Clinical features
|
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
|