Case Report An 8-year-old previously healthy boy presented 2 hours after he was kicked in the chest by a horse. He was awake, alert, and oriented with normal vital signs, including a heart rate of 84 bpm. Physical examination was significant for superficial abrasions over his left chest and left chin. He sustained an incomplete distal ulnar fracture. Chest radiograph and a computed tomography scan without contrast of the chest and abdomen demonstrated extensive bilateral pulmonary contusions and a small right-sided pneumothorax. The initial ECG demonstrated bifascicular block (right bundle branch block and left anterior fascicular block; Figure 1), a well described, albeit rare, transient conduction abnormality that can be seen secondary to myocardial edema after significant MCI. Troponin I level at presentation was elevated at 11.2 ng/mL (normal range, 0–0.1 ng/mL), creatine kinase MB of 58.5 ng/mL (range, 0–4 ng/mL), and creatine kinase total of 605 U/L (normal range, 21–232 U/L). Transthoracic echocardiogram showed normal intracardiac anatomy, competent intracardiac valves, no pericardial effusion, normal proximal coronary artery origins, normal biventricular systolic function, with mild left apical inferior segmental wall hypokinesia (Movie I in the Data Supplement). He was admitted to the intensive care unit for 48 hours of telemetry. At 24 hours after admission, the left anterior fascicular block resolved but ECG continued to demonstrate right bundle branch block (Figure 2). On day 3, the right bundle branch block resolved (Figure 3). He had no arrhythmias during his hospitalization. The troponin I peaked at 70 ng/mL at 9 hours post injury and started to downtrend but remained elevated 36 hours after injury (11.1 ng/mL). The transthoracic echocardiogram demonstrated persistent but improving left apical inferoseptal hypokinesia. Cardiac MRI (CMR) was performed with a 1.5-T scanner (Ingenia MR; Philips Medical Systems, Best, the Netherlands) on day 3 to assess the mechanism of myocardial injury and demonstrated mild thinning and hypokinesia of the apical septal segment of the left ventricle. The hypokinesia corresponded to an area of abnormal, increased enhancement in the subendocardial region on T2-weighted turbo spin echo images (Figure 4), signifying acute myocardial injury and edema. First-pass perfusion imaging was performed after contrast injection (0.2 mL/kg of gadoteridol) and did not show any perfusion defects at rest. Images using a phase-sensitive inversion recovery sequence were obtained ≈6 minutes after contrast and demonstrated abnormal myocardial hyperenhancement in the same location (Figure 5). Given CMR findings consistent with myocardial changes secondary to coronary ischemia, a coronary angiogram was performed, which showed unobstructed filling of his coronaries to the apex (Figure 6). It is possible the CMR changes were secondary to transient coronary vasospasm.