Laboratory Diagnosis of Patients with Acute Chest Pain

Abstract

The enzyme activities of creatine kinase (CK), its isoenzyme MB (CK-MB) and of lactate dehydrogenase isoenzyme 1 (LD-1) have been used for years in diagnosing patients with chest pain in order to differentiate patients with acute myocardial infarction (AMI) from non-AMI patients. These methods are easy to perform as automated analyses, but they are not specific for cardiac muscle damage. During the early 90's the situation changed. First creatine kinase MB mass (CK-MB mass) replaced the measurement of CK-MB activity. Subsequently cardiac-specific proteins troponin T (cTnT) and troponin I (cTnI) appeared on the scene, displacing LD-1 analysis. However, troponin concentrations in blood increase only from four to six hours after onset of chest pain. Therefore a rapid marker such as myoglobin, fatty acid binding protein or glycogen phosphorylase BB could be used in early diagnosis of AMI. On the other hand, CK-MB isoforms alone may also be useful in rapid diagnosis of cardiac muscle damage. Myoglobin, CK-MB mass, cTnT and cTnI are nowadays widely used in diagnosing patients with acute chest pain. Myoglobin is not cardiac-specific and therefore requires supplementation with some other analyses such as troponins to support the myoglobin value. Troponins are very highly cardiac-specific. Only the sera of some patients with severe renal failure, which requires hemodialysis, have elevated cTnT and/or cTnI without there being any evidence of cardiac damage. On the other hand, the latest studies have shown that elevated troponin levels in sera of hemodialysis patients point to an increased risk of future cardiac events in a similar manner to the elevated troponin values in sera of patients with unstable angina pectoris. In addition, the bedside tests for cTnT and cTnI alone or together with myoglobin and CK-MB mass can be used instead of quantitative analyses in the diagnosis of patients with chest pain. These rapid tests are easy to perform and they do not require expensive instrumentation. For routine clinical laboratory practice we suggest that in diagnosis of patients with chest pain, myoglobin and CK-MB mass measurements should be performed whenever they are requested (24 h/day) and cTnT or cTnI on admission to the hospital and then 4-6 and 12 hours later.

How Well Do Laboratories Adhere to Recommended Clinical Guidelines for the Management of Myocardial Infarction: The CARdiac MArker Guidelines Uptake in Europe Study (CARMAGUE)

“…Similarly, it has been shown that serial troponin measurement is equivalent to measurement of CK-MB for detection of reinfarction (29 ). Measurement of CK-MB by activity measurement is clinically and methodologically inadequate (30,31 ) and is not recommended (2 ) but was cited as performed on cost grounds and clinician familiarity. In sum, there is no longer justification for CK-MB activity or mass measurement.…”

Effect of hemodialysis on traditional and innovative cardiac markers

“…In the present investigation blood samples were drawn immediately before and 5 min after the end of the HD session. Therefore, due to the specific release pattern of troponin following myocardial injury (HD lasted less than 4 hr and troponin concentrations in blood increase only from 4 to 6 hr after onset of chest pain) (43), the changes observed could be most conceivably attributed to HD. At variance with previous investigations that used the lower limit of the analytical sensibility of the assay, we applied a more reliable diagnostic threshold, corresponding to the lowest cTnT concentration associated with a 10% total imprecision (33).…”

Effect of Renal Failure on Peak Troponin Ic Level in Patients with Acute Myocardial Infarction

“…Nevertheless, cTnI will undergo multiple biological transformations (phosphorylation, oxidation or proteolysis) that could induce smaller molecules, possibly eliminated by the kidney [21]. Moreover, cTnI molecular weight is around 24 kDa, allowing this molecule to be theoretically filtered by kidney glomerules [22]. Thus, we may hypothesize that during chronic kidney disease, alteration in the integrity of the filtration barrier could be responsible for a defect in renal clearance leading to the accumulation of cTnI or its degradation products.…”