Enzymes cardiaques et marqueurs de l'infarctus du myocarde

Cardiac biomarkers should be measured in all patients who present with chest discomfort consistent with syndrome coronarien aigu (SCA). Elevations of cardiac enzyme levels should be interpreted in the context of clinical and ECG findings.¹

• High sensitivity cardiac troponin I is the preferred marker for myocardial injury as it has the highest sensitivity and specificity for the diagnosis of acute myocardial infarction.

• Patients with negative ECG findings but suggestive history for acute coronary syndrome should have high sensitivity troponin measured at presentation and after 2 hours.²

Indications for measurement of cardiac enzymes

• Any patient presenting with a possible ACS.

• Routinely following percutaneous coronary intervention (PCI).

• Routinely following surgical revascularisation (coronary artery bypass graft (CABG)).

Cardiac troponin I and T have displaced myoglobin and creatine kinase-MB as the preferred markers of myocardial injury.³

Troponin is a protein released from myocytes when irreversible myocardial damage occurs. It is highly specific to cardiac tissue and accurately diagnoses myocardial infarction with a history of ischaemic pain or ECG changes reflecting ischaemia. Cardiac troponin level is dependent on infarct size, thus providing an indicator for the prognosis following an infarction.³

High-sensitivity cardiac troponin assays have been developed that can measure troponin values at much lower levels. High-sensitivity cardiac troponin (hs-cTn) is a marker of cardiomyocyte injury, and is recommended in all patients with suspected ACS.⁴ If the clinical presentation is compatible with myocardial ischaemia, then a rise and/or fall in hs-cTn above the 99th percentile of healthy individuals points to a diagnosis of MI as per the criteria in the fourth universal definition of MI. In patients with MI, levels of hs-cTn rise rapidly (i.e. usually within 1 h) after symptom onset and remain elevated for a variable period of time (usually several days).

With the use of these high-sensitivity assays, more patients with unstable angina will be classified as having non-ST-elevation myocardial infarction. These assays may therefore define a high-risk patient population and may lead to more appropriate therapy and improved outcomes in these patients.

• Cardiac troponins T and I are highly sensitive and specific for cardiac damage. Troponin I and T are of equal clinical value.

• Troponin levels should be measured at presentation and again at 2 hours after the onset of symptoms.⁴

• The risk of death from an ACS is directly related to troponin level and patients with no detectable troponins have a good short-term prognosis.

Problems with troponin estimation⁵

Anything that causes damage to cardiac muscle can cause troponin to spill into circulation. The most common cause of injury is oxygen supply and demand mismatch. Many other conditions can cause this mismatch, for example, tachycardia can cause decreased perfusion due to reduced diastolic time when coronary blood flow occurs and oxygen demand increases.

• Patients in shock can also have a supply and demand mismatch due to low blood volume, and elevated troponins in these patients are indicative of worse outcomes.

• Another cause of elevated troponin levels is cardiac muscle injury due to non-ischemic causes. Direct, blunt trauma to the chest can cause significant myocardial damage and, in turn, can lead to increased troponin.

• Inflammatory conditions such as viral myocardite and infiltrative diseases such as sarcoidosis have also been shown to cause elevations in troponins.

• Chronic kidney disease (CKD) also complicates the measurement of troponins.

• 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.

• Creatinine kinase is no longer used in the assessment of chest pain.

• 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 two hours after an acute myocardial infarction.

• Myoglobin has high sensitivity but poor specificity.
  

• Studies in several types of ACS have shown that elevated levels of natriuretic peptides - eg, B-type natriuretic peptide (BNP) - are independently associated with adverse outcomes - especially mortality.^{6 7}

• Leukocytosis may be seen within several hours after an acute myocardial infarction. It peaks in 2-4 days and returns to normal levels within one 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 three 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. Examples include:

• Heart-type fatty acid-binding protein (H-FABP) is involved in fatty acid metabolism in cardiac myocytes. The sensitivity of H-FABP in detecting ACS between 4 to 12 hours after symptom onset has been found to be 86.96%, comparable to (normal) troponin (90.9%) but the specificity of H-FABP was less than that of troponin.³ Despite its high sensitivity in detecting myocardial ischemia, H-FABP is not currently used clinically as it has yet to be tested against high-sensitivity troponin (hs-TnT) assays.

• Growth differentiation factor-15 has been shown to be useful in assessing prognosis following an ACS.⁸