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Abstract
Background Therapeutic hypothermia (TH) has shown potential in cardiac intervention for years; however, its adoption into the neurovascular space has been limited. Studies have pointed to slow cooling and limited depth of hypothermia negatively affecting the studies. Here an insulated catheter that allows for consistent infusion of chilled saline directly to the brain, avoids the above drawbacks. By delivering the cold saline directly to the target tissue a faster depth of hypothermia can be achieved, and we believe this will have a direct benefit to the growth of the ischemic lesions after reperfusion in a large vessel occlusion model.
Methods Ten dogs were randomized to either receive local brain cooling or no adjunctive care. Each animal underwent a temporary middle cerebral artery occlusion (MCAO) for a total of 45 minutes using an aneurysm coil. Five minutes prior to flow restoration, cold saline is injected through the ipsilateral internal carotid artery (ICA), to ensure the chilled saline reached the brain, an insulated catheter was used. The treatment is continued for a total of 25 minutes, at which point the animal is transferred to a 3T MRI for post ischemia imaging. Diffusion weighted (DWI) MRI was done immediately upon entering the MRI, and then repeated 1 hour later. To confirm flow restoration, time of flight MRI was acquired.
Results Of the 10 animals that received temporary MCAO, 8 were successfully enrolled (n = 4 per group), due to two unsuccessful reperfusions. There was no significant difference in the size of the infarct immediately upon entering the MRI (p = 0.34). After the 1 hour delayed MRI the rate of growth on the infarct size was significantly greater in the control animals compared to the local hypothermia animal (161.3% vs 13.8%, p = 0.016, figure 1). The infarct growth in all 4 of the control animals was greater than any of the cooled animals.
Conclusions Localized hypothermia was able to reduce the post MCAO infarct progression in a canine model of temporary MCAO. The reduction in infarct growth is most likely due to the protection of the blood brain barrier, which is known to break down in both the infarct core and penumbra in this model.
Diffusion weighted MRI repeated at 1 hr. The green area shows the tissue that was infarcted after reperfusion, and the blue area shows the growth over 1 hour. A) selective hypothermia B) no cooling
Disclosures R. King: None. V. Anagnostakou: None. M. Shazeeb: None. S. Hornibrook: 4; C; FocalCool. 5; C; FocalCool. M. Epshtein: None. C. Raskett: None. A. Puri: 2; C; Medtronic, Stryker. N. Henninger: None. T. Merrill: 4; C; FocalCool. 5; C; FocalCool. M. Gounis: 1; C; Research support from the NIH, the United States – Israel Binational Science Foundation, Anaconda, ApicBio, Arsenal Medical, Axovant, Balt, Cerenovus, Ceretrieve, CereVasc LLC, Cook Medical, Galaxy Th. 2; C; Consultant on a fee-per-hour basis for Alembic LLC, Astrocyte Pharmaceuticals, BendIt Technologies, Cerenovus, Imperative Care, Jacob’s Institute, Medtronic Neurovascular, Mivi Neurosciences, phenox G. 4; C; Imperative Care, InNeuroCo, Galaxy Therapeutics, and Neurogami, and Synchron.