2 and 4 chamber cines show a lesion adherent to the left ventricular apex, which is akinetic.
On first pass perfusion, this lesion is seen to be of low signal throughout gadolinium passage into the right ventricle, left ventricle and myocardium; this is consistent with an avascular lesion. Better demonstration of the lesion would have been achieved by acquiring the images in 4-chamber rather than short axis.
For early gadolinium imaging (< 4 minutes), a long inversion time of ~440ms is chosen to null any non-vascular lesions that do not contain gadolinium. This accentuates thrombus by making it very hypointense compared to surrounding tissues that contain gadolinium. The homogenous low signal is consistent with thrombus or microvascular obstruction (no-reflow phenomenon).
In late gadolinium imaging (>8 minutes), a short inversion time is initially chosen to null the gadolinium-rich myocardium, so that any areas of myocardial enhancement are accentuated. This also incidentally results in some fat suppression as fat has a short T1 value (~150ms). The inversion time is progressively increased as late gadolinium imaging progresses, because gadolinium washes out of the myocardium, and myocardial T1 value increases back to baseline. In this case, transmural enhancement of the apex is seen, consistent with previous LAD infarct and non-viable myocardium. Overall the appearances are those of previous silent infarct causing akinesis,with resulting apical thrombus formation adjacent to the akinetic and damaged myocardium.