035 in. diameter hydrophilic wires. The 6F guiding catheter was introduced subsequently into the target brain supplying vessel over the same hydrophilic wire and microcatheter with a support of a 0.014 in./300 microwire was advanced behind the occluded intracranial vessel segment. Occlusion of MCA or BA was classified according to the Thrombolysis in Cerebral Ischemie (TICI) criteria. The intraluminal position of the microcatheter was always checked. All catheters were continuously flushed with heparinized saline. The microcatheter was then replaced with the EKOS endovascular catheter terminated with the emitter of ultrasonic waves and connected to the central unit. The EndoWave System Entinostat mouse manufactured
by EKOS Corporation (Bothell, WA, USA) was used (Fig. 2a and b). It consists of a 5.2F, 106 cm long
infusion catheter, an ultrasound core wire, and a control unit with catheter interface cables. The ultrasound wire delivers pulsed high frequency (1.7–2.1 MHz) and low-intensity (400 mW/cm2) ultrasound waves. Special care was taken for the location of a tip of the catheter into the occluded segment of the artery (Fig. 3). Both the insonation and the local administration of tPA directly into the thrombus were simultaneously started. In this study, a dose of 15 mg/h of tPA was delivered selleck kinase inhibitor by an infusion pump with a maximal calculated total dosage not exceeding 20 mg of tPA. Patients with partial recanalization after EKOS
treatment were further treated by angioplasty and stent implantation. The recanalization status at the end of DSA was evaluated Depsipeptide nmr by blinded independent radiologist using the TICI criteria. TICI IIc and III were evaluated as complete recanalization (Fig. 4), TICI IIa and IIb were evaluated as partial recanalization. Neurological and physical examinations were done before therapy start and 24 h, 30 and 90 days after the start of treatment. Certified neurologist performed evaluation of neurological symptoms using NIHSS in all visits. Modified Rankin score was used for the evaluation of disability at days 30 and 90. Good clinical outcome was defined as a mRS 0–3, poor clinical outcome as a mRS 4–6. All adverse events were recorded. All changes in physical examinations, worsening of neurological symptoms (>4 points in NIHSS) and all disorders prolonging or requiring hospitalization were recorded as adverse events. Intracranial bleeds detected in the control brain CT examination 24 h after therapy onset were recorded. Intracranial bleeding with worsening of neurological symptoms > 4 points in the NIHSS were evaluated as SICH (ECASS 3 criteria). Other intracranial bleeds were evaluated as asymptomatic intracranial hemorrhage (AICH). In the control brain CT scan, detected brain edema associated with worsening of neurological symptoms > 4 points in the NIHSS was evaluated as “symptomatic”.