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.
There is an 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.
There are a variety of infection conditions and tissue damage that can be diagnosed by the b-globulin family of human proteins. C-Reactive Protein is one of these major proteins (~ 105,000 Mw) of which the levels increase dramatically in concentration during many acute phase conditions. The protein is produced mainly in the liver, and in serum it may be elevated 2000 fold by various inflammatory events. The protein is so called because of its ability to bind to and be precipitated by the C-polysaccharide of streptococcus pneumoniae in the presence of calcium. The molecular weight of the subunit is around 21,000kD and each subunit associates in a discoid arrangement composed of five such units; as portrayed within our logo.
The measurement of CRP in serum has important diagnostic applications for the following disorders:
- Septicemia, Meningitis, other serious infections
- Post surgical tissue trauma
- Rheumatoid arthritis
- Rheumatic fever
- Skeletal muscle damage
- Myocardial infarction
Research has shown that patients with stable angina who have high circulating levels of CRP are at greater risk of experiencing myocardial infarction and sudden cardiac death. Patients with CRP levels greater than 3.6mg/L had about a two-fold increase in their risk of an MI or sudden death compared to patients with lower levels. A recent study indicates that men with elevated CRP concentrations had a two-fold increase in the risk of stroke, a three-fold increase in the risk of MI, and a four-fold increase in the risk of developing peripheral vascular disease. Additionally, baseline CRP concentration is an independent risk factor for cardiovascular disease among apparently healthy postmenopausal women. The predictive value of a model including CRP as a cardiac risk factor is superior to models using usual risk factors only. CRP predicts vascular events even among low-risk subgroups of women with no readily apparent markers for disease.
Studies Indicate that CRP, a Marker for low-grade inflammation, is also a marker for subsequent cardiovascular events.
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.
Carcino-Embryonic Antigen (CEA) is a tumor associated antigen which has been characterized as a glycoprotein of approximately 200,000 molecular weight. Development of the radio-immunoassay (RIA) made it possible to detect very low concentrations of CEA in blood, body fluids, and in normal and diseased tissues. Results of clinical studies indicate that CEA, although originally thought to be specific for digestive tract cancers, may also be elevated in other malignancies and in some non-malignant disorders. CEA testing can have significant value in the monitoring of patients with diagnosed malignancies in whom changing concentrations of CEA are observed. A persistent elevation in circulating CEA following treatment is strongly indicative of occult metastatic and/or residual disease. A persistent elevation of CEA value may be associated with progressive malignant disease and poor therapeutic response. A declining CEA value is generally indicative of a favorable prognosis and good response to treatment. Patients who have low pre-therapy CEA levels may later show elevations in CEA as an indication of progressive disease. The clinical relevance of CEA monitoring has been shown in the follow-up management of patients with colorectal, breast, lung, prostatic, pancreatic, and ovarian carcinomas. Additionally, studies suggest that pre-operative CEA levels of patients with colorectal, breast and lung carcinoma have prognostic significance. As a point of reference, it has been shown that 99% of healthy subjects have CEA concentrations of less than 5 ng/mL.