COILUMICA: coil embolization of a coronary artery to pulmonary artery fistula via novel dual lumen micro catheter technique.

BACKGROUND: Management of coronary artery fistula (CAF) is based on obliterating the fistula communication between the cardiac arteries and other thoracic vessels. CASE PRESENTATION: We describe the presentation of an 85-year-old female with progressive exertional dyspnea on a background of a long standing left anterior descending diagonal to pulmonary artery fistula. We utilized neuro-interventional techniques to perform coil embolization via use of a Scepter XC dual lumen micro catheter. CONCLUSIONS: Dual lumen balloon catheters allow for super-selective artery interrogation, stability of balloon positioning, with less trauma to vessel architecture and accurate embolization. There were no complications and the patient reported improvement of symptoms on review.

Antiplatelet Drugs for Neurointerventions: Part 1 Clinical Pharmacology.

The development of endovascular treatment for intracranial aneurysms has established new techniques such as balloon and stent-assistance, flow diversion and endosaccular occlusion devices. Antiplatelet treatment is an important aspect to reduce risk of thrombus formation on microcatheters and implanted devices when utilizing these methods. It is particularly relevant for flow diverting stents to prevent early and late stent thrombosis. Consideration of platelet physiology and appropriate selection of antiplatelet medication is important as platelet dysfunction drives many of the pathological processes and complications of neurointerventional procedures. Part one of this review focuses on basic platelet physiology, pharmacology of common antiplatelet medications and future directions and therapies. Part two focuses on clinical applications and evidence-based therapeutic regimens.

A Review of the Management of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Despite decades of research, cerebral vasospasm (CV) continues to account for high morbidity and mortality in patients who survive their initial aneurysmal subarachnoid hemorrhage. OBJECTIVE: To define the scope of the problem and review key treatment strategies that have shaped the way CV is managed in the contemporary era. METHODS: A literature search was performed of CV management after aneurysmal subarachnoid hemorrhage. RESULTS: Recent advances in neuroimaging have led to improved detection of vasospasm, but established treatment guidelines including hemodynamic augmentation and interventional procedures remain highly variable among neurosurgical centers. Experimental research in subarachnoid hemorrhage continues to identify novel targets for therapy. CONCLUSIONS: Proactive and preventive strategies such as oral nimodipine and endovascular rescue therapies can reduce the morbidity and mortality associated with CV.

Mecamylamine prevents neuronal apoptosis induced by glutamate and low potassium via differential anticholinergic-independent mechanisms.

Neuronal loss via apoptosis caused by various stimuli may be the fundamental mechanism underlying chronic and acute neurodegenerative diseases. A drug inhibiting neuronal apoptosis may lead to a practical treatment for these diseases. In this study, treatment with mecamylamine, a classical antagonist of nicotinic acetylcholine receptors (nAChRs), prevented neuronal apoptosis induced by 75 microM glutamate and by low potassium (LK) in cerebellar granule neurons (CGNs) with EC(50)s of 35 and 293 microM, respectively. Two other antagonists of nAChRs, dihydro-beta-erythroidine and tubocurarine, failed to inhibit these two kinds of apoptosis. Mecamylamine inhibited the NMDA (30 microM)-evoked current and competed with [(3)H]MK-801. Furthermore, two inhibiters of the c-Jun N-terminal kinase (JNK) pathway prevented LK-induced apoptosis. Mecamylamine reversed the phosphorylation levels of JNK and c-Jun as well as the expression of c-Jun caused by LK in a Western blot assay. In addition, the JNK/c-Jun pathway was not involved in glutamate-induced cell death of CGNs. Our results suggest that mecamylamine prevents glutamate-induced apoptosis by blocking NMDA receptors at the MK-801 site and LK-induced apoptosis by inhibiting the activation of the JNK/c-Jun pathway.