Blood tests can rapidly detect heart attacks.

Over 500,000 people die annually as a result of heart attacks after coming to an emergency room. This is approximately one-third of the people who are diagnosed in an emergency room as having had an acute myocardial infarction (AMI). Chances for recovery can be greatly increased with more rapid and accurate diagnosis. Clinical studies have proven that heart attacks release proteins into the bloodstream which can be measured by emergency room physicians to rapidly establish whether a patient has actually suffered heart damage. The rapid and accurate identification of heart attack victims greatly improves chances for recovery and the evaluation of cardiac markers by emergency room physicians is significant.

Recently there's been increased emphasis on developing blood tests to detect injury to the heart muscle as early as possible among people with chest discomfort or other signs of a potentially serious heart problem. Blood tests confirm or refute suspicions raised in the early stages of evaluation that may occur in an emergency room, intensive care unit or urgent care setting. Such tests are sometimes called heart damage markers or cardiac enzymes.

In recent years tests have been developed to measure the level of cardiac muscle proteins called Troponins. The troponin complex is made of 3 different proteins:  Troponin-I (inhibitory protein), Troponin-T (tropomyosin-binding protein), and Troponin-C (calcium-binding protein). These proteins regulate the calcium-dependent interaction between actin and myosin, which contracts the heart muscle. Troponins specific to heart muscle have been found, allowing the development of blood tests or assays that can detect heart muscle injury with great sensitivity and specificity. Normally the level of Tn-T and Tn-I in the blood is very low. They increase substantially within several hours (on average 4-6 hours) of heart damage. They peak at 10 to 24 hours and can be detected for a week or more after.

Creatine Kinase isoenzyme, CK-MB, is the in-hospital gold standard for making the diagnosis of myocardial infarctions. However, their acceptance and applicability to the early evaluation of cardiac damage remains controversial. CK is present in very high concentrations in skeletal muscle and in lower concentrations in heart muscle. It is also present in brain and other tissues unlike cardiac troponin-I, which is only found in cardiac muscle and is a more specific marker of myocardial injury. CK is a dimer and has 3 different isoenzymes:  CK-BB, CK-MB, and CK-MM. Minor elevations in CK-MB are sometimes seen in unstable angina, but activities more than twice the upper limit of normal are specific for MI.

Cardiac Myoglobin is released into the blood stream earlier than CK-MB from damaged myocardial cells (within 4-6 hours) but it disappears about the time of the expected CK-MB elevation (6-18 hours). Like CK-MB, it is also non-specific because it also arises from skeletal muscle. Myoglobin is a globular protein important for its ability to bind oxygen in muscle tissue, contains 153 amino acids, and has a molecular mass of 17,500 kD. Blood myoglobin tests are used for estimating the extent of damage caused by a myocardial infarct or skeletal-muscle injury.

Fatty Acid Binding Protein (FABP) is a small intracellular protein, MW 15kD, that is released immediately upon MI. Its kinetic profile is similar to myoglobin except FABP has a higher cardiac specificity. Acceptance of FABP as a viable diagnostic tool is limited at present but is expected to increase.

The use of sensitive biochemical markers should allow a more reliable estimation of the rate of the remodeling process of the myocardium (heart) and may lead to refinement of therapeutic strategies.

We offer a wide variety of Troponin based products, and can provide custom preparations per client specifications.