ECG localisation and cardiac biomarkers in myocardial infarction
THE CONTEXT
ECG lead distribution helps localise myocardial infarction, while serial troponin measurements and other laboratory tests support assessment.
Anterior and inferior ECG patterns
•
The illustrated acute transmural anterior infarction shows ST elevation in I, aVL and V2–V6, with Q waves in V3–V5.
•
Anterior infarcts with prominent changes in V2–V4 are sometimes called anteroseptal; anterolateral infarcts have changes predominantly in V4–V6.
•
ECG changes are best seen in leads facing the affected myocardium. Anteroseptal abnormalities may occur in one or more leads from V1 to V4, while anterolateral changes occur in V4–V6, aVL and I.
•
Inferior infarction is best shown in II, III and aVF. Reciprocal ST depression may occur in I, aVL and anterior chest leads.
Posterior and right ventricular involvement
•
Posterior left ventricular infarction does not produce ST elevation or Q waves in standard leads; reciprocal ST depression and a tall R wave in V1–V4 can identify it.
•
Some infarctions, especially inferior infarctions, also involve the right ventricle. Additional leads over the right precordium may identify this involvement.
Troponin interpretation
•
Serial cardiac troponin measurements should be obtained.
•
Unstable angina has no detectable troponin rise; diagnosis relies on clinical features and investigations such as ECG or coronary angiography.
•
Myocardial infarction raises plasma troponin T and I or cardiac muscle enzymes.
•
Troponins T and I rise within 3–6 hours, peak at about 12–36 hours and remain elevated for up to 2 weeks.
Other laboratory findings
•
Leucocytosis may occur and peaks on the first day. The erythrocyte sedimentation rate and C-reactive protein are also elevated.
•
Lipids should be measured within 24 hours because cholesterol often falls transiently during the 3 months following infarction.