Unstable angina non ST elevation myocardial infarction biomarkers
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S.; Lakshmi Gopalakrishnan, M.B.B.S.VD
Overview
Cardiac markers are biomarkers that are measured to evaluate heart function. Their levels increase in blood when the heart muscle is necrosed, as in MI. Clinically the most commonly used cardiac markers include troponins and creatine kinase-MB (CK-MB). Other markers are lactate dehydrogenase, aspartate transaminase, myoglobin, ischemia modified albumin, pro-brain natriuretic peptide and glycogen phosphorylase isoenzyme. Cardiac biomarker measurement is one of the initial tests in a patient with heart attack.
Cardiac Biomarkers
If there is an elevation of a marker of myocardial necrosis (CK-MB or troponin), then the patient does not have unstable angina, but instead has a syndrome of either ST elevation MI or Non ST elevation MI depending upon the electrocardiogram changes.
According to consensus document in 2007[1] from the joint task force of the ESC, ACC, AHA and World Heart Federation (WHF), the term myocardial infarction is defined as myocardial necrosis in clinical setting consistent with myocardial ischemia with an elevation of troponin above the 99th percentile of normal together with any one of the following signs of ischemia:
- Symptoms of ischemia
- ECG changes indicative of new ischemia (new ST - T wave changes or new left bundle branch block)
- Development of pathological Q wave in ECG
- Imaging evidence of new wall motion abnormalities
Creatine Kinase-MB
CK-MB is a cytosolic carrier protein for high energy phosphates, which has long been the standard marker for the diagnosis of MI. However, it is less sensitive and less specific for MI than cardiac troponins. CK-MB is useful in special clinical situations such as in the diagnosis of early infarct extension (reinfarction), because the short half-life of CK-MB compared with troponin permits the detection of a diagnostic new increase after initial peak. Another scenario it has been found to be helpful is in the diagnosis of a periprocedural MI, and the diagnostic and prognostic value of CK-MB in these situations have been validated.
Cardiac Troponins
Cardiac troponin provides highly sensitive and specific result in detecting cell necrosis. There are 3 types of troponins- Troponin T(cTnT), troponin I(cTnI) and troponin C(cTnC). Cardiac troponins refers specifically to either TnT or TnI. Because cTnT and cTnI generally are not detected in the blood of healthy persons, the cutoff value for elevated cTnT and cTnI levels may be set to slightly above the upper limit of the performance characteristics of the assay for a normal healthy population. Therefore, physicians need to know the sensitivity and the cut-off of the test used in their hospital.
Brain Natriuretic Peptide (BNP)
Measurement of brain natriuretic peptide (BNP) levels has a prognostic importance in unstable angina. The TACTICS (Treat Angina With Aggrastat and Determine Cost of Therapy With an Invasive or Conservative Strategy) study has shown an association of BNP levels and short and long term mortality and CHF risk in patients with unstable angina. Also, a significant link exists between elevated BNP levels and significant coronary artery lesions.[2]
2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes (DO NOT EDIT) [3]
Early Risk Stratification
| Class I |
| "1. Serial cardiac troponin I or T levels (when a contemporary assay is used) should be obtained at presentation and 3 to 6 hours after symptom onset in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern of values. (Level of Evidence: A)" |
| "2. Additional troponin levels should be obtained beyond 6 hours after symptom onset in patients with normal troponin levels on serial examination when changes on ECG and/or clinical presentation confer an intermediate or high index of suspicion for ACS. (Level of Evidence: A)" |
| Class IIb |
| "1. Measurement of B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide may be considered to assess risk in patients with suspected ACS. (Level of Evidence: B)" |
Biomarkers: Diagnosis
| Class I |
| "1. Cardiac-specific troponin (troponin I or T when a contemporary assay is used) levels should be measured at presentation and 3 to 6 hours after symptom onset in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern. (Level of Evidence: A)" |
| "2. Additional troponin levels should be obtained beyond 6 hours after symptom onset in patients with normal troponins on serial examination when electrocardiographic changes and/or clinical presentation confer an intermediate or high index of suspicion for ACS. (Level of Evidence: A)" |
| "3. If the time of symptom onset is ambiguous, the time of presentation should be considered the time of onset for assessing troponin values. (Level of Evidence: A)" |
Biomarkers: Prognosis
| Class III: No Benefit |
| "1. The presence and magnitude of troponin elevations are useful for short- and long-term prognosis. (Level of Evidence: A)" |
| Class I |
| "1. The presence and magnitude of troponin elevations are useful for short- and long-term prognosis. (Level of Evidence: B)" |
| Class IIb |
| "1. It may be reasonable to remeasure troponin once on day 3 or day 4 in patients with MI as an index of infarct size and dynamics of necrosis. (Level of Evidence: B)" |
| "2. Use of selected newer biomarkers, especially B-type natriuretic peptide, may be reasonable to provide additional prognostic information. (Level of Evidence: B)" |
References
- ↑ Thygesen K, Alpert JS, White HD, Jaffe AS, Apple FS, Galvani M, Katus HA, Newby LK, Ravkilde J, Chaitman B, Clemmensen PM, Dellborg M, Hod H, Porela P, Underwood R, Bax JJ, Beller GA, Bonow R, Van der Wall EE, Bassand JP, Wijns W, Ferguson TB, Steg PG, Uretsky BF, Williams DO, Armstrong PW, Antman EM, Fox KA, Hamm CW, Ohman EM, Simoons ML, Poole-Wilson PA, Gurfinkel EP, Lopez-Sendon JL, Pais P, Mendis S, Zhu JR, Wallentin LC, Fernández-Avilés F, Fox KM, Parkhomenko AN, Priori SG, Tendera M, Voipio-Pulkki LM, Vahanian A, Camm AJ, De Caterina R, Dean V, Dickstein K, Filippatos G, Funck-Brentano C, Hellemans I, Kristensen SD, McGregor K, Sechtem U, Silber S, Tendera M, Widimsky P, Zamorano JL, Morais J, Brener S, Harrington R, Morrow D, Lim M, Martinez-Rios MA, Steinhubl S, Levine GN, Gibler WB, Goff D, Tubaro M, Dudek D, Al-Attar N (2007). "Universal definition of myocardial infarction". Circulation. 116 (22): 2634–53. doi:10.1161/CIRCULATIONAHA.107.187397. PMID 17951284. Retrieved 2011-04-11. Unknown parameter
|month=ignored (help) - ↑ Ahmed W, Zafar S, Alam AY, Ahktar N, Shah MA, Alpert MA (2007). "Plasma levels of B-type natriuretic Peptide in patients with unstable angina pectoris or acute myocardial infarction: prognostic significance and therapeutic implications". Angiology. 58 (3): 269–74. doi:10.1177/0003319707302543. PMID 17626979.
- ↑ Ezra A. Amsterdam, MD, FACC; Nanette K. Wenger, MD et al.2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. JACC. September 2014 (ahead of print)