & Francis, 2013).

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Cerebrovascular diseases (strokes)

The other major cause of cardiovascular death is cerebrovascular diseases, mostly stroke, resulting from blockages in blood vessels supplying the brain (ischaemic stroke) or leakage or rupture of a vessel (haemorrhagic stroke). While all the risk factors for IHD are also causative for stroke, hypertension is particularly important, especially for haemorrhagic strokes.

Mortality from strokes has also decreased significantly over the past 50 years (see graph below). In 1968 there were 15,363 deaths from stroke, compared with 10,186 in 2017, with corresponding death rates of 218.6 deaths per 100,000 persons in 1968, compared to 32.2 in 2017. Similar to IHD, this 85.3% reduction in the rate of death due to stroke illustrates the impact of various medical interventions and medications used to manage risk factors (e.g. hypertension), as well as public health campaigns aimed at promoting the importance of heart and circulatory health. If the 1968 age-specific mortality rates had persisted in 2017, there would have been 56,000 (84.6%) additional stroke deaths in 2017, and 18,400 additional deaths occurring in persons aged under 75.

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Age-specific mortality for cerebrovascular diseases

Similar to IHD, the proportion of premature mortality due to stroke has decreased over time. Between 1968-1972 42.8% of stroke deaths occurred before age 75 years. This compares to 16.6% of deaths occurring prematurely in 2013-2017. The proportional decline has been most marked in respect of haemorrhagic strokes in persons younger than 65 years of age.

Substantial changes in age-specific mortality from stroke have also occurred over the last fifty years, with the table below showing this decline for those 45 years of age and older. Rate decreases of more than 70% have occurred across all these age groups (declines in all ages other than 85 and over have been more than 85%). The largest decrease in stroke mortality is in the 65-74 year age group, with a rate 11.2 times lower in 2013-2017 than 1968-1972.

While the proportionate decrease in mortality rates is highest among the younger age cohorts, it is important to note that strokes most commonly affect the elderly. The table also shows higher death rates among those aged 85 and over compared to younger age cohorts (although both rates have declined). Although this is partly related to success in medical interventions and treatment, cerebrovascular incidences are closely related to dementia which has seen an increase over time.

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In 1968, cardiovascular diseases such as IHD and stroke had a very high impact on life expectancy, with IHD accounting for almost one-third of all deaths, and more than two in five deaths among people 45-64 years of age. IHD deaths were most commonly from acute events, mostly heart attacks, and the median age at death for IHD was 72.2 years of age.

Since 1968, deaths from both IHD and stroke have reduced in number and the average age at which people have died from these conditions has increased. In 2017, IHD deaths were more commonly due to chronic heart disease and the median age for IHD deaths had increased to 85.0 years of age. Despite this, heart disease is still the second highest contributor to premature mortality in Australia.

The decreases in age-specific mortality for acute IHD and stroke, especially among younger age cohorts, have contributed to a large scale shift in the pattern of mortality in Australia over the past 50 years. They have also contributed to Australia having one of the longest life expectancies of any country. For individuals, this increased life expectancy is positive, but it also highlights the importance of maintaining cardiovascular health for a longer time to be able to make the most of those extra years


Preventing cardiovascular deaths

The increase in life expectancy over the latter half of the twentieth century is largely related to the steep decline in deaths due to cardiovascular diseases, in particular acute ischaemic heart disease.

Changes in mortality rates over time link to either reduced incidence of an event or increased survivability from an event. Among cardiovascular diseases it is a combination of both. The World Health Organization’s Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) study attributed approximately two-thirds of the reduction to decreased incidence and one third to a reduction in case fatality (Tunstall-Pedoe, 1999).

More recent international studies have confirmed that reduced incidence and improved survivability have both contributed substantially to the declining mortality rates of cardiovascular diseases (Yeh et al., 2010). These studies indicate that both primary prevention (risk factor identification and reduction) and secondary prevention (medical treatment to reduce mortality of acute disease) have been key drivers of increased life expectancy over the last 50 years.

The figure below provides a timeline highlighting selected key events in primary and secondary cardiovascular prevention that would have contributed to reduced mortality and increased life expectancy, alongside the initially rising cardiovascular mortality rate and subsequent decline post-1968

Death rate from heart disease and major health interventions

Graph depicting death rates from heart disease and major health interventions from 1940 to 2017.
1948 - Framingham study starts 1956 - Mortality rate directly linked to smoking 1962 - Australia sets up coronary care units 1970-72 - Coronary bypass surgery used following heart attacks 1975 - Beta blockers used for hypertension 1984 - Framingham shows 50% increase in heart attack risk from previous 'safe' levels of hypertension 1984 - MONICA study starts in Australia 1989 - Statins shown to lower cholesterol 1990 - Statins and ACE-inhibitors available on PBS 2003 - Statins most prescribed drug on PBS (a) All causes of death data from 2006 onward are subject to a revisions process - once data for a reference year are 'final', they are no longer revised. Affected data in this table are: 2008-2014 (final), 2015 (revised), 2016-2017 (preliminary). See Methodology page 57-60 in Causes of Death, Australia, 2017 (cat. no. 3303.0); A More Timely Annual Collection: Changes to ABS Processes (Technical Note) and Causes of Death Revisions, 2013 Final Data (Technical Note) in Causes of Death, Australia, 2015 (cat. no. 3303.0). (b) See Methodology page 75-106 in Causes of Death, Australia, 2017 (cat. no. 3303.0) for further information on specific issues related to interpreting time-series and 2017 data. (c) The standardised death rates (SDRs) presented in this graph for 1940 to 1967 were taken from the General Record of Incidence of Mortality (GRIM) books, published by the Australian Institute of Health and Welfare (AIHW). The SDRs for 1968 to 2017 were calculated by the ABS, and differ slightly from those published in the GRIM books. This is due to a difference in the methodology used for calculating SDRs: the ABS prorates deaths for which the age was not stated across age groups, while SDRs presented in the GRIM books exclude deaths for which the age was not stated. This causes a small break in series for SDRs between 1967 and 1968. (d) The ICD undergoes periodic revisions by the World Health Organization to reflect changes in medical terminology, medical knowledge and death certification. Although large disease groups can be mapped between different versions of the ICD there may be slight differences in disease groupings between versions. ICD-8, ICD-9 and ICD-10 codes are included in this publication. (e) See the 'Population Estimates Used in Calculating Rates, 1968 to 2017' data downloads in this publication for information on the population estimates used in calculating rates.

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This article examines the main initiatives by which this huge improvement has been achieved, focusing on:

  • Risk factor identification and reduction (primary prevention)
  • Acute treatment for heart attacks (secondary prevention)
  • Ongoing management of diagnosed disease (tertiary prevention)

Risk factor identification and reduction (primary prevention)

At the end of World War II, almost nothing was understood of the predisposing risks for heart attacks and strokes while treatments for established disease were elementary. It was acknowledged in 1950 by the American Public Health Association that there was very little understanding of the epidemiology of hypertensive and atherosclerotic vascular diseases (Dawber, Meadors & Moore, 1951).

In an endeavour to generate good data to examine this matter, a longitudinal study of 6,000 volunteers who were “free of any detectable cardiovascular condition” was commenced in the town of Framingham, Massachusetts in 1948. The Framingham study serially recorded differences in lifestyle and health parameters between those who did and did not develop disease (Dawber et al., 1951).

Within a few years, data from Framingham (and other studies) were confirming that frequency of and mortality from heart attacks and strokes were associated with high blood pressure, tobacco smoking and high levels of circulating cholesterol (Mahmood, Levy, Vasan & Wang, 2014). In 1951, pioneering research in California identified the fractions of “good” and “bad” fats within cholesterol and the strong links between the latter and cardiovascular diseases (Gofman et al., 1956). It was noted that smoking amplified the risk of high cholesterol and high blood pressure (Castelli, 1984), and early studies in Australia showed declining incidence and up to 50% decline in age-specific mortality in association with reductions in cigarette smoking, systolic blood pressure, and cholesterol levels (Dobson, 1987).

Risk factors for heart disease are now well documented. The Heart Foundation outlines modifiable risk factors as smoking, high cholesterol, high blood pressure, diabetes, inactivity, obesity, unhealthy diet and depression and isolation. Unmodifiable risk factors include age, sex, ethnicity and family history of disease. Combinations of risk factors progressively increase the likelihood of a life-threatening cardiovascular event (Castelli, 1984; Lloyd-Jones et al., 2006; National Vascular Disease Prevention Alliance (NVDPA), 2012).

Although debate continues over the precise proportional contribution of these biological and behavioural risk factors to the reduction in cardiovascular mortality, there is consensus that risk factor reductions account for a large component of the overall decrease. In particular the protective values of controlling hypertension, high cholesterol and smoking are all strong (Lloyd-Jones et al., 2006; Yeh et al., 2010).

Hypertension (high blood pressure)

Blood pressure refers to the pressure of circulating blood within the artery walls. Systolic blood pressure refers to the maximum pressure inside the arteries when the heart is in active contraction (systole). Diastolic blood pressure measures the minimum pressure inside the arteries when the heart is relaxed between pulses or beats (diastole). The measurement of blood pressure is presented as systolic pressure over diastolic pressure and measured in millimetres of mercury, being the pressure exerted by the height of a mercury column in original measurement devices.

Data such as that published from the Framingham study in 1984 confirmed that persons with blood pressure in the range of 140-159 systolic and 90-94 diastolic had up to 50% increase in risk for heart attack and threefold increase in risk of stroke compared with persons with lower readings (Castelli, 1984). By 1990 it was shown that, regardless of the baseline blood pressure level, reductions in diastolic pressure in the order of 5-6 mm Hg were associated with 35-40% fewer strokes and 20-25% fewer coronary heart events (Collins et al., 1990). The Heart Foundation (2012) recommends treatment for blood pressure levels which are consistently at or above 140/90 with the aim of reduction to below 130/80.

The association between blood pressure and stroke is, in many situations, stronger than that for heart diseases. The increase in risk of disease events was calculated for a very large UK population of NHS patients, registered between 1997 and 2010 (Rapsomaniki et al., 2014). After extensive adjustment for other factors, increments of 20 mmHg in systolic pressure increased risk by 44% for intracerebral haemorrhage (a type of haemorrhagic stroke), 35% for ischaemic strokes, and 29% for heart attacks. The relative impacts were similar for a 10 mmHg increase in diastolic pressure, and all effects were most severe for persons under 60 years of age. A recent analysis of large randomised controlled trials showed that reductions in systolic pressure of 10 mmHg were associated with 27% reduced risk of stroke, 17% risk of coronary heart disease and 13% reduction in all-cause mortality (Ettehad et al., 2016).

Hypertension is one of the most commonly diagnosed conditions in general practice in Australia although often unsuspected by the patient. In the National Health Survey of 2014-15, 11.3% of respondents reported having hypertension but a much higher proportion (23%) had readings above 140/90 (ABS, 2015).

Treatment of hypertension (high blood pressure)

Since 1970, much more effective and patient-acceptable medications have progressively become available for the control of blood pressure. Prior to 1970, drugs which blocked the actions of the sympathetic nervous system or its chemical messengers were, in partnership with diuretic agents, the main weapons against hypertension. While often effective in lowering systolic pressure, there were often severe side effects, notably dizziness when standing, nausea, diarrhoea and impotence in some men. For these reasons, failure to comply with prescribed medication regimes was common. In 1975, beta-adrenergic blocking drugs and newer diuretics provided much more acceptable treatment (Moser, 2006).

After 1990, another class of medicines which act to oppose blood pressure raising chemicals originating from the kidney (renin and angiotensin) were approved by the Pharmaceutical Benefits Scheme (PBS). Over the next ten years the rate of use of these agents (ACE-Inhibitors) in the management of hypertension tripled, while the use of most older anti-hypertensive drugs, such as beta-blockers, remained relatively stable (Commonwealth Department of Health & Aged Care, 1999). Further developments have improved the effectiveness of this class of medicines. ACE-inhibitors were the second most commonly taken prescribed drug class in 2015 (Mabott & Storey, 2016). Further improvements in existing classes of medicines and developments of new therapeutic tools, including targeted gene therapies are constantly being advanced, with high prospects for better patient outcomes (Israili, Hernandez-Hernandez & Valasco, 2007).

While medical treatments have become increasingly effective, there is also increasing emphasis upon lifestyle factors in the prevention or control of hypertension. Weight reduction, regular exercise and limits to salt and alcohol intake now comprise the recommended baseline upon which medications are added if necessary (Heart Foundation, 2016).

Cholesterol and other blood lipids

Cholesterol is a lipid (fat-like substance) which circulates in the blood. Cholesterol is both produced by the liver naturally to build cells and is also found in many foods. Cholesterol is categorised as “good” (high density lipoprotein, HDL), and “bad” (low density lipoprotein, LDL). The density refers to the amount of fat in the lipoprotein, with low density lipids containing more fat. LDL excess in the blood is the main cause of build-up of cholesterol and artery blockage.

Pioneering laboratory work to identify and classify the various fractions of lipids circulating in plasma was published in 1950 by Gofman and colleagues from the University of California (Gofman et al., 1950). This was closely followed by data which aligned concentrations of cholesterol and the fraction later designated as LDL as directly and positively predictive of clinical complications of atherosclerosis-heart attacks and strokes (Gofman et al., 1956). One of the earliest confirmed and strongest risk-factor combinations has been that between increasing levels of smoking and increasing cholesterol concentrations (Dawber, Moore & Mann, 1957). A huge volume of research data has since confirmed this association, and the intake of dietary fat, as well as genetic factors has been confirmed as related to, if not directly causative of, abnormal lipid levels (Law, Wald & Rudnika, 2003).

Treatment of cholesterol and other blood lipids

Measures to control cholesterol were initially confined almost entirely to reduction of dietary fats. Nicotinic acid and various fibre preparations were also prescribed but without any marked success (Dwyer & Hetzel, 1980). In 1989 the first reports of the effectiveness of statins in lowering cholesterol levels and the more pathogenic LDL were published in Australasia (Lintott et al.,1989). In the following year the first of these agents was made available on the PBS. Further developments of statins have produced higher effectiveness and greater patient acceptability. Statins now rank among the five most commonly prescribed agents on the Australian PBS being taken by more than 30% of Australians aged 50 years or older (Schaffer, Buckley, Dobbins, Banks & Pearson, 2016).

For patients in whom acceptable levels of LDL cannot be achieved, treatment with targeted antibodies such as PCSK9 and a number of other agents have been shown to have additional effectiveness, although definite additional reductions in cardiac or all-cause mortality have not been fully proven (Lloyd-Jones et al., 2016; Hess et al., 2018). Concerns that persistent or excessive lowering of cholesterol may increase risks for dementia, haemorrhagic strokes or cataracts have been discounted by recent systematic reviews and trials in large populations (Mach et al., 2018) although caution is advised for patients aged over 75 years and those on blood-thinning treatment in addition to statins (NVDPA, 2012).

Despite continued education programs and more effective medication, approximately one-third of adult Australians continue to have levels of total cholesterol, and particularly LDL, above desired limits: for persons aged 55-64 years the proportion was 47.8% in 2011-12 (ABS, 2013). Continued and increased efforts to promote good habits of diet and activity, and patient-targeted medications provide potential for further improvement.


Tobacco smoke contains a complex mix of chemicals, many of which have harmful impacts on the blood vessels and their regulation. These include acceleration of structural damage to vessel walls, increased reactivity of small vessels and increases in factors which enhance blood clotting (Ambrose & Barua, 2004).

While the initial recognition of health hazards from tobacco focussed on lung cancer and chronic lung disease, the impacts upon the circulation were progressively recognised from 1940 and well documented by 1960. Although the early results from the Framingham studies failed to prove a definite relationship this was soon rectified. By 1958 the American Heart Association was able to report that heavy smoking was associated with a 50-150% increase in mortality from heart attacks, while also pointing out that this did not prove any causative role for tobacco (Katz, Allen, Cherkovsky, Davis & Dawber, 1960).

Serial surveys from 1964 to 2014-15 have reported decreases in rates of smoking for Australians adults from 58% to 16.9% for males and from 28% to 12.1% for females (Woodward, 1984; ABS, 2015). In 2014, 10% of secondary school students aged 16-17 were smokers, and fewer than 4% of younger students. These values were one-third or less of reported rates from 30 years prior (White & Williams, 2015).

Australia has a long history of strong anti-smoking advocacy and public health strategies targeted at raising awareness of the negative health effects of smoking and consequentially reducing smoking rates (Chapman, Byrne & Carter, 2003). Voluntary limits on advertising were introduced in 1966, made mandatory with regard to television in 1976 and limited to all but point-of-sale promotion in 1992. Promotion of sporting activities by tobacco companies was especially targeted (Scollo & Winstanley, 2012).

National tobacco campaign

Acute treatment for heart attacks (secondary prevention)

In addition to successful treatment of cardiovascular risk factors, major advancements in medical and surgical interventions have contributed to improved survivability from cardiovascular conditions. Early cardiac surgeries, such as those performed by Sir Benjamin Edye in Australia in 1943 on people with patent ductus arteriosus (a type of congenital heart disease), were widely celebrated when ten of fourteen patients survived. In 2015-16, the common nature of cardiac surgery is highlighted by the fact that approaching 1 in 10 (8.2%) of the 556,638 hospitalisations for cardiovascular diseases involved a surgical procedure (AIHW, 2018).

The first coronary care units were established in America in 1962. In Australia at that time, continuous monitoring by electrocardiograph of heart attack patients had commenced in Sydney Hospital and other centres, as had use of dedicated hospital areas with specialist staff (Julian, 2001). In-hospital mortality rates following acute heart attack at that time were 30-40% (Killip & Kimball, 1967; Goble, Sloman & Robinson, 1966). Risk factors for late arrhythmias and cardiac arrest (at > 7 days after onset of heart attack) were being recognised and addressed (Thompson & Sloman, 1971). In the period 1975-84 in-hospital fatality rates in the range of 15-17% were being reported and by 1995 were lower again in the order of 12%. The age-adjusted risk of dying during the initial hospital admission had more than halved in this 20-year period. Adjusted rates of survival to one year after discharge from hospital had also improved by 50% between 1975 and 1995 (Goldberg et al, 1999).

Surgical interventions to re-establish blood flow in blocked coronary arteries were also being trialled and established. The first coronary bypass operations were performed in 1964 on patients with symptoms of coronary disease with a view (largely successful in the short-term) to forestalling heart attack. By 1970, bypass surgery and mechanical circulation support were also being performed on high risk patients following heart attacks, including some with incipient or established shock, with a desperately bad outlook for survival (Mundith, Buckley, Daggett, Sanders & Austen, 1972). Of the first 30 such patients operated upon at St Vincent's Hospital Sydney in 1971-72, 14 survived to leave hospital (O'Rourke et al., 1975).

In addition to successful treatment of cardiovascular risk factors, major advancements in medical and surgical interventions have contributed to improved survivability from cardiovascular conditions. Additional developments to restore coronary artery blood flow, by inflation of balloons or by inserting sleeves (stents) into the blocked arteries have had increasing success. At the same time, improvements in medications to control heart rhythms, to dissolve or prevent reformation of blood clots and to manage complications such as heart failure, have helped to reduce short-term mortality of heart attacks. The in-hospital fatality rate is now less than 5% in a high proportion of American hospitals (Kontos et al., 2014). The Australian 30-day mortality rate in 2014 was 4.0 % (males 3.9 %, females 4.2 %) based on unlinked admission data (Organization for Economic Co-operation and Development (OECD), 2016) and this was the third lowest of OECD countries after Denmark and Norway.

Ongoing management of diagnosed disease (tertiary prevention)

Continuation of treatment beyond hospital discharge has additionally resulted in improvements in long-term survival after heart attack. Additional studies with the MONICA patient cohort in Perth have demonstrated the effectiveness of specific medical and surgical treatments to the long-term survival of patients after heart attacks. Among 28-day survivors in the Perth MONICA study, the mortality from heart attack in the subsequent 12 years fell from 21% to under 14% between 1984 and 1993 (Briffa et al., 2009). In addition, a range of validated medications and surgical interventions in selected patients is now incorporated into best-practice guidelines for ongoing care of heart attack survivors (NVDPA, 2012).

Future opportunities

Medical and scientific advancements have been major contributors to the decline in cardiovascular mortality over the past 50 years, yet many of these advancement have only been possible because of the insights provided by good quality data. As patterns of mortality change, and especially as people live longer lives, the importance of adapting data to this changed circumstance is also important. For instance, over 30% of cardiovascular disease deaths have one or more risk factor, such as diabetes, smoking, hypertension, high cholesterol or obesity recorded by the certifying doctor as contributing to the death, yet this information on co-morbidities is not reflected in data based solely on underlying cause.

The absolute and relative decline in mortality rates from cardiovascular diseases have slowed in the last decade (O'Flaherty et al., 2012; AIHW, 2017), and IHD remains the second leading cause of premature death in Australia. More advanced datasets that provide insights into multiple co-morbidities and the prevalence of risk factors relating to cardiovascular deaths, may assist future policy and research and help reduce future mortality rates. The ABS is working with partners to advance this work and will make results available as progress is made


Data downloads

1. Age-standardised death rates, cardiovascular diseases,1968 to 2017

2. Age-specific death rates, cardiovascular diseases, 1968-1972 to 2013-2017

3. Population estimates used in calculating rates, 1968 to 2017

Previous catalogue number

This release previously used catalogue number 3303.0.55.003

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