Cardiac Enzymes and Markers for Myocardial Infarction

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Cardiac biomarkers should be measured in all patients who present with chest discomfort consistent with acute coronary syndrome (ACS). Elevations of cardiac enzyme levels should be interpreted in the context of clinical and ECG findings.[1]

  • Cardiac troponins T and I are the preferred markers for myocardial injury as they have the highest sensitivities and specificities for the diagnosis of acute myocardial infarction.[1]
  • Patients with negative cardiac biomarkers within 6 hours of the onset of symptoms that are consistent with ACS should have biomarkers remeasured in the timeframe of 8 to 12 hours after the onset of symptoms.[2]
  • Peak circulating enzyme levels tend to occur earlier and are often higher following successful thrombolytic therapy.
  • Any patient presenting with a possible acute coronary syndrome (ACS).
  • Routinely following percutaneous coronary intervention (PCI).
  • Routinely following surgical revascularisation (coronary artery bypass graft (CABG)).

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  • Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.[3]
  • Cardiac troponins T and I are highly sensitive and specific for cardiac damage. Troponin I and T are of equal clinical value.
  • Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.[1] 
  • Troponin levels may not be detectable for six hours after the onset of myocardial cell injury. The most sensitive early marker for myocardial infarction is myoglobin.
  • Troponin levels should be measured at presentation and again 10-12 hours after the onset of symptoms. When there is uncertainty regarding the time of symptom onset, troponin should be measured at 12 hours after the presentation.
  • The risk of death from an acute coronary syndrome (ACS) is directly related to troponin level and patients with no detectable troponins have a good short-term prognosis.
  • Elevated troponin levels can occur in patients without an ACS and are associated with adverse outcomes in many other clinical situations, including congestive heart failure, sepsis, acute pulmonary embolism and chronic kidney disease. Other cardiac causes include myocarditis and aortic dissection.
  • Myocardial muscle creatine kinase (CK-MB) is found mainly in the heart.
  • CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours.
  • Sensitivity and specificity are not as high as for troponin levels.
  • Myoglobin is found in cardiac and skeletal muscle.
  • It is released more rapidly from infarcted myocardium than troponin and CK-MB and may be detected as early as 2 hours after an acute myocardial infarction.
  • Myoglobin has high sensitivity but poor specificity. It may be useful for the early detection of myocardial infarction.
  • Studies in several types of acute coronary syndromes (ACSs) have shown that elevated levels of natriuretic peptides, eg B-type natriuretic peptide (BNP), are independently associated with adverse outcomes - especially mortality.[4][5]
  • Leukocytosis may be seen within several hours after an acute myocardial infarction. It peaks in 2-4 days and returns to normal levels within 1 week.
  • Patients without biochemical evidence of myocardial necrosis but with elevated C-reactive protein (CRP) level are at increased risk of a subsequent ischaemic event.
  • Erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for weeks.

There are a number of novel biomarkers under investigation, but none has been tested and proven to alter outcome of therapeutic intervention.[6] Although some have improved prediction of outcome in acute myocardial infarction, none has been demonstrated to alter the outcome of a particular therapy or management strategy.

  • Heart-type fatty acid binding protein and copeptin (in combination with cardiac troponin) diagnose myocardial infarction or acute coronary syndrome (ACS) in the early hours following symptoms.
  • Mid-regional pro-atrial natriuretic peptide, ST2, C-terminal pro-endothelin 1, mid-regional pro-adrenomedullin and copeptin all provide information in predicting death and heart failure.
  • Growth differentiation factor-15 and high-sensitivity C-reactive protein (CRP) may predict death following an acute coronary syndrome (ACS).
  • Pregnancy-associated plasma protein A levels following chest pain predict risk of myocardial infarction and revascularisation.[7]

Aspartate transaminase and lactate dehydrogenase were used in the past, but have been superseded.

Further reading & references

  1. Chest pain of recent onset; NICE Clinical Guideline (March 2010)
  2. American College of Cardiology, American Heart Association; Guidelines for the management of patients with unstable angina/non ST-Elevation myocardial infarction, 2007
  3. Hillis GS, Fox KA; Cardiac troponins in chest pain can help in risk stratification. BMJ. 1999 Dec 4;319(7223):1451-2.
  4. Wiviott SD, de Lemos JA, Morrow DA; Pathophysiology, prognostic significance and clinical utility of B-type natriuretic peptide in acute coronary syndromes. Clin Chim Acta. 2004 Aug 16;346(2):119-28.
  5. Bassan R, Tura BR, Maisel AS; B-type natriuretic peptide: a strong predictor of early and late mortality in Coron Artery Dis. 2009 Mar;20(2):143-9.
  6. Chan D, Ng LL; Biomarkers in acute myocardial infarction. BMC Med. 2010 Jun 7;8:34.
  7. Heeschen C, Dimmeler S, Fichtlscherer S, et al; Prognostic value of placental growth factor in patients with acute chest pain. JAMA. 2004 Jan 28;291(4):435-41.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Last Checked:
Document ID:
8734 (v4)