Cynthia B Zevallos1, Biyue Dai2, Sudeepta Dandapat3, Darko Quispe-Orozco1, Andrea Holcombe1, Sameer Ansari1, Mudassir Farooqui1, Colin P Derdeyn3, Edgar A Samaniego3, Santiago Ortega-Gutierrez4. 1. Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA. 2. Department of Biostatistics, University of Iowa, Iowa City, IA, USA. 3. Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA; Department of Neurosurgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA; Department of Radiology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA. 4. Department of Neurology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA; Department of Neurosurgery, University of Iowa Hospitals and Clinics, Iowa City, IA, USA; Department of Radiology, University of Iowa Hospitals and Clinics, Iowa City, IA, USA. Electronic address: santy-ortega@uiowa.edu.
Abstract
BACKGROUND: Contrast-induced neurotoxicity (CIN) is a rare complication of neurointerventional procedures and its understanding remains limited. We evaluated the association of CIN with systemic hemodynamics in patients undergoing neuroendovascular interventions. METHODS: We conducted a 1:2 matched case-control study from a prospectively collected database of 2510 neurointerventional patients. We defined CIN as new neurological deficits presented ≤24 h post-operation after excluding other possible etiologies. We obtained demographic, clinical and imaging data, and baseline and intraprocedural blood pressures (BP) from medical records. The area between baseline and intraprocedural BP was used to measure sustained variability of BP over time. A generalized linear mixed model and generalized estimating equation were used to analyze the BP difference between groups over time. RESULTS: We evaluated 11 CIN cases and 22 controls. 2746 and 5837 min of continued BP data were analyzed for cases and controls, respectively. CIN cases had higher measurements and greater variability for: Systolic BP (SBP) [median 125 (IQR:121-147) vs. 114 (IQR:107-124) mmHg], median area above baseline [median 350 (IQR:25-1328) vs. 52 (IQR:0-293) mmHg*minutes] and mean arterial pressure (MAP) [median 85 (IQR:79-98) vs. 80 (IQR:74-89) mmHg]. CIN cases demonstrated a significant mean increase in SBP and MAP of 23.41 mmHg (p < 0.01) and 13.79 mmHg (p < 0.01) when compared to controls, respectively, over the perioperative time. CONCLUSION: Sustained hypertension and high BP variability may contribute to the pathophysiology of CIN. Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms.
BACKGROUND: Contrast-induced neurotoxicity (CIN) is a rare complication of neurointerventional procedures and its understanding remains limited. We evaluated the association of CIN with systemic hemodynamics in patients undergoing neuroendovascular interventions. METHODS: We conducted a 1:2 matched case-control study from a prospectively collected database of 2510 neurointerventional patients. We defined CIN as new neurological deficits presented ≤24 h post-operation after excluding other possible etiologies. We obtained demographic, clinical and imaging data, and baseline and intraprocedural blood pressures (BP) from medical records. The area between baseline and intraprocedural BP was used to measure sustained variability of BP over time. A generalized linear mixed model and generalized estimating equation were used to analyze the BP difference between groups over time. RESULTS: We evaluated 11 CIN cases and 22 controls. 2746 and 5837 min of continued BP data were analyzed for cases and controls, respectively. CIN cases had higher measurements and greater variability for: Systolic BP (SBP) [median 125 (IQR:121-147) vs. 114 (IQR:107-124) mmHg], median area above baseline [median 350 (IQR:25-1328) vs. 52 (IQR:0-293) mmHg*minutes] and mean arterial pressure (MAP) [median 85 (IQR:79-98) vs. 80 (IQR:74-89) mmHg]. CIN cases demonstrated a significant mean increase in SBP and MAP of 23.41 mmHg (p < 0.01) and 13.79 mmHg (p < 0.01) when compared to controls, respectively, over the perioperative time. CONCLUSION: Sustained hypertension and high BP variability may contribute to the pathophysiology of CIN. Acute hypertension can increase blood-brain barrier permeability and potentially allow contrast to leak into the brain parenchyma causing direct toxicity and CIN symptoms.