Table 5 Summary of the main CMR findings in various NICMP

HCM

Localised area of hypertrophy LV apical aneurysms

Normal

Circumferential defects (microvascular dysfunction)

Normal or hyposignal intensity in the area of perfusion defect

Patchy or confluent in regions of maximal wall thickening and LV/RV insertion points

Amyloidosis

Homogeneously thickened LV wall Thickened RV wall, interatrial septum, valves Pericardial effusion

Myocardial hypointensity

Diffuse perfusion defect

Diffuse perfusion defect

Widespread circumferential (commonest) Mid-wall Sub-epicardial Inter-atrial septum RV wall

Anderson-Fabry

Concentric hypertrophy

Normal

Not assessed with CMR

Normal

Mid-wall in basal inferolateral wall

Sub-epicardial (rarely)

DCM

Dilated LV and/or RV Reduced LVEF

Normal

Normal

Normal or hyposignal intensity within the LV if thrombus

Mid-wall septal (commonest) Epicardial Diffuse

ARVC

Dilated RV

RV dysfunction

-

-

RV free wall (difficult to image)

Focal aneurysms

Mid-wall septal, inferolateral or inferior

Local hypo or akinesia

LV wall (ALVC)

Myocarditis

Wall motion abnormalities

Focal epicardial or transmural hypersignal intensity

Not performed in the acute setting

Global EGE

Focal sub-epicardial

Localised thickened myocardium

LV dysfunction

Pericardial effusion

Tako-tsubo

Mid and apical akinesia (ballooning)

Focal, transient transmural

Normal

Normal

Normal

Compensatory basal hyperkinesia

hyper-intensity (apical segments)

Sarcoidosis

Normal or

Focal areas of hypersignal intensity

-

Focal

Focal patchy, mid-wall or sub-epicardial or subendocardial

Wall motion abnormalities or thinning

Basal and mid-septum mostly

LV and/or RV dysfunction

Sub-endocardium of RV side of the septum and RV free wall

LVNC

Hyper-trabeculation (non-compacted over compacted > 2.3)

Normal

Sub-endocardial perfusion defects

Sub-endocardial lack of EGE

Sub-endocardial, mid-wall or transmural trabecular enhancement

Absence of well-formed papillary muscles