Approximately every 42 seconds an American will suffer from a myocardial infarction. A MI occurs in a hypoxic state and sections of the heart are unable to get the oxygen it needs. According to the CDC about 610,000 die of heart disease in the United States every year, an occurrence of about 1 in every 4 deaths. Heart disease is the leading cause of death in both men and women.
Also about 47% of sudden cardiac deaths occur outside a hospital environment suggesting that many people with acute heart disease either don’t recognize the early signs or they don’t act on them.
There are cardiac markers that can give a physician a better picture of what is going on. These are routinely measured in a clinical laboratory and are almost all of the time STAT tests. The quick turn-around-time of these tests is imperative, because the sooner a patient with a heart condition gets treated, the better their prognosis.
The Troponin test is the most sensitive and specific test for myocardial damage. Troponin is released during and MI from the cytosolic pool of the myocytes. Its release is prolonged by the degradation of the actin and myosin filaments. Isoforms of protein, T, and I are specific markers for myocardium. After myocardial injury, troponin is released in 2-4 hours and peaks after 12 hours. It persists for up to 7 days after MI.
The Creatine Kinase-MB test is relatively specific when skeletal muscle damage is not present. Creatine kinase is an enzyme that is present in various tissues and cell types. It catalyzes the conversion of creatine to phosphocreatine utilizing adenosine triphosphate (ATP). The phosphocreatine serves as an energy reservoir in tissues that consumes ATP, especially the skeletal muscle and the brain. When mitochondrial creatine kinase is involved in the formation of phosphocreatine from mitochondrial ATP, cytosolic CK regenerates ATP from ADP and phosphocreatine kinase. In this instance, CK acts as an ATP regenerator. Clinically creatine kinase levels are assayed as a marker for damage of the CK-rich tissues in pathological states of myocardial infarction, rhabdomyolysis, muscle dystrophy, autoimmune diseases, and acute kidney injuries. There are two subunits of the cytosolic CK enzymes; Brain type (B) or Muscle type (M). The two subunits create three different isoenzymes CK-MM, CK-BB, and CK-MB. The different isoenzymes are present in different levels in various tissues. In skeletal tissue CK-MM is predominantly expressed, and in myocardial tissue, CK-MM and CK-MB is measured. Therefore measuring CK-MB levels is a good diagnostic test for heart damage from myocardial infarctions. CK-MB peaks about 10-24 hours after the attack and normalizes within 2-3 days.
Lactate dehydrogenase (LDH) was talked about in one of my previous posts and it can aid in the diagnosis of MI. Although it has been most recently replaced by the more specific and sensitive troponin test. LDH catalyzes the conversion of pyruvate to lactate. LDH-1 is found in the myocardium and LDH-2 is found in the serum. Normally LDH-2 is the predominate isoenzyme, but in cases of MI, LDH-1 is the predominate isoenzyme assayed and found. LDH takes about 72 hours to peak and normalizes within 10-14 days.
Myoglobin is an iron and oxygen binding molecule found in the muscle tissue. Myoglobin is a cytoplasmic protein that only harbors one heme group, although in contrast it has a much higher affinity for oxygen than does hemoglobin because its primary role is to store oxygen, where hemoglobins function is to transport oxygen. It contains a porphyrin ring with a proximal histidine group attached to the iron in its center. Myoglobin is only found in the bloodstream after muscle injury such as rhabdomyolysis. Myoglobin is a sensitive marker for muscle injury, making it a potential marker for MIs. However it lacks specificity and should be taken into account with other clinical findings to make a diagnosis. Myoglobin peaks the earliest of all other cardiac markers, that is within two hours, but it also falls quickly, usually before troponin or CK-MB.
Pro-brain natriuretic peptide is used as marker for acute congestive heart failure. The BNP is a hormone secreted by the cardiomyocytes in the ventricles of the heart in response to stretching caused by increased ventricular blood volume. The actions of BNP cause a decrease in systemic vascular resistance and venous pressure which causes a drop in blood pressure and causes after load. This causes a decrease in cardiac output.
Cardiac markers should be used to add to a clinical diagnosis, they should not be solely used to diagnose a patient with MI or CHF.