Table 1

The new ACC/ESC definition of myocardial infarction (MI)1

ACC, American College of Cardiology; CK, creatine kinase; ESC, European Society of Cardiology; MI, myocardial infarction
Clinical features
  • Spontaneous ischaemic episode (usually) lasting>20 minutes

  • Coronary artery intervention

Biochemistry
  • The preferred cardiac markers are troponin I or T because of their specificity

  • CK-MB has lower specificity than troponins T and I, but may be used

  • Myoglobin or CK-MB isoforms should be considered for rapid diagnosis

  • Total CK, aspartate transaminase (serum glutamate oxaloacetate transaminase) and LDH have low specificity and are less satisfactory

  • Elevation of troponin or CK-MB is defined as a value exceeding the 99th centile of a reference control group

  • Sampling of troponins or CK-MB should be done at presentation, at 6–9 hours, and at 12–24 hours.

Electrocardiography
  • Electrocardiographic criteria are not specific enough to identify non-ST elevation MI

  • ST elevation MI is indicated by new ST elevation in at least two contiguous leads, measuring ⩾0.2 mV in leads V1–V3, or ⩾0.1 mV in all other leads

  • Established MI (in the absence of confounders) is indicated by any Q wave in leads V1–V3 or by Q waves of ⩾1 mm for ⩾30 ms in two other contiguous leads

  • Presumed new left bundle branch block may not be accompanied by ST segment deviation; the characteristic changes indicative of acute MI in patients with prior left bundle branch block require further definition

Pathology
  • It takes 6 hours for myocyte necrosis to become evident on histopathology

  • The pathological identification of MI depends in part on the staging of the inflammatory cell infiltrate: acute = neutrophils; healing = mononuclear cells; healed = collagen without cellular infiltration

  • Infarcts are classified by size: microscopic (focal necrosis); small (<10% of the left ventricle); medium (10–30% of the left ventricle); large (>30% of the left ventricle)

Imaging
  • Manifestations of MI include regional wall motion abnormalities on echocardiography, contrast angiography, radionuclide scanning or magnetic resonance imaging

  • These abnormalities may include evidence of “infarct zone” wall thinning, changes in tissue texture, and/or abnormalities in wall motion