Type:
Educational Exhibit
Keywords:
Cardiac, MR, Imaging sequences, Diagnostic procedure, Inflammation, Connective tissue disorders, Congenital
Authors:
A. Mirakhur, N. Merchant; Calgary, AB/CA
DOI:
10.1594/ecr2013/C-2257
Imaging findings OR Procedure details
The technique for LGE-CMR involves intravenous administration of gadolinium chelate contrast material (0.05-0.2 mmol/kg) followed 8-30 minutes later by a cardiac-gated T1-weighted pulse sequence.
The typical LGE pulse sequence is a cardiac-gated segmented inversion-recovery-prepared fast gradient-echo sequence: an inversion recovery preparatory pulse nulls normal myocardium,
followed by a segmented k-space gradient-echo acquisition.
Retention of contrast material results in T1 shortening and thus increased signal intensity on T1-weighted images relative to that of the normal myocardium.
Typical values for inversion time (TI) are 150-400 milliseconds (ms),
varying from patient to patient based on their cardiac and renal function.
Phase-sensitive inversion recovery (PSIR) reconstruction algorithm can also be applied to reduce the effects of dynamic changes in TI,
resulting in consistently good image quality [2].
Unlike in ischemic heart disease,
delayed enhancement in non-ischemic myocardial disease generally does not correspond to any particular coronary artery distribution and is often midwall rather than subendocardial or transmural [3,
4].
In advanced cardiac sarcoidosis,
LGE can be seen,
as areas of focal,
patchy hyperenhancement,
usually located subepicardial or in the midwall (Figures 1-3).
Fabry Disease,
an X-linked disorder of lysosomal metabolism,
is a relatively common cause of left ventricular (LV) hypertrophy in middle-aged men.
Fibrosis from an unclear cause results in patients with severe disease showing focal inferolateral midwall LGE (Figure 4) [5].
Systemic sclerosis,
a subtype of scleroderma, can result in myocardial fibrosis,
likely throughfibroblast proliferation and collagen accumulation [6].
Midwall enhancement of predominantly the basal and midcavity segments of left ventricle (LV) is the most commonly described LGE pattern (Figures 5-7) [6].
Non-compaction cardiomyopathy is a complex,
not fully understood,
entity characterised by the presence of numerous and prominent trabeculations together with deep intertrabecular recesses in a portion of the ventricular wall,
thought to be a result of a congenital anomaly of endomyocardial development [7].
LGE is seen in areas of myocardial fibrosis (Figure 8).
LGE-CMR also has an important role in other congenital cardiac conditions.
Delayed enhancement of the right ventricle (RV) in association with reduced function or an aneurysm is highly suggestive of arrhythmogenic right ventricular cardiomyopathy (ARVC) in patients with non-sustained ventricular tachycardia and left bundle-branch block [8] (Figures 9-12).
LGE has also been described in muscular dystrophy cases,
where cardiac myocyte dystrophin deficiency leads to fibre necrosis causing replacement of morbid myocardium with connective tissue and fat [9].
This manifests as high signal intensity on LGE-CMR imaging,
predominantly in the midwall (Figures 13-15) [9].
In patients with suspected endocardial fibroelastosis,
accurate identification has previously required endomyocardial biopsy,
though LGE-CMR,
with its ability to demonstrate subendocardial fibrosis and mural thrombus (Figure 16),
has become relevant to diagnosis and prognosis [10].