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1.  Endovascular Coil Embolization of Segmental Arteries Prevents Paraplegia After Subsequent TAAA Repair – An Experimental Model 
To test a strategy for minimizing ischemic spinal cord injury (SCI) following extensive thoracoabdominal aneurysm (TAAA) repair, we occluded a small number of segmental arteries (SAs) endovascularly one week before simulated aneurysm repair in an experimental model.
30 juvenile Yorkshire pigs (25.2±1.7kg) were randomized into three groups. All SAs—intercostal and lumbar—were sacrificed by a combination of surgical ligation of the lumbar SAs and occlusion of intercostal SAs with thoracic endovascular stent grafting (TEVAR). 7–10 days before this simulated TAAA replacement, SAs in the lower thoracic/upper lumbar region were occluded using embolization coils: 1.5±0.5 SAs in Group 1 (T13/L1), and 4.5±0.5 in Group 2 (T11-L3). No SAs were coiled in the controls. Hind limb function was evaluated blindly from daily videotapes using a modified Tarlov score: 0=paraplegia; 9=full recovery. After sacrifice, each segment of spinal cord was graded histologically using the 9-point Kleinman score: 0=normal, 8=complete necrosis.
Hind limb function remained normal after coil embolization. After simulated TAAA repair, paraplegia occurred in 6/10 control pigs, but only 2/10 pigs in Group 1: no pigs in Group 2 had SCI. Tarlov scores were significantly better in Group 2 (Control vs 1 p=0.06; Control vs 2 p= 0.0002; 1 vs 2 p=0.05). A dramatic reduction in histologic damage—most prominently in the coiled region—was seen when SAs were embolized before simulated TAAA repair.
Endovascular coiling of 2–4 SAs prevents paraplegia in an experimental model of extensive hybrid TAAA repair, and helps protect the spinal cord from ischemic histopathological injury. A clinical trial in a selected patient population at high risk for postoperative SCI may be appropriate.
PMCID: PMC3918675  PMID: 24220154
2.  Mathematical model for describing cerebral oxygen desaturation in patients undergoing deep hypothermic circulatory arrest 
Surgical treatment for aortic arch disease requiring periods of circulatory arrest is associated with a spectrum of neurological sequelae. Cerebral oximetry can non-invasively monitor patients for cerebral ischaemia even during periods of circulatory arrest. We hypothesized that cerebral desaturation during circulatory arrest could be described by a mathematical relationship that is time-dependent.
Cerebral desaturation curves obtained from 36 patients undergoing aortic surgery with deep hypothermic circulatory arrest (DHCA) were used to create a non-linear mixed model. The model assumes that the rate of oxygen decline is greatest at the beginning before steadily transitioning to a constant. Leave-one-out cross-validation and jackknife methods were used to evaluate the validity of the predictive model.
The average rate of cerebral desaturation during DHCA can be described as: Scto2[t]=81.4−(11.53+0.37×t) (1−0.88×exp (−0.17×t)). Higher starting Scto2 values and taller patient height were also associated with a greater decline rate of Scto2. Additionally, a predictive model was derived after the functional form of a×log (b+c×δ), where δ is the degree of Scto2 decline after 15 min of DHCA. The model enables the estimation of a maximal acceptable arrest time before reaching an ischaemic threshold. Validation tests showed that, for the majority, the prediction error is no more than ±3 min.
We were able to create two mathematical models, which can accurately describe the rate of cerebral desaturation during circulatory arrest at 12–15°C as a function of time and predict the length of arrest time until a threshold value is reached.
PMCID: PMC2791548  PMID: 19933513
brain, ischaemia; brain, oxygen consumption; hypothermia

Results 1-2 (2)