A chronic (or remote) myocardial infarct is generally defined as occurring ≥ 8 weeks prior. Unlike acute infarcts (which preserve wall thickness and show edema), chronic MIs exhibit distinct morphological changes due to scarring and fibrosis.
1 Three hallmark indicators
The necrotic tissue scars down, leading to pronounced regional thinning of the myocardium — ranging from a few millimeters to near-normal thickness.
Linear low attenuation (fat density — characterized by negative HU) replacing the subendocardial layers of the left ventricular myocardium.
Linear calcifications depositing directly within the infarcted myocardial wall.
Linear myocardial calcification or subendocardial fatty metaplasia is highly specific and considered diagnostic for a remote MI. When you see either, the patient had an infarct — even if it isn’t in the history.
2 LV aneurysms
A remote, transmural infarct frequently leads to aneurysmal remodeling. On cine CCTA, this appears as an akinetic or dyskinetic (outward bulging during systole) segment of well-demarcated, thinned, and scarred myocardium.
3 Mural thrombus
The static blood flow within an aneurysm or severely hypokinetic region makes it highly prone to clot formation.
| Tissue | Density (HU) |
|---|---|
| Mural thrombus | 35–50 HU |
| Normal myocardium | 80–100 HU |
On CT, a thrombus appears as a low-attenuation filling defect lining the infarcted wall. The HU spread between thrombus and healthy myocardium is what makes the distinction reliable.
Old thrombi may also calcify — a calcified mural component does not exclude clot.
For acute-phase findings (the culprit lesion, hypoperfusion, preserved wall thickness) and acute mechanical complications (free wall rupture, post-infarct VSD, papillary muscle rupture), see Acute MI.