National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people


Chapter 11: Cardiovascular disease prevention
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☰ Table of contents


Recommendations for people without an established diagnosis of cardiovascular disease

Preventive intervention type

Who is at risk?

What should be done?

How often?

Level/ strength of evidence

References

Screening

People aged 30–74 years in communities where local risk factor prevalence rates and CVD incidence rates are high (eg remote areas) When using the FRE, consider adding 5% to the calculated five-year CVD risk score As part of a health assessment and review according to level of risk (refer below) GPP 29, 31
People aged 30–74 years There is insufficient evidence to recommend routine CVD risk screening with additional tests such as coronary artery calcium scores, C-reactive protein, Ankle Brachial Pressure Index (ABPI), 24-hour ambulatory BP monitoring. Such tests may have some use in people identified at intermediate risk, and the decision to conduct these tests should be based on clinical judgement§   IA 23, 24, 2,5 26, 27

Behavioural

People with low absolute five-year CVD risk (<10%) Advise lifestyle risk reduction as needed for the following (refer to Chapter 1: Lifestyle):
  • physical activity
  • weight loss
  • smoking cessation
  • salt reduction to less than 4 gm salt/ day (1600 mg sodium/day)
  • diet rich in fruit and vegetables, whole grain cereals, nuts and seeds, legumes, fish, lean meat, poultry, low-fat dairy products, and limiting saturated and trans fat intake
  • limit alcohol intake to ≤2 standard drinks/day
Review risk every two years IA 13–5, 1820, 30, 31
  People with the following:
  • absolute fiveyear CVD risk moderate or high (≥10%)
  • presence of any clinically high-risk conditions (Box 2)
Advise lifestyle risk reduction as above

Provide intensive intervention support (refer to Chapter 1: Lifestyle)
Review according to clinical context IB 13–15, 18, 20, 30, 31

Chemo-prophylaxis

People at low absolute risk:
<10% five-year CVD risk and with BP persistently ≥160/100 mmHg
Consider commencing a BP-lowering medication unless contraindicated Review according to clinical context GPP 10, 30, 33
People at moderate absolute CVD risk:
10–15% five-year CVD risk
Review individual risk factor profile (in particular, sub-optimal BP and lipids levels) and recommend commencing BP-lowering treatment and/or lipid-lowering medication unless contraindicatedII Review according to clinical context IB 1011, 15–18, 20, 30, 31
People at high absolute CVD risk:
>15% five-year CVD risk or presence of any clinically high-risk conditions (Box 2)
 
Recommend commencing both a BPlowering medication and lipid-lowering medication regardless of risk factor levels unless contraindicatedII Review according to clinical context IB 1011, 15–18, 20, 30, 31
Aspirin is not routinely recommended for primary prevention of CVD#   IB 20
Patients with atrial fibrillation (AF) without prior CVD Determine the cause of AF and manage rate and rhythm control. Assess and manage CVD risk as above. Consider oral anticoagulant treatment if:
  • valvular heart disease is present or
  • a CHA2DS2-VASc score of ≥2 (Box 3) is present and
  • risk of bleeding is low

 

IA 34, 35
*Although absolute CVD risk assessment using the FRE is currently not validated for people aged <30 years, a multifactorial assessment of CVD risk factors is still recommended to guide management decisions. Treatment on the basis of elevated single risk factors may still be appropriate depending on the clinical context.
Although the FRE is validated for people aged 30–74 years, the Australian absolute risk charts start from age 35 years. Some calculators embedded in clinical software and the CARPA charts (refer below) can be used to assess risk in those aged 30–34 years.

It is important to distinguish between absolute and relative risk increase. While the absolute risk remains constant at 5%, the relative risk increase will vary depending on the baseline risk. For example, if the initial risk estimate is 5%, an absolute increase of 5% equates to a 100% relative risk increase. If the initial risk estimate is 10%, an absolute increase of 5% equates to a relative risk increase of 50%. If the initial risk estimate is 15%, an absolute increase of 5% equates to a relative risk increase of 33%.

§At the time of writing, there are no Medicare Benefits Schedule rebates for coronary artery calcium scores, highly sensitive C-reactive protein, or 24-hour ambulatory BP monitoring.

IISpecific choice of BP and lipid-lowering agents and guidelines on treatment targets is beyond the scope of this guideline. In general, however, low-dose dual BP therapy is preferred as first-line therapy because treatment effects are at least as beneficial and tolerance is greater than when using higher dose single-agent treatment. Refer to ‘Resources’ for links to specific management guidelines. If BP or lipid levels are extreme or non-responsive to treatment, further investigation for underlying causes is recommended.

#The US Preventive Services Task Force makes a level IB recommendation for the use of aspirin in people aged 50–59 years at moderate to high CVD risk for the primary prevention of CVD and colon cancer if there is no increased risk of bleeding.36 This is not currently recommended in Australian guidelines, and clinical judgement is recommended in making decisions for aspirin use. Further trials are currently underway to more comprehensively understand the risks and benefits of aspirin in primary CVD and cancer prevention (refer also to Chapter 15: Prevention and early detection of cancer).

Recommendations for people with an established diagnosis of cardiovascular disease

Preventive intervention type

Who is at risk?

What should be done?

How often?

Level/ strength of evidence

References

Screening

People with CVD Calculation of the absolute CVD risk using the FRE is not recommended. Five-year risk of a subsequent CVD event is assumed to be high      

Behavioural

People with CVD
 
Intensive lifestyle risk factor management as for patients without an established diagnosis of CVD (refer to ‘Recommendations for people without an established diagnosis of cardiovascular disease [CVD]’) Review at every visit IB 37,38
A tailored cardiac rehabilitation program should be offered to all people post– myocardial infarction and other acute coronary syndromes, and to those who have undergone re-vascularisation procedures Post-CVD event IA 39

Chemo-prophylaxis

People with CVD

 
Commence blood pressure (BP)-lowering treatment if systolic BP is >120–130 mmHg unless contraindicated by symptomatic hypotension* Lifelong IA 38, 40
Commence lipid-lowering treatment with a statin at any cholesterol level unless contraindicated* Lifelong IA 38, 41
Commence low-dose aspirin treatment (75– 150 mg) unless contraindicated. Consider alternative antiplatelet agents such as clopidogrel (75 mg) if aspirin hypersensitivity is present 

For people with ischaemic stroke combination, aspirin/dipyridamole may also be considered
Lifelong IA 38, 4243
People with recent acute coronary heart disease Recommend dual antiplatelet therapy (clopidogrel or ticagrelor) in combination with aspirin For 12 months IA 38, 4243
People with stroke/ transient ischaemic attack Oral anticoagulant treatment is recommended if atrial fibrillation or cardio-embolic stroke is present unless contraindicated. Consultation of specific management guidelines is recommended (refer to ‘Resources’) Lifelong IA 34, 35, 38
*Specific choice of BP and lipid-lowering agents and guidelines on treatment targets is beyond the scope of this guideline. Refer to ‘Resources’ for links to specific management guidelines. If BP or lipid levels are extreme or non-responsive to treatment, further investigation for underlying causes is recommended.

 

 

Box 1. Commonly used international risk prediction equations13

 

Framingham

SCORE

ASSIGNSCORE

QRISK 1 and QRISK2

Pooled cohort studies equations

Data

Prospective studies:

Framingham

Heart Study and Framingham offspring study

12 pooled prospective studies

SHHEC

Prospective study

QRESEARCH database

Four pooled prospective studies:

  • ARIC
  • CHS
  • CARDIA
  • Framingham (original and offspring studies)

Population

General population,

Framingham,

Massachusetts, USA; baselines: 1968– 1971, 1971–75, 1984–87

12 prospective studies from 11 European countries; baselines: 1972–91

Random sample from general population in Scotland; baseline: 1984–87

Data collected from 1993–2008 from GP databases – imputation of missing data

Baselines 1987–89

(ARIC), 1990 and

1992–93 (CHS),

1985–86 (CARDIA),

1968–1971,

1971–75, 1984–87 (Framingham)

Sample size

3969 men and 4522 women

117,098 men and 88,080 women

6540 men and 6757 women

1.28 million (QRISK1)

2.29 million (QRISK2)

11,240 white women, 9098 white men, 2641 African-American women and 1647 African-American men

Calculates

10-year risk of CAD event; later versions 10-year risk of CVD event

(New Zealand and Australia derived 5-year risk)

10-year risk of CVD mortality

10-year risk of CVD events

10-year risk of CVD events

Lifetime risk

10-year risk for a first atherosclerotic CVD event

Lifetime risk

Age range (years)

30–75

40–65

30–74

35–74

20–79

Variables

Sex, age, total cholesterol, HDL-C, SBP, smoking status, DM, hypertensive treatment

Sex, age, total cholesterol or total cholesterol/ HDL-C ratio, SBP, smoking status. Versions for use in high and low-risk countries

Sex, age, total cholesterol, HDL-C, SBP, smoking – no. cigs, DM, area based index of deprivation, family history

QRISK1 – sex, age, total cholesterol to HDL-C ratio, SBP, smoking status, DM, area based index of deprivation, family history, BMI, BP treatment, ethnicity and chronic diseases

Age, sex, race (white or other/African American), total cholesterol, HDL-C, SBP, antihypertensive treatment, DM, smoking

Guidelines recommending its use

NCEP guidelines, Canadian CV guidelines, other national guidelines recommend adapted versions, including New Zealand

European SIGN Guidelines on CVD Prevention

SIGN

NICE guidelines on lipid modification

QRISK Lifetime risk recommended by JBS3 guidelines

2013 AHA ACC Guideline on the assessment of CVD risk

ACC, American College of Cardiology; AHA, American Heart Association; ARIC, Atherosclerosis Risk in Communities; ATP, Adult Treatment Panel; BMI, body mass index; BP, blood pressure; CAD, coronary artery disease; CARDIA, Coronary Artery Risk Development in Young Adults; CHS, Cardiovascular Health Study; CVD, cardiovascular disease; DM, diabetes mellitus; HDL-C, high-density lipoprotein cholesterol; JBS, Joint British Societies; LDL-C, low-density lipoprotein cholesterol; NCEP, National Cholesterol Education Program; NICE, National Institute for Health and Care Excellence; no. cigs, number of cigarettes; PROCAM, Prospective Cardiovascular Munster Study; SBP, systolic blood pressure; SIGN, Scottish Intercollegiate Guidelines Network; SHHEC, Scottish Heart Health Extended Cohort

Source: Extracted with permission from Piepoli MF, Hoes AW, Agewall S, et al. 2016 European Guidelines on cardiovascular disease prevention in clinical practice. The Sixth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of 10 societies and by invited experts) developed with the special contribution of the European Association for Cardiovascular Prevention & Rehabilitation (EACPR). Eur Heart J 2016;37(29):2315–81; Table 2.

Box 2. Framingham and non-Framingham cardiovascular disease (CVD) risk factors

Framingham Risk Equation factors*†19

Non-Framingham Risk Equation factors§20

Clinically high-risk conditions20

  • Age
  • Gender
  • Smoking status
  • Systolic blood pressure
  • Total cholesterol
  • HDL cholesterol
  • Diabetes status
  • Left ventricular hypertrophy (LVH)
  • Obesity (BMI >30 kg/m2 and/or waist circumference >102 cm men, >88 cm women)
  • Family history of CVD before age 55 years in a mother, father or sibling
  • Presence of albuminuriaII
  • Atrial fibrillation
  • Impaired fasting glucose ≥6.1 mmol and <7.0 mmol or glucose intolerance (twohour glucose ≥7.8 mmol and ≤11.0 mmol)
  • Socioeconomic hardship
  • Depression/other psychosocial stress
  • Excessive alcohol intake
  • Extreme risk factor elevations (SBP ≥180 or DBP ≥110, total cholesterol >7.5 mmol/L)
  • Type 2 diabetes and aged
  • >60 years
  • Type 2 diabetes and albuminuriaII
  • Moderate to severe chronic kidney disease (eGFR <45 ml/min/1.73 m2 or persistent proteinuria)
  • Familial hypercholesterolaemia

BMI, body mass index; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate; SBP, systolic blood pressure

*The 1991 Framingham Risk Equation (FRE) is intended for people without CVD. The most recently recorded pre-treatment measures for BP or lipids should be used to estimate CVD risk in people already receiving treatment. Where this is not possible, clinicians should make decisions on use of pharmacotherapy based on discussions with the patient and consideration of the individual context.

It is preferable to assess for LVH on the basis of echocardiography criteria rather than via an electrocardiogram.

A reasonable estimation of risk can be obtained from a non-fasting lipid sample in most circumstances.

§There are many additional risk factors that are independently associated with increased CVD risk, such as C-reactive protein, coronary calcium scores, and plasma homocysteine levels. Measurement of such factors can be costly and invasive, and there is limited evidence to suggest that assessment of these risk factors substantially improves risk prediction over those listed in Box 1. IIAlbuminuria is defined as an albumin excretion rate >20 mcg/min or urinary albumin to creatinine ratio >2.5 mg/mmol in males and >3.5 mg/mmol in females.

Box 3. Stroke risk assessment in people with atrial fibrillation*

Risk factors

Score

Congestive heart failure

1

Hypertension

1

Age ≥75 years

2

Age 65–74 years

1

Diabetes mellitus

1

Stroke/transient ischaemic attack/thromboembolism

2

Vascular disease

1

Sex female

1

*Consider oral anticoagluant treatment when total CHA2DS2-VASc score ≥2. Calculators are also available to assess harms from bleeding (refer to ‘Resources’).


Background


In this chapter, ‘cardiovascular disease’ (CVD) is a collective term that includes coronary heart disease, stroke and transient ischaemic attacks and peripheral vascular disease. Despite improving trends, CVD remains Australia’s biggest killer, accounting for 16% of the total disease burden, and is a major driver of national health system expenditure.1 Aboriginal and Torres Strait Islander peoples experience around five times greater vascular disease burden than other Australians.2–4 This vascular disease burden rises sharply from early adulthood. Although declining overall, mortality rates from coronary heart disease for Aboriginal and Torres Strait Islander people aged >25 years are twice as high as for the general population, and for those aged 40–54 years it is seven times higher than for the general population.2–4 CVD is the biggest contributor to the disease burden gap between Aboriginal and Torres Strait Islander peoples and non-
Indigenous people in Australia.3,5

Based on the Australian Aboriginal and Torres Strait Islander Health Survey (AATSIHS), approximately one in eight (13%) of Aboriginal and Torres Strait Islander people aged >2 years reported heart and/or circulatory diseases (including elevated blood pressure [BP]) in 2012–13.6 Over three successive surveys since 2000, the prevalence of self-reported heart and circulatory disorders has been rising in remote areas compared to non-remote areas (18% versus 11% in 2012–13).6 The 2012–13 National Aboriginal and Torres Strait Islander Health Measures Survey (NATSIHMS) is a sub-component of the overall AATSIHS, and includes nationally representative data for biomedical and physical measurements for 3293 people aged ≥18 years.7 It found that 65% of people had at least one risk factor for CVD, 18% had signs of chronic kidney disease (CKD) based on the presence of albuminuria and/or reduced estimated glomerular filtration rates (eGFR), and 11.1% had diabetes based on either a current diagnosis or a new diagnosis based in turn on biomedical test results.7 Targeting the risk factors associated with these conditions represents the ‘best buy’ in terms of preventive health opportunities. Reductions in the prevalence of seven risk factors (tobacco smoking, high body mass, physical inactivity, high blood cholesterol, excessive alcohol intake, high BP, low fruit and vegetable intake) are the most effective prevention strategies in closing the vascular disease burden gap for Aboriginal and Torres
Strait Islander peoples.3,4


Absolute risk approach to CVD prevention


Estimating the risk of CVD events requires simultaneous assessment of several risk factors. Based on largescale epidemiological studies, there has been a fundamental shift away from screening and managing single risk factor abnormalities (eg hypertension or hypercholesterolaemia, in which arbitrary cut-points are used for defining presence or absence of a condition) toward a global assessment of multiple risk factors to determine a person’s overall or ‘absolute’ risk of experiencing a cardiovascular event. This approach provides greater ability to predict who is at greatest risk of a first CVD event than the traditional single risk factor approach.8–11 Another important advantage of this approach is the ability to make accurate, treatment-relevant classifications of risk, thus focusing risk reduction efforts on the people who are most likely to benefit, while avoiding treatment for those likely to receive little risk reduction benefit.12

 

International evidence on CVD risk estimation


Several authoritative guidelines recently published have addressed the issue of CVD risk prediction for primary prevention.13–18 All of these guidelines are highly consistent in recommending an approach based on absolute risk, usually combined with recommendations for management of single risk factors at the extremes. The methods to estimate risk and the thresholds for defining high risk vary greatly. Box 1 provides a summary of the equations most commonly used internationally. Generally, these equations tend to perform similarly, particularly when the population to which they are applied is similar to that from whom the equations were derived. This issue is particularly important for Australia, as there are currently no Aboriginal and Torres Strait Islander population-specific risk prediction equations. Although research is underway to address this limitation, the 2012 National Vascular Disease Prevention Alliance (NVDPA) and the 2016 National Heart Foundation guidelines currently recommend the 1991 Anderson Framingham Risk Equation (FRE) for risk estimation in Australia.19,20 This equation should only be applied for people without established CVD. Although it outperforms single risk factor approaches, there are some limitations in its application to Aboriginal and Torres Strait Islander populations:

  • The FRE is validated for the age range 30–74 years only.
  • It may underestimate risk in populations where local risk factor prevalence rates and CVD incidence exceed that of the original Framingham cohort.
  • In areas where there is a high prevalence of additional risk factors that are not part of the FRE but are known to be independently associated with CVD, risk may be underestimated.

Non-FRE risk factors of known high prevalence in Aboriginal and Torres Strait Islander communities include family history of premature CVD, elevated body mass index (BMI), markers of CKD, socioeconomic hardship, depression and psychosocial stress, and impaired fasting glucose.7 Studies from the Tiwi Islands21 and North Queensland have demonstrated that the relative risk underestimate of FRE may be as great as 30%.22
Further, literature reviews conducted by the NVDPA have identified several clinical conditions that, if present, confer a high degree of risk regardless of the risk estimate using the FRE. Box 2 lists the FRE risk factors, additional risk factors for CVD that do not feature in the FRE, and a list of clinically high risk conditions for which absolute risk calculation can be assumed to be high.20

 

The role of additional tests in assessment of CVD risk


In addition to the FRE and non-FRE risk factors, a large number of tests have been proposed to further refine cardiovascular risk assessment. Most of these tests are not rebated under the Medicare Benefits Schedule (MBS) and are not routinely recommended for CVD risk screening.23 They may have a limited role in guiding management decisions for people at moderate CVD risk in primary prevention, but they should never be used in secondary prevention as all therapies are indicated irrespective of the results. Some of the most commonly mentioned tests are summarised below.

Coronary artery calcification (CAC) scores: Measurement of CAC using multi-detector computed tomography (CT) scanning uses a low dose of radiation to examine calcium content in artery walls, which is correlated with burden of atheroma. It does not directly measure artery obstruction (CT coronary angiography attempts to do this, but at much higher radiation doses and uses intravenous contrast), and can miss significant non-calcific atheroma. There is no evidence to justify routine screening with this test at present.24 The Cardiac Society of Australia and New Zealand has suggested there may be a role for this test in guiding treatment decisions for people at intermediate risk, where a high CAC score may reclassify someone to a higher risk status, while a zero or low CAC score indicates low probability of disease.24

Ankle Brachial Pressure Index (ABPI): ABPI is a measure of the relative pressures in lower and upper limbs, with a ratio of <0.9 being diagnostic of peripheral artery disease. High readings of >1.4 are also of potential concern as they are often associated with calcified, non-compressible arteries observed in peripheral artery disease. Although the presence of peripheral artery disease is significantly correlated with coronary and cerebrovascular disease, there is currently insufficient evidence to recommend routine population screening.25 If, however, this test is performed for clinical reasons and shows an abnormal ABPI, this should trigger a plan for lowering all reversible CVD risk factors, taking the same approach as for people identified at high CVD risk.

High-sensitivity C-reactive protein (hsCRP): C-reactive protein (CRP) is a non-specific inflammatory marker produced mainly by the liver in response to inflammatory cytokines. In the absence of acute inflammation, the levels in healthy persons are below the usual test thresholds of about 3 mg/L, so an hsCRP test is used, which has a detection limit around 0.3 mg/L, which is necessary for CVD risk stratification. Although many epidemiological studies show a correlation between CRP levels and risk of first or recurrent cardiovascular events, a meta-analysis has shown that measurement of hsCRP in addition to standard risk scoring would result in the prevention of one CVD event over 10 years for every 400–500 people screened, which makes this test difficult to justify as a standard screening test.26

Twenty-four–hour ambulatory BP: Ambulatory BP monitoring involves measuring BP at regular intervals over a 24-hour period while patients undergo normal daily activities, including sleep. Ambulatory BP measurement may be a useful method for diagnosing ‘white coat’ BP elevation, identifying ‘masked’ BP elevations that are not apparent on clinic measurements, and for treatment monitoring. It does not, however, play a major role in the assessment of CVD risk.27 Risk prediction equations are generally derived using officebased readings, and although ambulatory readings tend to be around 5 mmHg lower than clinic measures, this tends not to make a substantial difference to overall risk estimates given BP is just one of many risk factors used to assess risk.


Absolute CVD risk profile in Aboriginal and Torres Strait Islander communities


Using data from the NATSIHMS, the absolute risk profile for Aboriginal and Torres Strait Islander communities has recently been estimated using the NVDPA approach. It found that 9.6% of the sample aged 35–74 years with available data had prior CVD, and a further 15.7% were at high risk of CVD. Importantly, 1.1% and 4.7% of those in the age groups 18–24 years and 25–34 years respectively were also found to be at high risk of CVD (unpublished data). A major driver for being assessed at high CVD risk was the presence of clinically high-risk conditions (in particular, diabetes and age >60 years; diabetes and albuminuria). This pattern was similarly seen in a large primary care data set collected as part of a randomised controlled trial that included over 8000 Aboriginal and Torres Strait Islander people attending Aboriginal Community Controlled Health Services.28

Given the high prevalence of these clinically high-risk conditions and the early age at which they occur, a comprehensive vascular risk assessment of all risk factors (Box 2) is recommended from age 18 years. Further, because the FRE substantially underestimates risk in remote communities and there is a high likelihood that it will also underestimate risk in non-remote settings given the higher disease incidence and risk factor prevalence rates, the Central Australian Rural Practitioners Association (CARPA) and the National Heart Foundation have recommended a 5% loading to the FRE score.29,30 This aligns with approaches taken for Māori and Pacific populations in New Zealand.31

Consequently, there are three recommended options to estimate risk for Aboriginal and Torres Strait Islander populations:

  1. The NVDPA approach using a combination of the FRE and default clinically high-risk conditions (Box 2).
  2. The NVDPA approach plus a 5% absolute risk loading to the FRE scores for those without clinically highrisk conditions (CARPA approach – refer to ‘Resources’).29
  3. Use of recalibrated equations or new equations derived from local population data. There are research groups working on both recalibrating the FRE with local population data and deriving new, populationspecific risk prediction equations using Aboriginal and Torres Strait Islander–specific cohort data. These equations may provide alternative options for risk prediction purposes in the future.

Regardless of the approach taken, it should be noted that, given the heterogeneity of Aboriginal and Torres Strait Islander populations in Australia, it is likely that no single equation will be appropriate for everyone. A judicious clinical assessment will therefore involve both use of an appropriate risk prediction equation and tailored risk assessments that take into account an individual’s specific circumstances (clinical, psychological and socioeconomic).


Interventions


Although there is substantial work needed to improve the evidence base for absolute risk-based screening and management for Aboriginal and Torres Strait Islander peoples, the following recommendations have been made. For a detailed appraisal of the evidence base for medication recommendations, please consult the source guidelines in the reference list. Recommendations are provided for people without CVD in the first table and recommendations for those with established CVD are provided in the second table.

 

Resources

Absolute risk calculation

  • National Vascular Disease Prevention Alliance (NVDPA), Australian absolute cardiovascular disease risk calculator (refer to Appendix A: Australian cardiovascular risk charts, in this National Guide) and the Framingham Risk Equation (FRE) calculator modified to align with Australian guidelines
  • Although the FRE is validated for people aged 30–74 years, these charts start from age 35 years. Some calculators embedded in clinical software and the CARPA charts (refer below) can be used to assess risk in 30–34 year olds. For people aged 75 years and older without previous CVD, it is recommended to input 74 years of age to obtain a minimum risk score. Remote Primary Health Care Manuals (RPHCM), STM 4. Chronic diseases, ‘Assessing and reducing cardiovascular risk
  • The Indigenous-specific charts are identical to the NVDPA resources except for two features:
    • the corresponding colour has had a 5% absolute risk loading added (ie the lowest risk colour has been changed from <5% to <=9%)
    • the lower age limit has been changed from 35 years to 20 years. Although the FRE is validated for people aged 30–35 years, there are no empirical data assessing its use for those aged 20–29 years. 
  • National Heart Foundation, Guideline for the diagnosis and management of hypertension in adults: 2016
  • National Vascular Disease Prevention Alliance (NVDPA), Absolute cardiovascular disease risk management: Quick reference guide for health professionals

Blood pressure and lipid resources for patients

Oral anticoagulant management calculators and recommendations

National guide to a preventive health assessment for Aboriginal and Torres Strait Islander people

 





 
 
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