Troponin Test

Troponin tests are used, together with an electrocardiogram (ECG), in people with persistent chest pain taken to hospital as an emergency to see if they have had a heart attack. In a heart attack a blood clot stops the normal flow of blood and oxygen to the muscle. Without oxygen the heart muscle cells die and release troponin into the bloodstream. The more extensive the damage is, the greater the release and the higher the blood concentrations become. Concentrations can increase within two or three hours and may remain high for 10 to 14 days.

Until recently a standard cTnI or cTnT troponin blood test would have been used by the laboratory, but these two tests have now mostly been replaced by more sensitive tests producing results called high-sensitivity troponins, hs-cTnI or hs-cTnT. The benefit of the high-sensitivity troponin tests is that they can detect the highly specific marker of heart damage at very low levels which means that early and minor heart damage can be picked up much earlier than the previously used standard troponin tests.

The biochemical diagnosis of acute heart muscle damage requires an increase in the troponin concentration with time. If a high-sensitivity cardiac troponin (hs-cTn) test is used, a second specimen is taken in three hours or so after admission. Each laboratory purchases and uses different tests (depending on the manufacturer of the equipment used within the laboratory) which may mean that the timing of the blood samples and the values used to interpret the test will vary between hospitals. It is important that results are interpreted alongside local guidelines.

Even a small rise in high-sensitivity (hs-cTn) troponin may indicate some damage to the heart. When a patient has a large increase in troponin concentration, then it is highly likely that they have had a heart attack or some other form of heart damage. If a patient with chest pain and known stable angina has a normal and stable hs-cTn troponin result, it is likely that their heart has not been damaged.

Increased troponin concentrations should not be used by themselves to diagnose or rule out a heart attack. A physical examination, clinical history and electrocardiogram (ECG) or imaging investigations are also essential. The internationally agreed definition of heart attack requires evidence of a significant increase in troponin concentration with time together with evidence of a sudden reduction of heart muscle blood supply (ischaemia) from characteristic symptoms of the acute coronary syndrome (ACS) and new ECG changes or new imaging changes.

Without evidence of ischaemia, possible causes of rising troponin values include other causes of heart damage such as myocarditis (inflammation of the heart muscle), acute heart failure, an arrhythmia (abnormal heart rhythm), chest injury, stroke or pulmonary embolism (blood clot lodged in the lung). Elevated but unchanging values may be seen in chronic heart failure, high blood pressure (hypertension), severe infections, kidney disease and some chronic inflammatory conditions of muscle.

The test is not generally affected by damage to muscles other than the heart, so injections into muscle and accidents or drugs that damage muscle do not normally affect troponin concentrations.

Heart attack means that some of the muscle in your heart has died. The medical term for this is myocardial infarction. Most commonly, a heart attack starts with a feeling of heavy pressure or pain in the chest, often extending into the neck or left arm. You may have trouble breathing, and may feel weak and break into a cold sweat.

A heart attack usually occurs because one of the blood vessels (called coronary arteries) that carry blood to your heart muscle is blocked. This happens when a blood clot forms in a blood vessel that is already partially blocked. The partial blockage is usually due to atherosclerosis (often called hardening of the arteries). This partial blockage occurs gradually over many years as lipid plaques (cholesterol)are deposited along the walls of the blood vessels. These plaques narrow and stiffen the arteries and can break apart unexpectedly and then totally block the affected artery.