Glioblastoma treated with magnetic resonance imaging-guided laser interstitial thermal therapy: Safety, efficacy, and outcomes

BACKGROUND: Despite the multitude of available treatments, glioblastoma (GBM) remains an aggressive and uniformly fatal tumor. Laser interstitial thermal therapy (LITT) is a novel, minimally invasive treatment that holds promise for treating patients with GBM who are not candidates for traditional open craniotomy. However, due to the recent introduction of LITT into clinical practice, large series that evaluate safety and long-term outcomes after LITT are lacking. OBJECTIVE: To present our institution\u27s series of over 50 GBM patients treated with LITT, with regard to safety, efficacy, and outcomes. METHODS: We performed a retrospective descriptive study of patients with histologically proven GBM who underwent LITT. Data collected included demographics, tumor location and volume, tumor genetic markers, treatment volume, perioperative complications, and long-term follow-up data. RESULTS: We performed 58 LITT treatments for GBM in 54 patients over 5.5 yr. Forty-one were recurrent tumors while 17 were frontline treatments. Forty GBMs were lobar in location, while 18 were in deep structures (thalamus, insula, corpus callosum). Average tumor volume was 12.5 ± 13.4 cm3. Average percentage of tumor treated with the yellow thermal damage threshold (TDT) line (dose equivalent of 43°C for 2 min) was 93.3% ± 10.6%, and with the blue TDT line (dose equivalent of 43°C for 10 min) was 88.0% ± 14.2%. There were 7 perioperative complications (12%) and 2 mortalities (3.4%). Median overall survival after LITT for the total cohort was 11.5 mo, and median progression-free survival 6.6 mo. CONCLUSION: LITT appears to be a safe and effective treatment for GBM in properly selected patients

Inhalation of nitric oxide prevents ischemic brain damage in experimental stroke by selective dilatation of collateral arterioles

RATIONALE: Stroke is the third most common cause of death in industrialized countries. The main therapeutic target is the ischemic penumbra, potentially salvageable brain tissue that dies within the first few hours after blood flow cessation. Hence, strategies to keep the penumbra alive until reperfusion occurs are needed. OBJECTIVE:: To study the effect of inhaled nitric oxide on cerebral vessels and cerebral perfusion under physiological conditions and in different models of cerebral ischemia. METHODS AND RESULTS:: This experimental study demonstrates that inhaled nitric oxide (applied in 30% oxygen/70% air mixture) leads to the formation of nitric oxide carriers in blood that distribute throughout the body. This was ascertained by in vivo microscopy in adult mice. Although under normal conditions inhaled nitric oxide does not affect cerebral blood flow, after experimental cerebral ischemia induced by transient middle cerebral artery occlusion it selectively dilates arterioles in the ischemic penumbra, thereby increasing collateral blood flow and significantly reducing ischemic brain damage. This translates into significantly improved neurological outcome. These findings were validated in independent laboratories using two different mouse models of cerebral ischemia and in a clinically relevant large animal model of stroke. CONCLUSIONS:: Inhaled nitric oxide thus may provide a completely novel strategy to improve penumbral blood flow and neuronal survival in stroke or other ischemic conditions

Clinical relevance and treatment of carotid stent fractures

Objective: To review all published reports and investigate the clinical relevance and need for treatment of carotid stent fractures. Methods: Electronic and hand-searching of the published literature and the Manufacturer and User Facility Device Experience (MAUDE) database. Results: Thirteen articles were published. There are 10 case reports and 3 clinical studies. There are 26 reports of fractured stems in the MAUDE database. Fifty-five cases of carotid stent fractures are reported in total. A total of 201 carotid stents were examined in the 3 studies, and the incidence of fractures was 8.9% (18/201). Fractured stents were 22 Xact, 20 Acculink, 6 Precise, 2 Exponent, 1 Nexstent, 1 Genesis, 1 Symbiot, and 2 nonspecified nitinol self-expandable stents. Twenty-seven of the treated carotid lesions were atherosclerotic, 3 restenoses after carotid endarterectomy, 2 postradiational, 1 pseudoaneurysm, and 22 lesions of unknown pathology. Calcification was reported in 15 of the 27 atherosclerotic lesions (55.5%). Time from implantation to fracture ranged from 0 days (fracture during implantation) to 37 months. In 55% of the cases, stent fracture was associated with restenosis. Six patients presented with symptoms. Treatment was reported for 32 patients: 14 patients underwent de novo stent placement, 2 balloon angioplasty, 2 carotid endarterectomy, 2 bypass graft (1 vein, 1 polytetrafluoroethylene), 1 anticoagulation, and 11 patients were followed up. Conclusion: Carotid stent fractures are mainly reported in self-expandable nitinol stents. Plaque calcification may be a risk factor for stent fractures. No difference was observed between open and closed-cell design. Stent fractures were often associated with restenosis and usually were asymptomatic. The actual incidence, clinical relevance, and optimal treatment remain to be clarified from larger prospective studies designed to investigate the issue. (J Vasc Surg 2010;51:1280-5.