An inducible perfusion defect is subendocardial, in a coronary territory, and persists beyond peak myocardial enhancement; the LGE on the same study tells you whether that myocardium is viable.
Orient first
- Vasodilator stress (adenosine, regadenoson) raises flow in normal arteries; territories supplied by a stenosis enhance less on first-pass perfusion.
- The dark-rim artefact looks like a defect: it is transient (at peak contrast only), a thin subendocardial rim, present at rest too, and not confined to a territory.
- Viability is judged on LGE: scar transmurality < 50% predicts recovery after revascularisation; > 75% does not.
Acquire the study
- Rest cine; stress first-pass perfusion (3 short-axis slices every heartbeat) at peak vasodilator effect; rest perfusion (optional); LGE. Confirm adequate stress (heart-rate rise, symptoms, splenic switch-off).
The manoeuvre
- Check stress adequacy: splenic switch-off and heart-rate response — an inadequate stress makes a negative study non-diagnostic.
- Stress perfusion: subendocardial hypoenhancement in ≥ 1 segment of a coronary territory, persisting beyond peak myocardial enhancement — inducible ischaemia.
- Separate artefact: dark rim present only at peak blood-pool contrast, 1–2 pixels, and also at rest.
- LGE: match each defect — defect with no LGE = ischaemia; defect matching LGE = scar; defect larger than LGE = peri-infarct ischaemia.
- Count ischaemic segments (≥ 2 of 16, or ≥ 10% of myocardium, is significant ischaemia — verify the trial threshold used locally).
What confirms it
- An inducible subendocardial perfusion defect in a coronary territory persisting beyond peak enhancement after adequate stress, with the extent stated.
What licenses you to exclude it
- A normal stress perfusion study after documented adequate stress has a high negative predictive value for significant coronary disease.
The classic misread
- Calling dark-rim artefact ischaemia; calling a study negative when splenic switch-off shows the stress failed.