Troponins are specific proteins found in heart muscle. Troponin testing is done to diagnose heart attacks (myocardial infarctions).
When heart muscle is damaged, as in a myocardial infarction (MI), troponins leak out of cells and into the bloodstream. Increased troponin levels indicate myocardial infarction or injury in a person with chest pain or pressure. Some MIs are silent, manifesting few if any symptoms.
If infarction is ruled out in a person with continuing or recurring chest pain (unstable angina), an increased troponin level indicates the person has heart muscle ischemia (a decreased supply of oxygenated blood to the body), and is at an increased risk for a future serious heart event.
Although troponins also exist in other muscles, those in the heart are unique, and are measured separately in laboratory tests. Troponins in the heart are called cardiac troponins. There are two main types of cardiac troponins; T and I. T is also referred to as cTnT, while I is also referred to as cTnI.
Both troponin T and I are cardiac markers used to diagnose myocardial infarctions. Cardiac markers are substances whose blood levels increase after a myocardial infarction. Others include CK (creatine kinase), myoglobin, and CK-MB (one of three CK isoenzymes).
Like all cardiac markers, troponins have a unique diagnostic window (the timeline during which the marker rises, peaks, and returns to normal). Troponin levels rise within four to six hours after the beginning of chest pain or heart damage, and stay elevated for at least one week. This long elevation allows detection of a myocardial infarction that occurred days earlier, but prevents detection of a second infarction if it occurred only days after the first.
Troponins I and T are considered superior cardiac markers for several reasons. The most significant is that cardiac troponins are the only markers specific for heart muscle. Other markers also increase following damage to other muscles. Troponin levels help predict the extent of heart muscle damage; higher levels are associated with increased damage, lower levels with less damage. Levels in a healthy person are negligible, so an increase is easily detected.
The main difference between troponins I and T is that cardiac troponin I tests measure only cardiac troponin; tests for cardiac troponin T may cross-react with troponin found in other muscles and give positive or increased results in the absence of heart damage.
Two types of tests for troponins T and I are available: a traditional quantitative test that provides an actual measurement of troponin, and a newer qualitative test that simply reports the result as positive or negative. The quantitative test takes 45-90 minutes, and helps distinguish between myocardial infarction and unstable angina. The qualitative test takes 15 minutes and is used in emergency rooms in which rapid patient care decisions can be made based on the presence or absence of troponins.
Troponins tests require 5 mL of blood. Collection of the sample takes only a few minutes.
Discomfort or bruising may occur at the puncture site or the person may feel dizzy or faint. Pressure to the puncture site until the bleeding stops reduces bruising. Warm packs to the puncture site relieve discomfort.
People without heart damage have troponin levels less than 0.5 ng/mL.
Levels greater than 2.0 ng/mL indicate a person has had a significant myocardial injury, such as an infarction, and is at an increased risk for future serious heart events. Levels between 0.5 and 2.0 ng/mL indicate a diagnosis of unstable angina, other heart disorders, or chronic kidney failure.
Wu, Alan, editor. Cardiac Markers. Washington, DC:American Association of Clinical Chemistry (AACC) Press,1998.
Angina — A temporary chest pain caused by the heart not receiving enough oxygen.
Cardiac marker — A substance in the blood whose level rises following a myocardial infarction.
Myocardial infarction — Commonly known as a heart attack, a myocardial infarction is an episode in which some of the heart's blood supply is severely cut off or restricted, causing the heart muscle to suffer and die from lack of oxygen.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.