Figure 1. Panel of low resolution T1 scout images with increasing inversion time (TI) (from left to right, TI 130 ms, 190 ms, 250 ms, 310 ms, 370 ms.) Images (a–b) have TIs which are too short, revealing enhancement of the normal myocardium with nulling of the abnormal myocardium. Image (c) is acquired at the correct TI with nulling of the normal myocardium alone, creating good contrast with the high signal enhanced scar in the inferior and lateral walls. Images (d–e) have TIs which are too long, and there is reduced nulling of the normal myocardium and consequent loss of contrast with the abnormal tissue. In addition, increased signal from the blood pool makes delineation of the abnormal endocardium difficult.

Figure 2. Three consecutive short axis delayed hyperenhancement images (a–c.) The patient has undergone extensive full thickness infarction, and there is transmural enhancement within the septum and anterior wall of the left ventricle, indicative of LAD territory involvement.

Figure 3. Four chamber (a) and short axis (b) delayed hyperenhancement images reveal subendocardial hyperenhancement extending along the septum and inferior wall corresponding on cine images to an area of abnormal wall motion. The limited extent of scar (approximately 25% of the transmural thickness) suggests a high chance of functional improvement following revascularisation.

Figure 4. Short axis (a) and two chamber (b) delayed hyperenhancement images of a patient with full thickness LAD territory infarct. Subendocardial areas of absent enhancement are indicative of microvascular obstruction (the “no reflow” phenomenon.)

Figure 5. Short axis delayed enhancement image of a patient with hypertrophic cardiomyopathy. The myocardium is thickened, and delayed enhancement is seen at the right ventricular insertion points into the interventricular septum. These appearances are typical of this condition.

Figure 6. Short axis delayed enhancement image revealing diffuse global enhancement in this patient with biopsy proven amyloidosis.

Figure 7. Long (a) and short (b) axis delayed enhancement images in a patient with sarcoid demonstrating patchy partial and full thickness myocardial enhancement that is not in a segmental coronary distribution. Incidental note was made of multiple delayed enhancing foci within the spleen due to sarcoid granulomata (b).

Figure 8. Four chamber delayed enhancement image of a patient with presumed myocarditis. The appearances are non-specific, with patchy midwall hyperenhancement towards the apex. In the clinical context of chest pain, a Troponin rise and normal coronaries at angiography, appearances are consistent with myocarditis.

Figure 9. Short (a) and long (b) axis delayed hyperenhancement images demonstrate diffuse linear endocardial hyperenhancement in a patient with peripheral eosinophilia.

Figure 10. Two (a) and four (b) chamber delayed enhancement images of a patient with an aneurysmal apex secondary to a full thickness infarction. The incidental finding of a low signal, non-enhancing LV thrombus is shown.