Multiple telescoping flow diverter technique in endovascular treatment of a vertebrobasilar dissecting aneurysm: case report.

A 64-year-old man presented with headache and dizziness. A vertebrobasilar dissecting aneurysm was identified via computed tomography angiography and high resolution magnetic resonance imaging. Perioperatively, standard oral dual antiplatelet drugs were given. Two flow diverters were telespcoped for endovascular treatment of the aneurysm. Postoperatively, there were no signs of cerebral infarction and no new symptoms. At the 6-month follow-up, digital subtraction angiography showed that the aneurysm was almost completely occluded, with no other complications. This case serves as a reference for using the multiple telescoping flow diverter technique to treat vertebrobasilar dissecting aneurysm.

Cerebral arterial air embolism after computed tomography-guided hook-wire localization of a pulmonary nodule: A case report.

RATIONALE: Cranial arterial air embolism is a rare but potentially fatal complication after computed tomography (CT)-guided pulmonary interventions. PATIENT CONCERNS: A 64-year-old man was diagnosed with a pulmonary nodule (diameter: approximately 1 cm) in the right lower lobe. The patient developed convulsions after CT-guided hook-wire localization. DIAGNOSIS: Cranial CT revealed arborizing/linearly distributed gas in the territory of the right middle cerebral artery. INTERVENTIONS: The patient was administered hyperbaric oxygen, antiplatelet aggregation therapy, and dehydration treatment. OUTCOMES: Clinical death occurred 55 hours after air embolism. LESSONS: Systemic air embolism is a serious complication of lung puncture. Clinicians should improve their understanding of this complication and remain vigilant against air embolism.

IL-18 cleavage triggers cardiac inflammation and fibrosis upon ß-adrenergic insult.

Aims: Rapid over-activation of ß-adrenergic receptor (ß-AR) upon stress leads to cardiac inflammation, a prevailing factor that underlies heart injury. However, mechanisms by which acute ß-AR stimulation induce cardiac inflammation still remain unknown. Here, we set out to identify the crucial role of inflammasome/interleukin (IL)-18 in initiating and maintaining cardiac inflammatory cascades upon ß-AR insult. Methods and results: Male C57BL/6 mice were injected with a single dose of ß-AR agonist, isoproterenol (ISO, 5 mg/kg body weight) or saline subcutaneously. Cytokine array profiling demonstrated that chemokines dominated the initial cytokines upregulation specifically within the heart upon ß-AR insult, which promoted early macrophage infiltration. Further investigation revealed that the rapid inflammasome-dependent activation of IL-18, but not IL-1ß, was the critical up-stream regulator for elevated chemokine expression in the myocardium upon ISO induced ß1-AR-ROS signalling. Indeed, a positive correlation was observed between the serum levels of norepinephrine and IL-18 in patients with chest pain. Genetic deletion of IL-18 or the up-stream inflammasome component NLRP3 significantly attenuated ISO-induced chemokine expression and macrophage infiltration. In addition, IL-18 neutralizing antibodies selectively abated ISO-induced chemokines, proinflammatory cytokines and adhesion molecules but not growth factors. Moreover, blocking IL-18 early after ISO treatment effectively attenuated cardiac inflammation and fibrosis. Conclusion: Inflammasome-dependent activation of IL-18 within the myocardium upon acute ß-AR over-activation triggers cytokine cascades, macrophage infiltration and pathological cardiac remodelling. Blocking IL-18 at the early stage of ß-AR insult can successfully prevent inflammatory responses and cardiac injuries.