Acute ischemic myelopathy treated with intravenous thrombolysis: Four new cases and literature review.

BACKGROUND: Intravenous thrombolysis is a well-established treatment of ischemic stroke within 4.5 h. However, its effectiveness in acute ischemic myelopathy is unknown. PURPOSE: We describe a series of four acute ischemic myelopathy patients treated with intravenous thrombolysis within 4.5 h and review the current literature to explore this treatment feasibility, potential safety, and efficacy. METHODS: We reviewed all routinely collected clinical, radiological, and follow-up data of patients with a final acute ischemic myelopathy diagnosis who received acute intravenous thrombolysis in our stroke network. We also reviewed thrombolyzed acute ischemic myelopathy patients in the literature. RESULTS: Four patients (three women) aged 57 to 83 years presented with acute uni- or bilateral extremity paresis, considered initially as cerebral strokes in two of them. After excluding contraindications by brain imaging in three, spinal computed tomography in one and confirmation of acute ischemic myelopathy on spinal magnetic resonance imaging in one patient, intravenous thrombolysis was administered at 135, 190, 240, and 245 min accordingly. Subacute diffusion-weighted imaging-magnetic resonance imaging confirmed acute ischemic myelopathy in all but one patient. Favorable outcome was achieved in two patients rapidly and in three patients at three-month follow-up. We identified seven other thrombolyzed acute ischemic myelopathy patients in the literature, who showed variable recovery and no hemorrhagic complications. CONCLUSIONS: With appropriate acute imaging, intravenous thrombolysis after acute ischemic myelopathy is feasible and potentially safe within 4.5 h. Given the potential of benefit of thrombolysis in acute ischemic myelopathy, this treatment warrants further efficacy and safety studies.

Effects of continuous positive airway pressure treatment on coronary vasoreactivity measured by (82)Rb cardiac PET/CT in obstructive sleep apnea patients.

PURPOSE: Obstructive sleep apnea syndrome (OSA) increases the risk of cardiovascular disease. We aimed at evaluating the effect of continuous positive airway pressure (CPAP) treatment on coronary endothelium-dependent vasoreactivity in OSA patients by quantifying myocardial blood flow (MBF) response to cold pressure testing (CPT). METHODS: In the morning after polysomnography (PSG), all participants underwent a dynamic (82)Rb cardiac positron emitting tomography/computed tomography (PET/CT) scan at rest, during CPT and adenosine stress. PSG and PET/CT were repeated at least 6 weeks after initiating CPAP treatment. OSA patients were compared to controls and according to response to CPAP. Patients' characteristics and PSG parameters were used to determine predictors of CPT-MBF. RESULTS: Thirty-two untreated OSA patients (age 58 ± 13 years, 27 men) and 9 controls (age 62 ± 5 years, 4 men) were enrolled. At baseline, compared to controls (apnea-hypopnea index (AHI) = 5.3 ± 2.6/h), untreated OSA patients (AHI = 48.6 ± 19.7/h) tend to have a lower CPT-MBF (1.1 ± 0.2 mL/min/g vs. 1.3 ± 0.4 mL/min/g, p = 0.09). After initiating CPAP, CPT-MBF was not different between well-treated patients (AHI <10/h) and controls (1.3 ± 0.3 mL/min/g vs. 1.3 ± 0.4 mL/min/g, p = 0.83), but it was lower for insufficiently treated patients (AHI ≥10/h) (0.9 ± 0.2 mL/min/g vs. 1.3 ± 0.4 mL/min/g, p = 0.0045). CPT-MBF was also higher in well-treated than in insufficiently treated patients (1.3 ± 0.3 mL/min/g vs. 0.9 ± 0.2 mL/min/g, p = 0.001). Mean nocturnal oxygen saturation (ß = -0.55, p = 0.02) and BMI (ß = -0.58, p = 0.02) were independent predictors of CPT-MBF in OSA patients. CONCLUSIONS: Coronary endothelial vasoreactivity is impaired in insufficiently treated OSA patients compared to well-treated patients and controls, confirming the need for CPAP optimization.