Three cases of middle cerebral artery occlusion emergently revascularized with a balloon-expandable coronary bare stent after intravenous tissue plasminogen activator.

BACKGROUND: Revascularization with emergency stent placement in patients with acute middle cerebral artery occlusion is still controversial in Japan. METHODS: We placed balloon-expandable coronary bare stents in 3 patients in whom revascularization was not obtained after intravenous tissue plasminogen activator therapy (IV t-PA) for acute ischemic stroke (middle cerebral artery M1 occlusion). RESULTS: Patient 1 was an 87-year-old woman with left hemiplegia. Her National Institutes of Health Stroke Scale score (NIHSS) was 12, and her magnetic resonance imaging diffusion-weighted image Alberta Stroke Programme Early Computed Tomography Score (MRI DWI-ASPECTS) was 8. Adequate revascularization was not obtained with IV t-PA and adjunctive percutaneous transluminal angioplasty (PTA) for right M1 occlusion, and a stent was placed 368 minutes after onset. Her Thrombolysis in Myocardial Infarction Trial (TIMI) score was 2. After 90 days, her modified Rankin scale (mRS) score was 4. Patient 2 was a 65-year-old woman with left hemiplegia. Her NIHSS score was 16, and MRI DWI-ASPECTS was 9. A stent was placed 337 minutes after onset after IV t-PA and adjunctive PTA for right M1 occlusion. Her TIMI score was 3. After 90 days, her mRS score was 3. Patient 3 was a 61-year-old woman with left hemiplegia. Her NIHSS score was 18, and MRI DWI-ASPECTS score was 7. Arterial dissection was found after IV t-PA and adjunctive PTA for the right M1 occlusion, so a stent was placed 312 minutes after onset. Her TIMI score was 2. After 90 days, her mRS score was 0. CONCLUSIONS: Revascularization with emergency stent placement seems likely to be successful in patients with acute middle cerebral artery occlusion, but clinical symptoms do not always improve in some cases and care is needed in selecting patients for the procedure.

Clinical review of 37 patients with medullary infarction.

BACKGROUND: Clinical features of medullary infarction were compared between patients with lateral medullary infarction and medial medullary infarction METHODS: Thirty-seven patients with medullary infarction (29 with lateral medullary infarction and 8 with medial medullary infarction) who were admitted to our center between April 1, 2007 and March 31, 2010 were examined. Background factors, neurologic signs and symptoms, imaging findings, cause of disease, and outcomes were assessed for patients with lateral and those with medial medullary infarction. RESULTS: Examination of the clinical symptoms and neurologic findings suggested that among patients with medial medullary infarction, few demonstrated all of the symptoms of Dejerine syndrome at onset, and many had lesions that were difficult to locate based only on neurologic findings. Both lateral and medial medullary infarction were frequently caused by atherothrombosis. However, cerebral artery dissection was observed in 31% of patients with lateral medullary infarction and 12.5% of those with medial medullary infarction. In 13% of patients with lateral and 37% of patients with medial medullary infarction, magnetic resonance imaging diffusion-weighted images on the day of onset did not show abnormalities, and the second set of diffusion-weighted images confirmed infarction lesions. For lateral medullary infarction, a more rostral lesion location was correlated with a poorer 90-day outcome. For medial medullary infarction, a more dorsal lesion location was correlated with a poorer 90-day outcome. CONCLUSIONS: The diagnosis rate of medullary infarction using imaging examinations at onset--particularly medial medullary infarction--is not necessarily high. The imaging examinations need to be repeated for patients who are suspected to have medullary infarction based on neurologic signs and symptoms.

Factors related to recurrence of paradoxical cerebral embolism due to patent foramen ovale.

Patent foramen ovale (PFO) is an important etiology of ischemic stroke in young adults. We investigated factors contributing to recurrent ischemic stroke in patients with PFO. Subjects comprised 47 patients (mean age, 56.8 ± 14.2 years; range 23-74 years) with ischemic stroke due to PFO who were admitted to our hospital between April 2007 and February 2011. Mean duration of follow-up was 34.5 ± 13 months. Recurrence occurred in 11 cases. Annual recurrence rate was 23.4%. We investigated relationships between recurrence of ischemic stroke and size of PFO (large, >4 mm; medium, 2-3.9 mm; small, <1.9 mm; absent group), maximal number of microbubbles (determined as the number of microembolic signals: small, 0-5; moderate, 6-25; and multiple, ≥ 26), massive bubble on contrast transesophageal echocardiography or atrial septal aneurysm, D-dimer level and antithrombotic therapy. Univariate analysis showed size of the PFO (P = 0.013), number of microbubbles (P = 0.021), and presence of a massive bubble on echocardiography (P = 0.04) were related to recurrence of ischemic stroke. Logistic analysis identified size of the PFO (P < 0.05) and massive bubble on echocardiography (P < 0.05) as factors related to recurrence of ischemic stroke. In conclusion, size of the PFO and presence of a massive bubble were considered to be factors associated with recurrence of ischemic stroke due to PFO.

Evaluation of clopidogrel resistance in ischemic stroke patients.

OBJECTIVE: Clopidogrel has potent antiplatelet effects, but recent interest has focused on clopidogrel resistance, in which platelet function is not inhibited despite taking the drug. This study evaluated clopidogrel resistance in ischemic stroke patients. METHODS: After taking oral clopidogrel 75 mg/day for ≥1 week, platelet aggregometry was performed by turbidimetry in all patients, and by a screen filtration pressure method using whole blood in 37 patients. Using turbidimetry, resistance was defined as platelet maximum aggregation rate ≥34% with aggregation-inducing agent ADP 1 µmol/L, or ≥66% with ADP 4 µmol/L. Using the screen filtration pressure method, resistance was defined as a minimum concentration of ≤3 µmol/L ADP to induce secondary aggregation of platelets. PATIENTS: This study was conducted in 72 patients (52 men, 20 women; mean age, 69 ± 8 years; range, 50-84 years) with non-cardiogenic ischemic cerebrovascular disease. RESULTS: Based on turbidimetry, the rate of clopidogrel resistance was 8.3% with ADP 1 µmol/L and 18.1% with 4 µmol/L. Based on the screen filtration pressure, the rate of clopidogrel resistance was 8.1%. The differences between turbidimetry and screen filtration pressure methods, regarding the measurement of the presence of resistance in the same patient, were observed. CONCLUSION: Clopidogrel resistance varies greatly depending on the method of measuring platelet aggregation and the definition of resistance. Rates of 8-18% were obtained using our methods and criteria.