Echo and cardiac MR are typically first-line for cardiomyopathies, but Cardiac CT is a powerful tool when MR is contraindicated or echo is nondiagnostic. CT is particularly effective for:
- Excluding obstructive CAD to rule out an ischemic cause for the heart failure
- Quantifying ventricular volumes, myocardial mass, and ejection fraction via multiphase volume-rendered datasets
- Identifying patterns of myocardial fibrosis via delayed-enhancement CT and dual-energy CT — similar to late gadolinium enhancement on MR
1 Hypertrophic cardiomyopathy (HCM)
A genetic disease characterized by unexplained myocardial hypertrophy — defined by LV wall thickness > 15 mm. CT’s spatial resolution accurately defines the pattern and extent:
| Variant | Frequency | Pattern |
|---|---|---|
| Asymmetric septal | ~ 60% (most common) | Primarily thickens the basal interventricular septum |
| Apical | — | Abnormal apical thickening; LV cavity takes a “spade-like” configuration |
| Concentric | — | Uniform thickening — can be difficult to distinguish from hypertensive heart disease |
Functional complications. Multiphasic cine CT detects LVOT obstruction and systolic anterior motion (SAM) of the mitral valve leaflet.
2 Arrhythmogenic right ventricular cardiomyopathy (ARVC)
A genetic disorder where RV myocardium undergoes apoptosis and is replaced by fibrofatty tissue — predisposing to sudden cardiac death.
CT findings:
- Globally dilated RV with reduced systolic function
- RV/LV ratio > 0.9
- RV free wall is often severely thinned and scalloped
Caveat: while CT can detect prominent low-attenuation trabeculations and fat within the RV wall, intramyocardial fat visualization is no longer recommended as a primary diagnostic criterion — it frequently leads to misdiagnosis.
3 Left ventricular non-compaction (LVNC)
A persistent embryonic myocardial morphology resulting in a thick, hypertrabeculated inner myocardial layer.
CT findings:
- Extensive trabeculations predominantly at the apex and inferolateral walls — sparing the basal segments
- Noncompacted-to-compacted ratio > 2.3 : 1.0 measured during diastole
4 Dilated cardiomyopathy (DCM)
LV chamber dilation and global or regional systolic dysfunction.
The primary role of CT in new-onset DCM is to prove the etiology is non-ischemic. A true idiopathic DCM will present with an enlarged LV but completely normal, unobstructed epicardial coronaries, and will lack the wall thinning or calcifications that signify a prior MI.
5 Takotsubo (stress-induced) cardiomyopathy
Triggered by severe physical or emotional stress — causes reversible LV dysfunction that closely mimics an acute MI.
CT findings:
- Severe hypokinesis or “ballooning” of the LV apex with preserved contractility of the basal and mid segments
- Absence of obstructive CAD — the critical distinguishing feature from a true acute MI
6 Restrictive & infiltrative cardiomyopathies
Conditions that result in an abnormally stiff, noncompliant heart — restricting diastolic filling while initially preserving systolic function.
Characterized by extracellular fibrillar protein deposits. CT shows concentric LV thickening alongside thickening of the RV, atria, and interatrial septum. LV mass is increased, but LV volumes and ejection fraction remain normal.
On non-contrast CT (NECT), heavy iron deposition is detected as global hyperdensity of both the myocardium and the liver. Dual-energy CT attenuation values of the septum correlate closely with established MR T2* measurements.
Hallmark CT features:
- Fibrotic apical obliteration of the involved ventricles
- Massive atrial enlargement (restrictive physiology + tethered AV valves causing regurgitation)
- Normal-to-small ventricular cavities
- Intracavitary thrombi may be visible