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Cardiovascular Disease

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Cardiovascular disease causes half of all deaths in Europe

Cardiovascular disease (CVD) is the collective term used to describe any disorder of the heart and circulatory system; the most common cardiovascular diseases are coronary artery disease and stroke. 

Coronary artery disease is caused by a build up of fatty deposits and cholesterol on the inner artery walls over time. This build up can eventually lead to stenosis or narrowing of the arteries. As the arteries narrow it decreases the hearts ability to pump blood and oxygen to the body’s vital organs.   This process can occur to a greater extent in some people and can result in a blockage.  If the blockage is not cleared within 12 hours, it will result in cell death (necrosis) in the effected area. When this process occurs in the heart it is called a heart attack or myocardial infarction (MI). Symptoms include chest pain, shortness of breath, palpitations and nausea. In patients with diabetes however it is not unusual for myocardial ischaemia to be silent that is to occur without any symptoms due to associated nerve damage. There are several risk factors for CVD including high blood pressure, elevated cholesterol, diabetes, smoking, obesity and family history.

There are 2 types of stroke Ischaemic stroke and haemorrhagic stroke.  Ischaemic stroke is cased by a blockage in one of the arteries taking blood to the brain whereas haemorrhagic stroke is caused when a blood vessel bursts causing bleeding in the brain.  Common symptoms include slurred speech, paralysis of one side of the body, blurred vision or loss of sight. 

The World Health Organisation estimated that 17.1 million people died from CVD in 2004, this figure represents approx 29% of all deaths making CVD the number one cause of death globally.

Myocardial infarction is generally diagnosed using a combination of clinical symptoms, characteristic changes on the ECG and a rise and fall in biochemical markers (cardiac enzymes).

Cardiac enzymes are the term given to the proteins released into the blood by dying heart muscle. They are typically elevated in the blood several hours after the onset of MI and therefore can be used as markers to confirm the diagnosis of heart attack. 
The most commonly used diagnostic markers for cardiovascular disease are CK-MB, Myoglobin and Troponin. 

  • Troponin I (cTnl) – Troponin I is the current gold standard marker for MI, levels in the blood are raised 5-6 hours after the event and peak at around 12 hours.  Levels remain elevated for several days after the event, Troponin I can therefore be classified as a late marker of MI.
  • Creatinine Kinase-muscle brain (CK-MB) – Similarly to Troponin I CK-MB is highly specific to the heart and is classified as a late marker of MI.  Serum levels are raised 4-6 hours after the event and peak at around 18-24 hours.  They remain elevated for a few days after the event and usually return to normal within 4 days.
  • Myoglobin (MYO) – Due to its small size Myoglobin levels appear increased in the blood first with levels being raised only 2-3 hours after the event however unlike Troponin I and CK-MB Myoglobin is not heart specific

 

The fact Myoglobin is not specific to the heart and more specific markers like Troponin I and CK-MB do not peak until much later has led to extensive research into additional markers to improve diagnosis.   The following novel markers have proven to be highly specific early indicators of MI.

  • Heart Type Fatty Acid Binding protein (h-FABP) – research shows h-FABP to be more sensitive than Troponin I in patients presented within 4 hours of symptom onset.  h-FABP is highly specific for heart muscle and with increased levels detected in the blood only 1.5 – 3 hours after the event is an ideal early marker of MI.
  • Glycogen Phosphorylase BB (GP-BB) – GP-BB is highly specific for cardiac muscle, serum levels appear to increase very soon after the event (3 hours) and peak at around 6 hours.
  • Carbonic Anhydrase III (CA III) – CA III is a cytoplasmic protein found in the skeletal muscle, although it is not specific to cardiac muscle research has suggested the ratio of Myoglobin to CA III correlates closely to cardiac muscle damage.

 

Early diagnosis of acute myocardial infarction (AMI) is essential in providing patients with the appropriate treatment and preventing inadvertent discharge.  Early detection will also help reduce the number of patients unnecessarily admitted to hospital and treated for AMI.  Not only will healthy individuals not benefit from treatment, the unnecessary treatment could result in considerable harm.  The ability to detect or disregard AMI early will dramatically decrease costs and the risk of associated litigation.

In the majority of cases it is recommended blood is obtained and tested 6 to 9 hours after the onset of symptoms.  If results are negative and suspicion remains high blood should be sampled again at 12 to 24 hours. After AMI has been confirmed biochemical marker testing at a reduced frequency is valuable in determining the size of the infarction and the risk of re infarction. 

Randox offer two different cardiac arrays capable of simultaneously testing a single patient sample for multiple cardiac markers.

 

Cardiac Array

  • Troponin I
  • CK-MB
  • Myoglobin
  • h-FABP

Cardiac Plus Array 

  • h-FABP
  • Myoglobin
  • Troponin I
  • CA III
  • GP-BB
  • CK-MB

For more information please visit the Biochip immunoassays section of our website or alternatively contact us.

Further reading:

  • Joint British recommendations on prevention of coronary heart disease in clinical practice Heart 1998 Volume 2 Supplement 2
  • National Academy of Clinical Biochemistry Standards of Laboratory Practice: Recommendations for the use of Cardiac Markers in Coronary Heart Diseases. Clinical Chemistry 1999, 45:7; 1104-1121.
  • Myocardial Infarction Redefined-A Consensus Document of The Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. Journal of the American College of Cardiology 2000, 36:3; 959-969

 

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