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Your search keyword '"Ducruet, Andrew"' showing total 5 results
Start Over Author "Ducruet, Andrew" Publication Type Electronic Resources
5 results on '"Ducruet, Andrew"'

1. Treatment of Large Intracranial Aneurysms Using the Woven EndoBridge (WEB): A Propensity Score-Matched Analysis

Author

Musmar, Basel, Salim, Hamza, Adeeb, Nimer, Aslan, Assala, Aljeradat, Bahaa, Diestro, Jose, McLellan, Rachel, Algin, Oktay, Ghozy, Sherief, Dibas, Mahmoud, Lay, Sovann, Guenego, Adrien, Renieri, Leonardo, Cancelliere, Nicole, Carnevale, Joseph, Saliou, Guillaume, Mastorakos, Panagiotis, El Naamani, Kareem, Shotar, Eimad, Premat, Kevin, Möhlenbruch, Markus, Kral, Michael, Vranic, Justin, Chung, Charlotte, Salem, Mohamed, Lylyk, Ivan, Foreman, Paul, Vachhani, Jay, Shaikh, Hamza, Župančić, Vedran, Hafeez, Muhammad, Catapano, Joshua, Waqas, Muhammad, Tutino, Vincent, Ibrahim, Mohamed, Mohammed, Marwa, Ozates, M. Ozgur, Ayberk, Giyas, Rabinov, James, Ren, Yifan, Schirmer, Clemens, Piano, Mariangela, Kühn, Anna, Michelozzi, Caterina, Elens, Stéphanie, Starke, Robert, Hassan, Ameer, Ogilvie, Mark, Nguyen, Anh, Jones, Jesse, Brinjikji, Waleed, Nawka, Marie, Psychogios, Marios, Ulfert, Christian, Spears, Julian, Jankowitz, Brian, Burkhardt, Jan-Karl, Domingo, Ricardo, Huynh, Thien, Martinez-Gutierrez, Juan Carlos, Essibayi, Muhammed, Sheth, Sunil, Spiegel, Gary, Tawk, Rabih, Lubicz, Boris, Panni, Pietro, Puri, Ajit, Pero, Guglielmo, Nossek, Erez, Raz, Eytan, Killer-Oberfalzer, Monika, Griessenauer, Christoph, Asadi, Hamed, Siddiqui, Adnan, Brook, Allan, Altschul, David, Ducruet, Andrew, Albuquerque, Felipe, Regenhardt, Robert, Stapleton, Christopher, Kan, Peter, Kalousek, Vladimir, Lylyk, Pedro, Boddu, Srikanth, Knopman, Jared, Aziz-Sultan, Mohammad A, Tjoumakaris, Stavropoula, Clarençon, Frédéric, Limbucci, Nicola, Cuellar-Saenz, Hugo, Jabbour, Pascal, Pereira, Vitor, Patel, Aman, Dmytriw, Adam, Musmar, Basel, Salim, Hamza, Adeeb, Nimer, Aslan, Assala, Aljeradat, Bahaa, Diestro, Jose, McLellan, Rachel, Algin, Oktay, Ghozy, Sherief, Dibas, Mahmoud, Lay, Sovann, Guenego, Adrien, Renieri, Leonardo, Cancelliere, Nicole, Carnevale, Joseph, Saliou, Guillaume, Mastorakos, Panagiotis, El Naamani, Kareem, Shotar, Eimad, Premat, Kevin, Möhlenbruch, Markus, Kral, Michael, Vranic, Justin, Chung, Charlotte, Salem, Mohamed, Lylyk, Ivan, Foreman, Paul, Vachhani, Jay, Shaikh, Hamza, Župančić, Vedran, Hafeez, Muhammad, Catapano, Joshua, Waqas, Muhammad, Tutino, Vincent, Ibrahim, Mohamed, Mohammed, Marwa, Ozates, M. Ozgur, Ayberk, Giyas, Rabinov, James, Ren, Yifan, Schirmer, Clemens, Piano, Mariangela, Kühn, Anna, Michelozzi, Caterina, Elens, Stéphanie, Starke, Robert, Hassan, Ameer, Ogilvie, Mark, Nguyen, Anh, Jones, Jesse, Brinjikji, Waleed, Nawka, Marie, Psychogios, Marios, Ulfert, Christian, Spears, Julian, Jankowitz, Brian, Burkhardt, Jan-Karl, Domingo, Ricardo, Huynh, Thien, Martinez-Gutierrez, Juan Carlos, Essibayi, Muhammed, Sheth, Sunil, Spiegel, Gary, Tawk, Rabih, Lubicz, Boris, Panni, Pietro, Puri, Ajit, Pero, Guglielmo, Nossek, Erez, Raz, Eytan, Killer-Oberfalzer, Monika, Griessenauer, Christoph, Asadi, Hamed, Siddiqui, Adnan, Brook, Allan, Altschul, David, Ducruet, Andrew, Albuquerque, Felipe, Regenhardt, Robert, Stapleton, Christopher, Kan, Peter, Kalousek, Vladimir, Lylyk, Pedro, Boddu, Srikanth, Knopman, Jared, Aziz-Sultan, Mohammad A, Tjoumakaris, Stavropoula, Clarençon, Frédéric, Limbucci, Nicola, Cuellar-Saenz, Hugo, Jabbour, Pascal, Pereira, Vitor, Patel, Aman, and Dmytriw, Adam

Abstract

The Woven EndoBridge (WEB) device is primarily used for treating wide-neck intracranial bifurcation aneurysms under 10 mm. Limited data exists on its efficacy for large aneurysms. We aim to assess angiographic and clinical outcomes of the WEB device in treating large versus small aneurysms. We conducted a retrospective review of the WorldWide WEB Consortium database, from 2011 to 2022, across 30 academic institutions globally. Propensity score matching (PSM) was employed to compare small and large aneurysms on baseline characteristics. A total of 898 patients were included. There was no significant difference observed in clinical presentations, smoking status, pretreatment mRS, presence of multiple aneurysms, bifurcation location, or prior treatment between the two groups. After PSM, 302 matched pairs showed significantly lower last follow-up adequate occlusion rates (81% vs 90%, p = 0.006) and higher retreatment rates (12% vs 3.6%, p < 0.001) in the large aneurysm group. These findings may inform treatment decisions and patient counseling. Future studies are needed to further explore this area.

Published
2024

2. Spetzler-Martin Grade III Arteriovenous Malformations: A Multicenter Propensity-Adjusted Analysis of the Effects of Preoperative Embolization.

Author

Catapano, Joshua S, Catapano, Joshua S, Frisoli, Fabio A, Nguyen, Candice L, Wilkinson, D Andrew, Majmundar, Neil, Cole, Tyler S, Baranoski, Jacob F, Whiting, Alexander C, Kim, Helen, Ducruet, Andrew F, Albuquerque, Felipe C, Cooke, Daniel L, Spetzler, Robert F, Lawton, Michael T, Catapano, Joshua S, Catapano, Joshua S, Frisoli, Fabio A, Nguyen, Candice L, Wilkinson, D Andrew, Majmundar, Neil, Cole, Tyler S, Baranoski, Jacob F, Whiting, Alexander C, Kim, Helen, Ducruet, Andrew F, Albuquerque, Felipe C, Cooke, Daniel L, Spetzler, Robert F, and Lawton, Michael T

Abstract

BackgroundSpetzler-Martin (SM) grade III arteriovenous malformations (AVMs) are at the boundary of safe operability, and preoperative embolization may reduce surgical risks.ObjectiveTo evaluate the benefits of preoperative AVM embolization by comparing neurological outcomes in patients with grade III AVMs treated with or without preoperative embolization.MethodsAll microsurgically treated grade III AVMs were identified from 2011 to 2018 at 2 medical centers. Neurological outcomes, measured as final modified Rankin Scale scores (mRS) and changes in mRS from preoperative baseline to last follow-up evaluation, were compared in patients with and without preoperative embolization.ResultsOf the 102 patients with grade III AVMs who were treated microsurgically, 57 (56%) underwent preoperative embolization. Significant differences were found between the patients with and without embolization in AVM eloquence (74% vs 93%, P = .02), size ≥ 3 cm (47% vs 73%, P = .01), diffuseness (7% vs 22%, P = .04), and mean final mRS (1.1 vs 2.0, P = .005). Poor outcomes were more frequent in patients without embolization (38%) than with embolization (7%) (final mRS > 2; P < .001). Propensity-adjusted analysis revealed AVM resection without embolization was a risk factor for poor outcome (mRS score > 2; odds ratio, 4.2; 95% CI, 1.1-16; P = .03).ConclusionNonembolization of SM grade III AVMs is associated with an increased risk of poor neurological outcomes after microsurgical resection. Preoperative embolization of intermediate-grade AVMs selected because of large AVM size, surgical inaccessibility of feeding arteries, and high flow should be employed more often than anticipated, even in the context of increasing microsurgical experience with AVMs.

Published
2021

3. Mutations in Chromatin Modifier and Ephrin Signaling Genes in Vein of Galen Malformation.

Author

UCL - SSS/DDUV - Institut de Duve, Duran, Daniel, Zeng, Xue, Jin, Sheng Chih, Choi, Jungmin, Nelson-Williams, Carol, Yatsula, Bogdan, Gaillard, Jonathan, Furey, Charuta Gavankar, Lu, Qiongshi, Timberlake, Andrew T, Dong, Weilai, Sorscher, Michelle A, Loring, Erin, Klein, Jennifer, Allocco, August, Hunt, Ava, Conine, Sierra, Karimy, Jason K, Youngblood, Mark W, Zhang, Jinwei, DiLuna, Michael L, Matouk, Charles C, Mane, Shrikant, Tikhonova, Irina R, Castaldi, Christopher, López-Giráldez, Francesc, Knight, James, Haider, Shozeb, Soban, Mariya, Alper, Seth L, Komiyama, Masaki, Ducruet, Andrew F, Zabramski, Joseph M, Dardik, Alan, Walcott, Brian P, Stapleton, Christopher J, Aagaard-Kienitz, Beverly, Rodesch, Georges, Jackson, Eric, Smith, Edward R, Orbach, Darren B, Berenstein, Alejandro, Bilguvar, Kaya, Vikkula, Miikka, Gunel, Murat, Lifton, Richard P, Kahle, Kristopher T, UCL - SSS/DDUV - Institut de Duve, Duran, Daniel, Zeng, Xue, Jin, Sheng Chih, Choi, Jungmin, Nelson-Williams, Carol, Yatsula, Bogdan, Gaillard, Jonathan, Furey, Charuta Gavankar, Lu, Qiongshi, Timberlake, Andrew T, Dong, Weilai, Sorscher, Michelle A, Loring, Erin, Klein, Jennifer, Allocco, August, Hunt, Ava, Conine, Sierra, Karimy, Jason K, Youngblood, Mark W, Zhang, Jinwei, DiLuna, Michael L, Matouk, Charles C, Mane, Shrikant, Tikhonova, Irina R, Castaldi, Christopher, López-Giráldez, Francesc, Knight, James, Haider, Shozeb, Soban, Mariya, Alper, Seth L, Komiyama, Masaki, Ducruet, Andrew F, Zabramski, Joseph M, Dardik, Alan, Walcott, Brian P, Stapleton, Christopher J, Aagaard-Kienitz, Beverly, Rodesch, Georges, Jackson, Eric, Smith, Edward R, Orbach, Darren B, Berenstein, Alejandro, Bilguvar, Kaya, Vikkula, Miikka, Gunel, Murat, Lifton, Richard P, and Kahle, Kristopher T

Abstract

Normal vascular development includes the formation and specification of arteries, veins, and intervening capillaries. Vein of Galen malformations (VOGMs) are among the most common and severe neonatal brain arterio-venous malformations, shunting arterial blood into the brain's deep venous system through aberrant direct connections. Exome sequencing of 55 VOGM probands, including 52 parent-offspring trios, revealed enrichment of rare damaging de novo mutations in chromatin modifier genes that play essential roles in brain and vascular development. Other VOGM probands harbored rare inherited damaging mutations in Ephrin signaling genes, including a genome-wide significant mutation burden in EPHB4. Inherited mutations showed incomplete penetrance and variable expressivity, with mutation carriers often exhibiting cutaneous vascular abnormalities, suggesting a two-hit mechanism. The identified mutations collectively account for ∼30% of studied VOGM cases. These findings provide insight into disease biology and may have clinical implications for risk assessment.

Published
2019

4. Intranasal Delivery of Caspase-9 Inhibitor Reduces Caspase-6-Dependent Axon/Neuron Loss and Improves Neurological Function after Stroke

Author

American Heart Association, National Institutes of Health (US), Akpan, Nsikan, Serrano-Saiz, Esther, Zacharia, Brad E., Otten, Marc L., Ducruet, Andrew F., Snipas, Scott J., Liu, Wen, Velloza, Jennifer, Cohen, Greg, Sosunov, Sergeyi A., Frey II, William H., Salvesen, Guy S., Connolly Jr., E. Sander, Troy, Carol M., American Heart Association, National Institutes of Health (US), Akpan, Nsikan, Serrano-Saiz, Esther, Zacharia, Brad E., Otten, Marc L., Ducruet, Andrew F., Snipas, Scott J., Liu, Wen, Velloza, Jennifer, Cohen, Greg, Sosunov, Sergeyi A., Frey II, William H., Salvesen, Guy S., Connolly Jr., E. Sander, and Troy, Carol M.

Abstract

Despite extensive research to develop an effective neuroprotective strategy for the treatment of ischemic stroke, therapeutic options remain limited. Although caspase-dependent death is thought to play a prominent role in neuronal injury, direct evidence of active initiator caspases in stroke and the functional relevance of this activity have not previously been shown. Using an unbiased caspase-trapping technique in vivo, we isolated active caspase-9 from ischemic rat brain within 1 h of reperfusion. Pathogenic relevance of active caspase-9 was shown by intranasal delivery of a novel cell membrane-penetrating highly specific inhibitor for active caspase-9 at 4 h postreperfusion (hpr). Caspase-9 inhibition provided neurofunctional protection and established caspase-6 as its downstream target. The temporal and spatial pattern of expression demonstrates that neuronal caspase-9 activity induces caspase-6 activation, mediating axonal loss by 12 hpr followed by neuronal death within 24 hpr. Collectively, these results support selective inhibition of these specific caspases as an effective therapeutic strategy for stroke.

Published
2011

5. Temporal pattern of C1q deposition after transient focal cerebral ischemia

Author

Division of Cardiology, Department of Medicine, University of Michigan, Ann Arbor, Michigan, Department of Neurological Surgery, College of Physicians & Surgeons, Columbia University, New York, New York ; Dept. of Neurological Surgery, Columbia University, 710 West 168th Street, New York, NY 10032, Department of Neurological Surgery, College of Physicians & Surgeons, Columbia University, New York, New York, Department of Pediatrics, College of Physicians & Surgeons, Columbia University, New York, New York, Mack, William J., Sughrue, Michael E., Ducruet, Andrew F., Mocco, J., Sosunov, Sergey A., Hassid, Benjamin G., Silverberg, Joshua Z., Ten, Vadim S., Pinsky, David J., Connolly, E. Sander, Division of Cardiology, Department of Medicine, University of Michigan, Ann Arbor, Michigan, Department of Neurological Surgery, College of Physicians & Surgeons, Columbia University, New York, New York ; Dept. of Neurological Surgery, Columbia University, 710 West 168th Street, New York, NY 10032, Department of Neurological Surgery, College of Physicians & Surgeons, Columbia University, New York, New York, Department of Pediatrics, College of Physicians & Surgeons, Columbia University, New York, New York, Mack, William J., Sughrue, Michael E., Ducruet, Andrew F., Mocco, J., Sosunov, Sergey A., Hassid, Benjamin G., Silverberg, Joshua Z., Ten, Vadim S., Pinsky, David J., and Connolly, E. Sander

Abstract

Recent studies have focused on elucidating the contribution of individual complement proteins to post-ischemic cellular injury. As the timing of complement activation and deposition after cerebral ischemia is not well understood, our study investigates the temporal pattern of C1q accumulation after experimental murine stroke. Brains were harvested from mice subjected to transient focal cerebral ischemia at 3, 6, 12, and 24 hr post reperfusion. Western blotting and light microscopy were employed to determine the temporal course of C1q protein accumulation and correlate this sequence with infarct evolution observed with TTC staining. Confocal microscopy was utilized to further characterize the cellular localization and characteristics of C1q deposition. Western Blot analysis showed that C1q protein begins to accumulate in the ischemic hemisphere between 3 and 6 hr post-ischemia. Light microscopy confirmed these findings, showing concurrent C1q protein staining of neurons. Confocal microscopy demonstrated co-localization of C1q protein with neuronal cell bodies as well as necrotic cellular debris. These experiments demonstrate the accumulation of C1q protein on neurons during the period of greatest infarct evolution. This data provides information regarding the optimal time window during which a potentially neuroprotective anti-C1q strategy is most likely to achieve therapeutic success. © 2006 Wiley-Liss, Inc.

Published
2007

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