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Статті в журналах з теми "Endoarterectomia"

Автор: Grafiati
Опубліковано: 11 березня 2023

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1

Caputo, N., R. Scaroni, M. Hamam, P. Mazzi, R. Scatolini, P. Cao, F. Verzini, S. Ricci, M. Celani, and E. Signorini. "Lesioni ischemiche cerebrali TEA-correlate: Valutazione TC su 100 casi operati." Rivista di Neuroradiologia 6, no. 3 (August 1993): 331–36. http://dx.doi.org/10.1177/197140099300600314.

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Анотація:
Per valutare l'incidenza delle lesioni ischemiche cerebrali silenti che si realizzano in corso di intervento di tromboendoarterectomia carotidea è stata passata in revisione una serie con-secutiva di 100 casi, tutti studiati preoperatoriamente e nei periodo postoperatorio precoce con esame tomodensitometrico cerebrale. Sui 100 casi considerati, 7 hanno presentato nella TC postoperatoria una lesione ischemica non evidente nella TC preoperatoria; tali lesioni hanno avuto un corrispettivo clinico in 3 pazienti mentre in 4 sono passate asintomatiche. Gli autori discutono il ruolo dell'esame tomodensitometrico cerebrale nella quantificazione obbiettiva del rischio perioperatorio con breve commento sulla disparita dei dati segnalati in letteratura per quanto riguarda questo argomento. L'esame tomodensitometrico cerebrale effettuato prima e dopo l'intervento di endoarterectomia permette diindividuare le lesioni ischemiche TEA-correlate con possibilità di dimostrare, oltre alle lesioni che hanno un corrispettivo clinico, anche quelle clinicamente mute. Un ulteriore vantaggio offerto dall'esame TC è quello di distinguere agevolmente e immediatamente la complicanza ischemica perioperatoria da quella emorragica che si realizza nello 0,5–1%.
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2

Gagliardi, R., L. Benvenuti, A. Amadori, and L. Rossi. "TEA con tecnica microchirurgica sotto protezione barbiturica e monitoraggio intraoperatorio di EEG e PESS." Rivista di Neuroradiologia 9, no. 2_suppl (November 1996): 75–83. http://dx.doi.org/10.1177/19714009960090s209.

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Vari trials clinici recentemente conclusi hanno dimostrato l'efficacia della endoarterectomia carotidea nella prevenzione dello stroke, in pazienti sintomatici e non, con stenosi carotidea superiore al 70%. Il suddetto beneficio si realizza soltanto se l'incidenza percentuale di mortalità e morbilità viene mantenuta ragionevolmente bassa. Il ruolo del chirurgo è pertanto fondamentale e si estrinseca essenzialmente in due momenti: la selezione dei pazienti da sottoporre al trattamento chirurgico e l'accuratezza della tecnica chirurgica. In questo lavoro gli Autori riportano la loro esperienza relativa a 64 TEA (tromboendoarterectomie), eseguite in 59 pazienti negli anni compresi fra il 1991 ed il 1994, in cui era stato seguito un rigido protocollo per la selezione dei pazienti che erano poi stati sottoposti ad intervento con tecnica microchirurgica, protezione barbiturica e monitoraggio intraoperatorio di EEG e PESS. L'assenza di mortalità e morbilità operatorie come pure la mortalità a distanza, limitata ad un solo paziente deceduto per stroke vertebrobasilare alcuni mesi dopo l'intervento, incoraggiano gli autori a proseguire nel cammino intrapreso; i risultati ottenuti rappresentano una ulteriore conferma del fatto che una accurata selezione preoperatoria unita ad un rigido protocollo comportamentale perioperatorio sono fondamentali per garantire il successo di una procedura il cui scopo è profilattico più che terapeutico.
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3

TENJIN, Hiroshi, Takuya KAWABE, Yasuhiro HAYASHI, Yasuo INOUE, Yasuhiko OSAKA, Takashi HOURI, Yoshikazu NAKAHARA, Kanji TAKEMI, and Satoshi KUBO. "Carotid Endoarterectomy Using Patch Graft." Surgery for Cerebral Stroke 32, no. 1 (2004): 49–54. http://dx.doi.org/10.2335/scs.32.49.

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4

Ducati, A., E. Fava, A. Landi, M. Cenzato, E. Bortolani, R. Trazzi, and R. Villani. "SEPS and EEG monitoring during carotid endoarterectomy." Electroencephalography and Clinical Neurophysiology 61, no. 3 (September 1985): S26—S27. http://dx.doi.org/10.1016/0013-4694(85)90136-1.

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5

Giuliani, E., G. Coppi, S. Genedani, C. Bonvecchio, F. Mosca, and A. Barbieri. "S100-b levels after carotid endoarterectomy - pilot study." European Journal of Anaesthesiology 28 (June 2011): 99. http://dx.doi.org/10.1097/00003643-201106001-00315.

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6

Fanelli, Fabrizio, Pierleone Lucatelli, Massimiliano Allegritti, Alessandro Cannavale, Andrea Wlderk, and Roberto Passariello. "Percutaneous endoarterectomy: Unusual complication during thoracic endovascular repair." Clinical Radiology 67, no. 11 (November 2012): 1124–26. http://dx.doi.org/10.1016/j.crad.2012.03.004.

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7

Maiuri, Francesco, Biagio Gallicchio, Giorgio Iaconetta, Antonio Bernardo, and Lazzaro Luca Serra. "Ultrasonographic findings that predict carotid restenosis after endoarterectomy." European Journal of Ultrasound 2, no. 4 (October 1995): 261–67. http://dx.doi.org/10.1016/0929-8266(95)00111-4.

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8

Cofrancesco, Elisabetta, Eloisa Arbustini, Francesca Rossi, Andrea Negri, Elena Tremoli, Livio Gabrielli, Marina Camera, and Michele Cortellaro. "Atorvastatin and Thrombogenicity of the Carotid Atherosclerotic Plaque: the ATROCAP Study." Thrombosis and Haemostasis 88, no. 07 (2002): 41–47. http://dx.doi.org/10.1055/s-0037-1613151.

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SummaryStatins appear to have beneficial effects on fibrous cap stabilisation but their effects on plaque thrombogenicity have not been reported. To evaluate the thrombogenicity of human carotid plaques before and after atorvastatin treatment, 59 patients with bilateral carotid stenosis eligible for two-step carotid endoarterectomy (CEA) were randomly assigned to atorvastatin, 20 mg/day, or placebo. Histological and immunohistochemical analyses, Tissue Factor (TF), Tissue Factor Pathway Inhibitor (TFPI) antigens (Ag) and TF activity were determined in endoarterectomy specimens obtained at baseline and after treatment. Mean TFAg and TFPIAg levels from plaques removed at the first CEA were 55 ± 56 and 32 ± 26 pg/mg. After placebo, TFAg and TFPIAg content was higher in the second than the first CEA. Plaques removed at the second CEA from atorvastatin-treated patients had a lower macrophage content than plaques at the first CEA. TFAg and TFPIAg levels, and TF activity in plaques after atorvastatin treatment were lower (respectively 29, 18% and 56%) than after placebo. These findings indicate that atorvastatin reduce the inflammatory/thrombotic phenotype of carotid plaque, suggesting that these drugs may indeed have a beneficial effect on cerebrovascular events.We are indebted to Pfizer Italia for providing atorvastatin, 20 mg, and placebo.
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9

Fanelli, Fabrizio, Emanuele Boatta, Pierleone Lucatelli, and Roberto Passariello. "Limiting Complications During Carotid Artery Stenting in Complex Lesions." Interventional Cardiology Review 5, no. 1 (2010): 66. http://dx.doi.org/10.15420/icr.2010.5.1.66.

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Stroke is the third leading cause of death and permanent disability in the US and Europe. During the last decade, carotid artery stenting (CAS) has gained a role as an alternative option to carotid endoarterectomy (CEA). Both patient selection and plaque morphology are crucial to reduce the risk of complications. Technical aspects such as the employment and selection of different types of cerebral protection devices, distal occlusion balloons, filters, proximal protection systems and stent selection will be widely discussed.
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10

Nucci, Carlo, Eugenio Martelli, Annalisa Appolloni, and Stefano Palma. "A case of central retinal artery occlusion after carotid endoarterectomy." Eye 11, no. 5 (September 1997): 755–57. http://dx.doi.org/10.1038/eye.1997.192.

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11

DERIU, G. "17.1 Delayed insertion of the shunt during carotid endoarterectomy with patch." Cardiovascular Surgery 5 (September 1997): 85. http://dx.doi.org/10.1016/s0967-2109(97)89983-8.

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12

Ohno, Shingo, Yukio Ikeda, Hitoshi Izawa, Mamoru Murakami, Satoshi Nakajima, Hiroshi Nishioka, Takao Hashimoto, Toshiaki Onitsuka, and Jo Haraoka. "Endothelial Injury: Carotid Endoarterectomy Versus Carotid Artery Stenting in Carotid Artery Stenosis." Neurosurgery 58, no. 2 (February 2006): 404. http://dx.doi.org/10.1227/01.neu.0000310179.12787.4c.

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13

Miura, N., K. Yoshitani, Y. Ohnishi, and M. Kuro. "Factors of Hyperperfusion Syndrome after Carotid Endoarterectomy and Intraoperative Near Infrared Spectroscopy." Journal of Neurosurgical Anesthesiology 18, no. 4 (October 2006): 303–4. http://dx.doi.org/10.1097/00008506-200610000-00075.

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14

Properzi, G. "Blood endothelin-1 levels before and after carotid endoarterectomy for atherosclerotic stenosis." Atherosclerosis 154, no. 1 (January 2001): 137–40. http://dx.doi.org/10.1016/s0021-9150(00)00445-7.

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15

Minicucci, F., R. Chiesa, M. C. Giusti, M. Franceschi, M. A. Volonte, P. Spiegel, M. V. Meraviglia, and G. Comi. "EEG aspects during carotid endoarterectomy: Haemodynamic evaluation by means of transcranial doppler (TCD)." Electroencephalography and Clinical Neurophysiology 75 (January 1990): S98. http://dx.doi.org/10.1016/0013-4694(90)92072-5.

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16

Matsushita, K., F. Akai, Y. Teramoto, Y. Yokoi, A. Aoki, K. Nakanishi, and M. Taneda. "Stenting of the Extracranial Carotid Artery in a High-Risk Population." Interventional Neuroradiology 4, no. 1_suppl (November 1998): 31–36. http://dx.doi.org/10.1177/15910199980040s104.

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Анотація:
The results of nine patients with carotid stenosis in a high-risk surgical population that were treated by stent supported angioplasty are reported. There were eight males and one female between the ages of 53 to 74. A balloon expandable stent was deployed by a transfemoral approach. Technical success was achieved in all cases. There were no periprocedural complications. The mean % stenosis decreased from 84% to 5.2% after stenting. No arterial dissection was recorded and smooth contour of the vessel was demonstrated in all patients. We have observed long term patency for over 6 months in seven patients. Mean angiographic stenosis was 20% and 21% at 3 and 6 months, respectively (range, 5 to 32%). No further stenosis was recorded. Carotid stenting is an alternative strategy to carotid endoarterectomy (CEA) for high-risk patients, for whom the complications of CEA may exceed the potential benefits.
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17

Ramponi, Fabio, Michael Seco, Stella Harris, Bronwen Needham, Michael Wilson, and Michael Vallely. "Synchronous Anaortic Off-Pump Coronary Artery Bypass Surgery and Carotid Endoarterectomy: A Case Series." Heart, Lung and Circulation 26 (2017): S404—S405. http://dx.doi.org/10.1016/j.hlc.2017.03.146.

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18

Tamakawa, N., H. Sakai, and Y. Nishimura. "Evaluation of Carotid Artery Plaque Using IVUS Virtual Histology." Interventional Neuroradiology 13, no. 1_suppl (March 2007): 100–105. http://dx.doi.org/10.1177/15910199070130s114.

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Currently carotid artery stenting (CAS) as well as carotid endoarterectomy (CEA) have become widely accepted forms of treatment for carotid artery stenosis, although complications associated with distal embolism remain problematic. Therefore it is important to have an accurate understanding of the properties of carotid plaque before undertaking CAS in order to ensure the safety of such a therapeutic treatment. This study was undertaken to determine the efficacy of using IVUS Virtual Histology TM (VH-IVUS) to evaluate the pathological properties of plaque contained within carotid artery stenosis. VH-IVUS was performed for six cases undergoing CAS during the period of July to December, 2005. VH-IVUS displays plaque composition under four color mappings of fibrous, fibro-fatty, calcification and necrotic core, being able to offer detailed tissue characterization of soft to hard plaque components. Plaque evaluation by VH-IVUS is both reproducible and objective, and is considered to be an effective method for evaluating the risk complications associated with CAS.
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19

Cherchi, Manuela, Giulia Pistincu, Nellie Della Schiava, Palmina Petruzzo, and Patrick Feugier. "Eversion Carotid Endoarterectomy in Young People: What Happened to Our Patients after More Than 10 Years?" European Journal of Vascular and Endovascular Surgery 58, no. 6 (December 2019): e15. http://dx.doi.org/10.1016/j.ejvs.2019.06.516.

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20

Caporelli, S., G. Orsetti, E. Adrario, E. Giorgetti, and P. Pelaia. "Ropivacaine vs. bupivacaine in partial deep cervical plexus block and superficial cervical plexus block for carotid endoarterectomy." European Journal of Anaesthesiology 17, Supplement 19 (2000): 101. http://dx.doi.org/10.1097/00003643-200000002-00327.

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21

Artese, L., S. Ucchino, A. Piattelli, M. Piccirilli, V. Perrotti, A. Mezzetti, and F. Cipollone. "Factors Associated with Apoptosis in Symptomatic and Asymptomatic Carotid Atherosclerotic Plaques." International Journal of Immunopathology and Pharmacology 18, no. 4 (October 2005): 645–53. http://dx.doi.org/10.1177/039463200501800405.

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The aim of this study was to investigate the differences that are present between apoptosis in symptomatic (with symptoms of cerebral ischemic attack) and asymptomatic carotid atherosclerotic plaques. The apoptotic process in macrophages and smooth muscle cells was evaluated. Cellular markers and products of immune cells in symptomatic and asymptomatic atherosclerotic plaque and endoarterectomy specimen were analyzed by immunohistochemistry. No statistically significant differences were present regarding the mean SMC actin-positive area. Using double staining of α-smooth muscle actin and TUNEL techniques, the number of smooth muscle cells in apoptosis was statistically higher in symptomatic plaque as compared with asymptomatic plaque. Statistically significant differences (p=0.009) were also found in the CD45-positive cells in the inflammatory infiltrate. The CD68-positive macrophages showed statistically significant differences (p=0.0001). Similarly, the double staining with CD68 and TUNEL revealed that apoptotic macrophages were mainly present in asymptomatic plaques rather than symptomatic plaques. Statistically significant differences (p<0.001) were found in the Bcl-2 expression, with higher values in asymptomatic plaques. Our data showed that the increase of the inflammatory cells contributes to plaque instability and that death due to apoptosis of smooth muscle cells in symptomatic plaques could contribute to their destabilization and explains their tendency to fracture.
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22

Kawasaki, Masakazu, Yoshimitsu Ishibashi, Kiyotaka Morimoto, Hideyuki Kunishige, and Nozomu Inoue. "The Case of a Patient with Femoral Artery Stenosis Caused by Angio-Seal® Use Treated with Endoarterectomy." Japanese Journal of Cardiovascular Surgery 45, no. 1 (2016): 62–66. http://dx.doi.org/10.4326/jjcvs.45.62.

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23

Fukuda, T., A. Tsuji, T. Ogo, and N. Norifumi. "Balloon pulmonary angioplasty for the treatment of residual pulmonary hypertension after pulmonary endoarterectomy in patients with chronic thromboembolic pulmonary hypertension (CTEPH)." Journal of Vascular and Interventional Radiology 27, no. 3 (March 2016): S289—S290. http://dx.doi.org/10.1016/j.jvir.2015.12.734.

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24

Yamada, Kazuo, Toru Hayakawa, Kazutami Nakao, Kazuo Kataoka, and Heitaro Mogami. "Proliferation of smooth muscle cells of tunia media as a cause of arteriosclerosis. Immunohistochemical studies on cases showing recurrence of stenosis after endoarterectomy of the carotid artery." Nosotchu 10, no. 3 (1988): 227–31. http://dx.doi.org/10.3995/jstroke.10.227.

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25

Corsico, Angelo G., Andrea M. D’Armini, Valentina Conio, Antonio Sciortino, Maurizio Pin, Valentina Grazioli, Giulia Di Vincenzo, et al. "Persistent exercise limitation after successful pulmonary endoarterectomy: frequency and determinants." Respiratory Research 20, no. 1 (February 14, 2019). http://dx.doi.org/10.1186/s12931-019-1002-5.

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26

Ohno, Shingo, Yukio Ikeda, Hitoshi Izawa, Mamoru Murakami, Satoshi Nakajima, Hiroshi Nishioka, Takao Hashimoto, Toshiaki Onitsuka, and Jo Haraoka. "Endothelial Injury: Carotid Endoarterectomy Versus Carotid Artery Stenting in Carotid Artery Stenosis." Neurosurgery, February 2006, 397. http://dx.doi.org/10.1097/00006123-200602000-00040.

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27

Russo, R. "Carotid Endoarterectomy (CEA) and Carotid Artery Stenting (CAS): prophylaxis and treatment of stroke." BMC Geriatrics 10, S1 (May 19, 2010). http://dx.doi.org/10.1186/1471-2318-10-s1-a74.

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28

Modugno, Pietro, Veronica Picone, Enrico Maria Centritto, Eugenio Calvo, Carlo Canosa, Felice Piancone, Nicola Testa, et al. "Combined Treatment With Carotid Endoarterectomy and Coronary Artery Bypass Grafting: A Single-Institutional Experience in 222 Patients." Vascular and Endovascular Surgery, May 2, 2022, 153857442210941. http://dx.doi.org/10.1177/15385744221094148.

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Introduction Carotid atherosclerotic disease is a known independent risk factor of post operative stroke after coronary artery bypass grafting (CABG). The best management of concomitant coronary artery disease and carotid artery disease remains debated. Current strategies include simultaneous carotid endoarterectomy (CEA) and CABG, staged CEA followed by CABG, staged CABG followed by CEA, staged transfemoral carotid artery stenting (TF-CAS) followed by CABG, simultaneous TF-CAS and CABG and transcarotid artery stenting. Methods We report our experience based on a cohort of 222 patients undergoing combined CEA and CABG surgery who come to our observation from 2004 to 2020. All patients with >70% carotid stenosis and severe multivessel or common truncal coronary artery disease underwent combined CEA and CABG surgery at our instituion. 30% of patients had previously remote neurological symptoms or a cerebral CT-scan with ischemic lesions. Patients with carotid stenosis >70%, either asymptomatic or symptomatic, underwent CT-scan without contrast media to assess ischemic brain injury, and in some cases, if necessary, CT-angiography of the neck and intracranial vessels. Results The overall perioperative mortality rate was 4.1% (9/222 patients). Two patients (.9%) had periprocedural ipsilateral transient ischemic attack (TIA) which completely resolved by the second postoperative day. Two patients (.9%) had an ipsilateral stroke, while 7 patients (3.2%) had a stroke of the controlateral brain hemisphere. Two patients (.9%) patients were affected by periprocedural coma caused by cerebral hypoperfusion due to perioperative heart failure. There were no statistically significant differences between patients in Extracorporeal Circulation (ECC) and Off-pump patients in the onset of perioperative stroke. Conclusion Our experience reported that combined surgical treatment of CEA and CABG, possibly Off-Pump, is a feasible treatment procedure, able to minimize the risk of post-operative stroke and cognitive deficits.
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29

Yamazaki, Masako, Yoshikazu Okada, Akitsugu Kawashima, Koji Yamaguchi, Taku Yoneyama, and Shinichiro Uchiyama. "Abstract TP136: Cilostazol Inhibits Inflammation and Endothelial Cell Damage in Patients with Severe Carotid Disease." Stroke 44, suppl_1 (February 2013). http://dx.doi.org/10.1161/str.44.suppl_1.atp136.

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Background: Cilostazol is an antiplatelet agent, which is known also to have protective effects on endothelial cell. We studied effects of cilostazol on markers of inflammation and endothelial cell damage in patients with severe carotid disease, who underwent carotid endoarterectomy (CEA). Methods: We measured high sensitivity CRP (hsCRP), soluble vascular cellular adhesion molecule (VCAM)-1, soluble E-selectin, soluble intercellular adhesion molecule-1 and von Willebrand Factor antigen (vWF) in 45 patients who underwent CEA (38 males and 7 females, mean age was 69 years). Venous blood was taken from each patient before (Pre) and 3 days (Day3), 10 days (Day10), 4 weeks and 1 year (Post) after CEA. Each marker was compared between patients who were treated with aspirin alone (aspirin group, 18 cases) and those treated with cilostazol alone or cilostazol plus aspirin (cilostazol group, 17 cases). Results: The levels of hsCRP, VCAM-1, E-selectin and vWF at Day3 and the levels of hsCRP and VCAM-1 on Day10 were significantly higher than those at PreCEA. The alterations of those markers were not significantly different between the aspirin and cilotazol groups. The levels of hsCRP in the cilostazol group were significantly lower than those in aspirin group at both PreCEA and PostCEA. The levels of VCAM-1 at PreCEA in the cilostazol group were significantly lower than those in the aspirin group. Conclusions: The results suggested that cilostazol inhibits inflammation and endothelial cell damage in patients with severe carotid disease, although its protective effects did not reduce the endothelial cell damage induced by CEA when compared with aspirin.
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