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Person—high-density lipoprotein cholesterol level (measured), total millimoles per litre [N].NN

Identifying and definitional attributes

Metadata item type:Help on this termData Element
Short name:Help on this termCholesterol—HDL (measured)
METEOR identifier:Help on this term270401
Registration status:Help on this term
  • Health, Standard 01/03/2005
Definition:Help on this termA person's high-density lipoprotein cholesterol (HDL-C), measured in mmol/L.
Data Element Concept:Person—high-density lipoprotein cholesterol level

Value domain attributes

Representational attributes

Representation class:Help on this termTotal
Data type:Help on this termNumber
Format:Help on this term[N].NN
Maximum character length:Help on this term3
Supplementary values:Help on this term
ValueMeaning
9.99Not measured/inadequately described
Unit of measure:Help on this termMillimole per litre (mmol/L)

Data element attributes

Collection and usage attributes

Guide for use:Help on this term

When reporting, record whether or not the measurement of High-density Lipoprotein Cholesterol (HDL-C) was performed in a fasting specimen.

In settings where the monitoring of a person's health is ongoing and where a measure can change over time (such as general practice), the date of assessment should be recorded.

Collection methods:Help on this term

When reporting, record absolute result of the most recent HDL-Cholesterol measurement in the last 12 months to the nearest 0.01 mmol/L.

Measurement of lipid levels should be carried out by laboratories, or practices, which have been accredited to perform these tests by the National Association of Testing Authorities.

  • To be collected as a single venous blood sample, preferably following a 12-hour fast where only water and medications have been consumed.
  • Prolonged tourniquet use can artefactually increase levels by up to 20%.

Source and reference attributes

Submitting organisation:Help on this term

Cardiovascular Data Working Group

National Diabetes Data Working Group

Origin:Help on this termNational Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand, Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

Relational attributes

Related metadata references:Help on this term
Supersedes PDFCholesterol-HDL - measured, version 1, DE, NHDD, NHIMG, Superseded 01/03/2005.pdf (22.0 KB) No registration status
Is used in the formation of Person—low-density lipoprotein cholesterol level (calculated), total millimoles per litre N[N].N
  • Health, Standard 01/10/2008
Is used in the formation of Person—low-density lipoprotein cholesterol level (calculated), total millimoles per litre N[N].N
  • Health, Superseded 01/10/2008
Implementation in Data Set Specifications:Help on this term
All attributes +

Acute coronary syndrome (clinical) DSSHealth, Superseded 07/12/2005

Acute coronary syndrome (clinical) DSSHealth, Superseded 01/10/2008

Acute coronary syndrome (clinical) DSSHealth, Superseded 01/09/2012

Acute coronary syndrome (clinical) DSSHealth, Superseded 02/05/2013

Acute coronary syndrome (clinical) NBPDS Health, Recorded 15/05/2017

Acute coronary syndrome (clinical) NBPDS 2013-Health, Standard 02/05/2013

DSS specific attributes +

Implementation start date: 01/07/2013


Cardiovascular disease (clinical) DSSHealth, Superseded 15/02/2006

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Cardiovascular disease (clinical) DSSHealth, Superseded 04/07/2007

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Cardiovascular disease (clinical) DSSHealth, Superseded 22/12/2009

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Cardiovascular disease (clinical) DSSHealth, Superseded 01/09/2012

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Cardiovascular disease (clinical) NBPDSHealth, Superseded 17/10/2018

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Cardiovascular disease (clinical) NBPDS Health, Standard 17/10/2018

DSS specific attributes +

DSS specific information:

High-density Lipoprotein Cholesterol (HDL-C) is easily measured and has been shown to be a negative predictor of future coronary events.

An inverse relationship between the level of HDL-C and the risk of developing premature coronary heart disease (CHD) has been a consistent finding in a large number of prospective population studies. In many of these studies, the level of HDL-C has been the single most powerful predictor of future coronary events. Key studies of the relationship between HDLs and CHD include the Framingham Heart Study (Castelli et al. 1986), the PROCAM Study (Assman et al 1998), the Helsinki Heart Study (Manninen et al. 1992) and the MRFIT study (Stamler et al. 1986; Neaton et al 1992).

There are several well-documented functions of HDLs that may explain the ability of these lipoproteins to protect against arteriosclerosis (Barter and Rye 1996). The best recognised of these is the cholesterol efflux from cells promoted by HDLs in a process that may minimise the accumulation of foam cells in the artery wall. The major proteins of HDLs and also other proteins (e.g. paraoxonase) that co-transport with HDLs in plasma have anti-oxidant properties. Thus, HDLs have the ability to inhibit the oxidative modification of LDLs and may therefore reduce the atherogenicity of these lipoproteins.

Overall, it has been concluded from the prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%. For a review of the relationship between HDL-C and CHD, see Barter and Rye (1996). A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al. 1998). (Lipid Management Guidelines - 2001, MJA 2001; 175: S57-S88.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the Service contact date should be recorded.


Diabetes (clinical) DSSHealth, Superseded 21/09/2005

DSS specific attributes +

DSS specific information:

Lowered HDL-Cholesterol, with increased serum triglyceride and increased low-density lipoprotein cholesterol are important risk factors for vascular disease in type 2 diabetes.

In the New South Wales Principles of Care and Guidelines for the Clinical Management of Diabetes Mellitus, recommendations are that HDL, total cholesterol, triglycerides are to be measured:

  • every 1-2 years (if normal)
  • every 3-6 months (if abnormal or on treatment)

and the target is:

  • to increase HDL Cholesterol to more than or equal to 1.0 mmol/L
  • to reduce total Cholesterol to less than 5.5 mmol/L
  • to reduce triglyceride levels to less than 2.0 mmol/L.

If pre-existing cardiovascular disease (bypass surgery or myocardial infarction) total cholesterol should be less than 4.5 mmol/L. A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al, 1998), (Draft NHF Lipid Guidelines Paper 2001). It has been concluded from prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the date of assessment should be recorded.

References:

National Heart Foundation of Australia - Lipid Management Guidelines 2001.


Diabetes (clinical) NBPDSHealth, Standard 21/09/2005

DSS specific attributes +

DSS specific information:

Lowered HDL-Cholesterol, with increased serum triglyceride and increased low-density lipoprotein cholesterol are important risk factors for vascular disease in type 2 diabetes.

In the New South Wales Principles of Care and Guidelines for the Clinical Management of Diabetes Mellitus, recommendations are that HDL, total cholesterol, triglycerides are to be measured:

  • every 1-2 years (if normal)
  • every 3-6 months (if abnormal or on treatment)

and the target is:

  • to increase HDL Cholesterol to more than or equal to 1.0 mmol/L
  • to reduce total Cholesterol to less than 5.5 mmol/L
  • to reduce triglyceride levels to less than 2.0 mmol/L.

If pre-existing cardiovascular disease (bypass surgery or myocardial infarction) total cholesterol should be less than 4.5 mmol/L. A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al, 1998), (Draft NHF Lipid Guidelines Paper 2001). It has been concluded from prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the date of assessment should be recorded.

References:

National Heart Foundation of Australia - Lipid Management Guidelines 2001.


Diabetes (clinical) NBPDSHealth, Recorded 15/05/2017

DSS specific attributes +

DSS specific information:

Lowered HDL-Cholesterol, with increased serum triglyceride and increased low-density lipoprotein cholesterol are important risk factors for vascular disease in type 2 diabetes.

In the New South Wales Principles of Care and Guidelines for the Clinical Management of Diabetes Mellitus, recommendations are that HDL, total cholesterol, triglycerides are to be measured:

  • every 1-2 years (if normal)
  • every 3-6 months (if abnormal or on treatment)

and the target is:

  • to increase HDL Cholesterol to more than or equal to 1.0 mmol/L
  • to reduce total Cholesterol to less than 5.5 mmol/L
  • to reduce triglyceride levels to less than 2.0 mmol/L.

If pre-existing cardiovascular disease (bypass surgery or myocardial infarction) total cholesterol should be less than 4.5 mmol/L. A level below 1.0 mmol/L increases risk approximately 2-fold (Gordon et al. 1989; Assmann et al, 1998), (National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand 2001). It has been concluded from prospective population studies that for every 0.025 mmol/L increase in HDL-C, the coronary risk is reduced by 2-5%.

In settings such as general practice where the monitoring of a person's health is ongoing and where a measure can change over time, the date of assessment should be recorded.

References:

Assman 1998.

Gordon DJ, Probstfield JL, Garrison RJ, Neaton JD, Castelli MP, Knoke JD, Jacobs DR, Bangdiwala S & Tyroler HA 1989. High-density lipprotein cholesterol and chardiovascular disease. Four prospective American studies. Circulation 79(1).

National Heart Foundation of Australia & the Cardiac Society of Australia and New Zealand 2001. Lipid management guidelines—2001. Medical Jounral of Australia 175.


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