Standard CCTA is not typically the primary diagnostic modality for an acute MI — a STEMI goes straight to the catheterization lab. But CCTA is increasingly used to rule out CAD in patients presenting with acute chest pain who have low-to-intermediate pretest probability. When an acute MI is captured incidentally on a CCTA, several hallmark features identify it.
1 Hallmark CCTA findings
Typically an abrupt occlusion of the coronary lumen filled with noncalcified, low-density material representing acute thrombus. Often accompanied by pronounced positive remodeling (enlarged vessel diameter) at the site of thrombosis.
In the early phases of an acute MI, CT depicts the affected ischemic myocardial tissue as hypodense (darker than normal). This appears as a subendocardial attenuation/perfusion defect, typically measuring < 50% of the attenuation of normal, healthy myocardium.
Crucially, in an acute MI wall thickness is preserved — or occasionally appears mildly thickened due to acute edema. (This is the key feature that distinguishes an acute from a chronic infarct — chronic infarcts thin and scar.)
Multiphasic retrospective ECG-gated cine CT lets you visualize regional wall-motion abnormalities — focal hypokinesis or akinesis in the affected vascular territory.
2 Acute mechanical complications
CCTA is excellent for detecting the catastrophic mechanical complications of acute MI:
- Left ventricular free wall rupture — often contained by pericardial adhesions, presenting as a pseudoaneurysm.
- Post-infarct ventricular septal defect (VSD) — typically apical and irregular in geometry.
- Papillary muscle rupture — leading to a flail mitral valve leaflet and severe mitral regurgitation.
For chronic-phase findings (wall thinning, fatty metaplasia, calcification) and chronic complications (LV aneurysm, mural thrombus), see Chronic MI / scar.