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Introduction: Hyperdynamic therapy with dobutamine (DOB) administration on patients with subarachnoid hemorrhage (SAH) is a useful strategy for treating cerebral vasospasm and neurological deterioration. Even some reports have suggested that DOB administration caused the cerebral blood flow (CBF) augmentation by increasing cardiac output, microcirculatory behavior in brain remains unclear. Hypothesis: Red blood cell (RBC) velocity should be increased under DOB administration. To investigate the cortical microcirculation, two-photon laser scanning microscopy with successive line-scans was used for red blood cell (RBC) velocity estimation. Methods: SAH was induced in ten male wild-type C57BL/6 mice (23 - 25g) using endovascular perforation technique. Five days after SAH, a cranial window was prepared for optical access to the cortical vasculature. Then we observed two-photon microscopy with intravenously injected rhodamine-dextran. The RBC velocity was visualized as dark objects against the fluorescent plasma background. The velocity was estimated from dark objects angle in successive line-scans analyzed by Radon function based algorithm. DOB was administrated intravenously at the dose of 6 and 12 μg/kg/min. Results: RBC velocity was increased in 8 mice after the DOB administration and 2 mice were reduced. The RBC velocity in increased mice of baseline , 6 , and 12 μg/kg/min was 1.29±0.40, 1.70±0.74 and 1.37±0.53 mm/sec, respectively. In the reduced mice, the RBC velocity was dropped almost half value of baseline at the DOB administration. Conclusions: DOB administration was increased RBC velocity in cortical microcirculation. It indicates DOB hyperdynamic therapy on patients with SAH is effective in the viewpoint of cortical microcirculatory control.

Introduction: Subarachnoid hemorrhage (SAH) is a devastating form of stroke with high rates of mortality and disability. Evidence suggests that acute failure to restore cerebral blood flow (CBF) after SAH may be setting the stage of delayed cerebral ischemia. Despite increasing number of experiments using rodent models, little is known about the effect of CBF and neuro-behavioral profile on ischemic brain injury, vasospasm and neurological outcome for precise grading of this model to mimic clinical severity in humans. Hypothesis: To investigate the feasibility of MRI-based assessment of clot distribution and CBF for grading SAH severity in a mouse endovascular perforation model. Methods: SAH was induced by endovascular perforation in adult male C57BL/6 mice. CBF was estimated by MRI continuous arterial spin labeling with short delay after tagging. Neurological deficit and behavioral data were recorded by adhesion removal test and open field test, respectively. MRI and neuro-behavioral performance were assessed immediately after SAH induction and at 24, 72 hours after SAH. The time-course changes of each parameter and their relationships with MRI-based grading score using T2*-weighted image at 24 hours, new ischemic lesion detected by diffusion-weight image (DWI) at 72 hours, day 7 and 14, cortical vasospasm visualized by two-photon laser microscopy (performed between 48-72 hours), and final outcome based on the modified Garcia score at day 21 after SAH were analyzed. Results: Among a total of 60 mice, the mortality rates at 24 hours and day 21 were 17% and 30%, respectively. There were strong correlations between the CBF value at 72 hours after SAH and MRI grading (24% scored as grade 1, 18% as grade 2, 30% as grade 3, and 28% as grade 4) (r=0.75; P Conclusions: Non-invasive MRI-based grading that includes both CBF and neuro-behavioral performance at 24 hours enables more accurate in vivo evaluation of SAH severity based on the prevalence of vasospasm and functional outcome.

Takotsubo cardiomyopathy (TCM) is a life-threatening systemic consequence early after subarachnoid hemorrhage (SAH), but precise hemodynamics and related outcome are not well-understood. We aimed to investigate the TCM-induced cardiac function by transpulmonary thermodilution and its impact on clinical outcome of SAH. Forty-six consecutive SAH patients who developed TCM and treated surgically or endovascularly were analyzed retrospectively. Patients were divided into two groups of LVEF r = 0.82, P P P -1 had a sensitivity of 82% and specificity of 84% for detecting LVEF -1 was associated with delayed cerebral ischemia (DCI) (odds ratio [OR], 2.14; 95% confidence interval [CI], 1.33-2.86; P = 0.004) and poor 3-month functional outcome on modified Rankin Scale of 4-6 (OR, 1.87; 95% CI, 1.06-3.29; P = 0.02). An ELWI >14 mL/kg after day 4 increased the risk of poor functional outcome at 3-month follow-up (OR, 2.10; 95% CI, 1.11-3.97; P = 0.04). In conclusion, prolonged cardiac dysfunction and pulmonary edema increased the risk of DCI and poor 3-month functional outcome in patients with SAH suffering from TCM. Serial measurements of CFI and ELWI by transpulmonary thermodilution may provide an easy bedside method of detecting early changes of the cardiopulmonary function in directing proper post-SAH treatment.

Intensive hemodynamic augmentation by increasing cardiac output (CO) is a valuable method of elevating cerebral blood flow and oxygenation in the dysautoregulated vascular territories after subarachnoid hemorrhage (SAH). We prospectively assessed the effect of hyperdynamic therapy with dobutamine (DOB) or milrinone (MIL) on regional cerebral oxygenation (rSO 2 ) for reversing clinical deterioration induced by delayed cerebral ischemia, using an integrative monitoring with uncalibrated pulse contour CO analysis and multi-channel near-infrared spectroscopy. One-hundred ten SAH patients diagnosed to have clinical deterioration due to delayed cerebral ischemia were assigned to receive hemodynamic augmentation with DOB or MIL (n=56 per each group). For hyperdynamic therapy, each inotrope was initiated at low dose (DOB: 3μg/kg/min; MIL 0.15μg/kg/min) and then increased in each dose increment until resolution of the symptoms unless any adverse effects occur during the therapy, based on our predefined hemodynamic regimen to induce similar dose-related increase in CO. Real-time CO and rSO 2 changes in conjunction with the assessment of neurological improvements were compared. A total of 425 dose increment challenges (DOB, n=197; MIL, n=228) were performed. In spasm-affected territories, decreased and/or fluctuating rSO 2 was detected compared with recordings in other brain region. Patients who exhibited rapid elevation of CO by each challenge had subsequent uptake and stabilization of rSO 2 . The responses (total number and degree of neurological improvements) were more significant in patients treated with DOB than those treated with MIL ( P < 0.05), although tachycardia that may affect stroke volume depression during the DOB therapy was more evident (DOB 28% vs. MIL 9%). Area under the ROC curve to predict rSO 2 elevation or neurological improvement for both drug groups were significant ( P < 0.0001) and the values were significantly greater in DOB than in MIL ( P < 0.05). In conclusion, DOB can provide more effective hemodynamic augmentation in relieving focal cerebral ischemia in patients after SAH. MIL is also effective in the hyperdynamic therapy but may be used as a second line in a patient subgroup when DOB was contraindicated.

Purpose: Plaque protrusion may cause thrombo-embolic events following carotid artery stenting (CAS). We evaluated the temporal profile and the treatment options of plaque protrusion (PLP) in our series. Methods: In 32 consecutive cases since April 2009 to December 2011, we checked intravascular status using ultrasound (US) and CT angiography (CTA) within 1 week after CAS. For these cases, medical risk factors, procedural factors, and pre-operative CTA and plaque MRI were also evaluated. Results: As for medical factors including hypertension, diabetes mellitus and hyperlipidemia, there were no significant effects on PLP. Effects of neurological and radiological factors on post procedural PLP are shown in table1. Symptomatic and ulcerative plaque were the risk factor of the post procedural PLP (symptomatic plaque, RR 2.33; 95% CI, 1.31-4.16; p=0.01; ulceration, RR 2.33; 95% CI, 1.31-4.16; p=0.01). High intensity of T1-black blood (BB) MRI tended to induce PLP (RR 1.62; 95% CI, 1.03-2.54; p=0.09). Pre-dilatation may reduce PLP (RR, 0.53; 95% CI, 0.21-1.34; p=0.09). All cases of PLP were treated by reinforcement of anticoagulation and/or antiplatelet therapy, and one case needed stenting following balloon angioplasty for progression of plaque protrusion in spite of medical treatments. In 8 cases of PLP, 7 cases were uneventful and 1 case had a minor stroke in the post-operative course. Conclusions: 1. In terms of plaque characteristics, ulceration and symptomatic plaque relevant to post procedural PLP. 2. Post procedural neuroimaging studies such as CTA and US are crucial to detect plaque protrusion. 3. In case of plaque protrusion, careful managements including reinforcement of thrombotic therapy and endovascular procedures are required.

Background and Purpose— Early goal-directed hemodynamic therapy is of particular importance for adequate cerebral circulation of patients with vasospasm after subarachnoid hemorrhage but is often precluded by the invasiveness of established cardiac output determination using a pulmonary artery catheter. This study was undertaken to validate the usefulness of less invasive goal-directed hemodynamic monitoring by transpulmonary thermodilution technique in patients after subarachnoid hemorrhage. Methods— One hundred sixteen patients with subarachnoid hemorrhage who underwent surgical clipping within 24 hours of ictus were investigated. Validation of transpulmonary thermodilution-derived intermittent/continuous cardiac output and cardiac preload (global end diastolic volume) were compared with pulmonary artery catheter-derived reference cardiac output and pulmonary capillary wedge pressure or central venous pressure in 16 patients diagnosed with vasospasm. In a subsequent trial of 100 consecutive cases, clinical results between the new and standard management paradigms were compared. Results— Transpulmonary thermodilution-derived intermittent cardiac output and transpulmonary thermodilution-derived continuous cardiac output showed close agreement to catheter-derived reference cardiac output with high correlation ( r =0.85 and 0.77) and low percentage error (13.5% and 18.0%). Fluid responsiveness to defined volume loading was predicted better with global end diastolic volume than with pulmonary capillary wedge pressure and central venous pressure for larger receiver operating characteristic curve area. Patients receiving early goal-directed management by transpulmonary thermodilution experienced reduced frequencies of vasospasm and cardiopulmonary complications compared with those managed with standard therapy ( P P =0.06). Conclusions— Goal-directed hemodynamic management guided by transpulmonary thermodilution appears to have a therapeutic advantage for optimizing the prognosis of patients with subarachnoid hemorrhage with vasospasm over conventional methods.