Acute carotid T occlusion in a young patient: cryptogenic origin?

A 32-year-old man without previous medical problems had acute global aphasia and right-sided hemiplegia (National Institutes of Health Stroke Scale [NIHSS] score 16 points) shortly after carrying a heavy mirror. Smoking (8 pack-years) was his only vascular risk factor. Computed tomographic angiography demonstrated a left carotid T occlusion (occlu-sion of the carotid artery, middle and anterior cerebral artery). Ninety minutes after symptom onset, intravenous thromboly-sis was initiated with 80 mg recombinant tissue-type plasmin-ogen activator, but successful reperfusion (Thrombolysis in Cerebral Infarction scale 3) was achieved only after thrombec-tomy with a Solitaire Stent (puncture 236 minutes and reper-fusion 263 minutes after symptom onset). The thrombus was 20 mm long. Immediately after the intervention, his symptoms started to improve, and head MRI on the day after showed a residual 3.5 cm×1.5 cm×1.5 cm lesion in the left-sided basal ganglia on diffusion weighted imaging and that the recana-lized carotid T stayed open (Figure 1). Secondary prevention with aspirin 100 mg/d and atorvastatin 40 mg/d was initiated. The sudden onset of physical straining and the large thrombus were suspicious for a cardioembolic source. Admission and follow-up ECG, 24-hour ECG recordings, and transesopha-geal echocardiography were normal. The only abnormalities of ancillary investigations were borderline-elevated high-sensitivity troponin T (hs troponin T; 0.015 μg/L; normal value <0.014 μg/L) and >3-fold elevated creatine kinase levels (750 U/L; normal value <190 U/L). Creatine kinase levels declined, and troponin T levels were normal at follow-up examinations. Neurological signs continued to improve, and on day 4, clinical examination was essentially normal. The next night, transient aphasia and weakness of the right arm recurred for 2 hours. MRI did not show any new diffusion weighted imaging lesion but new irregularities of the left proximal and distal M1 segment of the middle cerebral artery, which were suspicious for spontaneously recanalized recurrent embolization (Figure 1). On transcranial Doppler on day 5 after stroke, there were microembolic signals in the left intracranial carotid artery and left anterior cerebral artery but not on the right side. Therefore, we decided to perform a cardiac MRI (CMR) on day 6 to search further for a cardiac source of emboli. CMR showed regional left ventricular (LV) apical wall thinning with dyski-nesia and an apical thrombus (0.9×1.8 mm in size; Figure 2). LV ejection fraction was slightly reduced to 58%, and there was transmural late enhancement of the LV apex indicating subacute myocardial infarction (MI). Unfractionated heparin in therapeutic dosage …