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• W2106905206 abstract "Remote ischemic preconditioning is a physiologic mechanism in mammalian species whereby brief exposure to nonlethal ischemia in one tissue confers protection against a prolonged ischemic insult in a distant tissue. first described almost 15 years ago, it has been slow to translate into clinical practice. several clinical trials have recently reported that remote ischemic preconditioning reduces myocardial injury after major cardiovascular surgery. in addition, a randomized trial in patients undergoing open abdominal aortic aneurysm repair reported a significant reduction in perioperative myocardial infarctions. remote ischemic preconditioning is easily performed and likely to prove highly cost-effective. large-scale trials of the technique are warranted in patients undergoing major vascular surgery. Remote ischemic preconditioning is a physiologic mechanism in mammalian species whereby brief exposure to nonlethal ischemia in one tissue confers protection against a prolonged ischemic insult in a distant tissue. first described almost 15 years ago, it has been slow to translate into clinical practice. several clinical trials have recently reported that remote ischemic preconditioning reduces myocardial injury after major cardiovascular surgery. in addition, a randomized trial in patients undergoing open abdominal aortic aneurysm repair reported a significant reduction in perioperative myocardial infarctions. remote ischemic preconditioning is easily performed and likely to prove highly cost-effective. large-scale trials of the technique are warranted in patients undergoing major vascular surgery. Patients undergoing major vascular surgery represent a high-risk surgical population because of the presence of generalized arterial disease. In particular, vascular patients are susceptible to ischemia–reperfusion injury (IRI), which is an integral part of most vascular procedures. Perioperative death and major morbidity rates for patients undergoing index vascular procedures such as open and endovascular aneurysm repair, carotid endarterectomy, and infrainguinal bypass range from about 3% to 25%.1Prinssen M. Verhoeven H.L. Buth J. Cuypers P.W. van Sambeek M.R. Balm R. et al.A randomized trial comparing conventional and endovascular repair of absominal aortic aneurysms.N Engl J Med. 2004; 351: 1607-1618Crossref PubMed Scopus (1565) Google Scholar, 2Paciaroni M. Eliasziw M. Kappelle L.J. Finan J.W. Ferguson G.G. Barnett H.J. Medical complications associated with carotid endarterectomy North American Symptomatic Carotid Endarterectomy Trial (NASCET).Stroke. 1999; 30: 1759-1763Crossref PubMed Scopus (126) Google Scholar, 3Adam D.J. Beard J.D. Cleveland T. Bell J. Bradbury A.W. Forbes J.F. et al.Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised controlled trial.Lancet. 2005; 366: 1925-1934Abstract Full Text Full Text PDF PubMed Scopus (1445) Google Scholar An ageing population means that the demand for major vascular interventions is steadily increasing, and by 2030, it is anticipated that 1 to 2 million such procedures will be performed in the United States, resulting in about 18,000 deaths.4Anderson P.L. Gelijns A. Moskowitz A. Arons R. Gupta L. Weinberg A. et al.Understanding trends in inpatient surgical volume: vascular interventions, 1980-2000.J Vasc Surg. 2004; 39: 1200-1208Abstract Full Text Full Text PDF PubMed Scopus (129) Google Scholar In addition, large numbers of patients will have complications that may have adverse effects, ranging from an extra day in hospital to life-long hemodialysis dependence. Multiple mechanisms produce perioperative complications. For example, during open aneurysm repair, renal injury may result from a low-flow state in the renal vasculature due to systemic hemodynamic instability, a no-flow state arising from direct interference with renal blood flow due to suprarenal or juxtarenal clamping, or indirectly due to the release of toxic metabolites into the general circulation when the lower limbs are reperfused.5Seal J.B. Gewertz B.L. Vascular dysfunction in ischemia-reperfusion injury.Ann Vasc Surg. 2005; 19: 572-584Abstract Full Text Full Text PDF PubMed Scopus (165) Google Scholar Similarly, myocardial injury may result from a low-flow state across a hemodynamically significant coronary artery stenosis, fissuring of a plaque producing acute thrombosis, or excessive demands on the myocardium exceeding the compensatory ability of diseased coronary vasculature to supply adequate oxygen to the cells.6Devereaux P.J. Goldman L. Cook D.J. Gilbert K. Leslie K. Guyatt G.H. Perioperative cardiac events in patients undergoing noncardiac surgery: a review of the magnitude of the problem, the pathophysiology of the events and methods to estimate and communicate risk.CMAJ. 2005; 173: 627-634Crossref PubMed Scopus (440) Google Scholar Most strategies to reduce complications target a specific etiological mechanism. Attempts to reduce perioperative cardiac morbidity by preoperative cardiac intervention have failed to produce the expected results.7McFalls E.O. Ward H.B. Moritz T.E. Goldman S. Krupski W.C. Littooy F. et al.Coronary-artery revascularization before elective major vascular surgery.N Engl J Med. 2004; 351: 2795-2804Crossref PubMed Scopus (921) Google Scholar Perioperative β-blockade attempts to reduce myocardial injury by limiting myocardial oxygen demand,8Brady A.R. Gibbs J.S. Greenhalgh R.M. Powell J.T. Sydes M.R. Perioperative β-blockade (Pobble) for patients undergoing infrarenal vascular surgery: results of a randomized double-blind controlled trial.J Vasc Surg. 2005; 41: 602-609Abstract Full Text Full Text PDF PubMed Scopus (294) Google Scholar aspirin may reduce the risk of coronary thrombosis by platelet inhibition,9Anti-thrombotic Trialists' CollaborationCollaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar and statins reduce the risk of plaque rupture.10Schouten O. Bax J.J. Dunkelgrun M. Feringa H.H. van Urk H. Poldermans D. Statins for the prevention of perioperative cardiovascular complications in vascular surgery.J Vasc Surg. 2006; 44: 419-424Abstract Full Text Full Text PDF PubMed Scopus (44) Google Scholar These strategies will only ever produce small incremental improvements in outcome because they only address single etiologic mechanisms. Thus, although aspirin will reduce the risk of thrombosis and statins will stabilize plaques and reduce the risk of plaque fissuring, neither will protect against a hemodynamic myocardial injury due to low flow across a significant but otherwise asymptomatic stenosis. IRI is the final common pathway that leads to end-organ damage regardless of the mechanism that led to ischemia in the first place.5Seal J.B. Gewertz B.L. Vascular dysfunction in ischemia-reperfusion injury.Ann Vasc Surg. 2005; 19: 572-584Abstract Full Text Full Text PDF PubMed Scopus (165) Google Scholar, 11Carden D.L. Granger D.N. Pathophysiology of ischaemia-reperfusion injury.J Pathol. 2000; 190: 255-266Crossref PubMed Scopus (1329) Google Scholar If the cells in delicate end organs such as the heart, kidneys, and brain could be induced to convert to an ischemia–reperfusion resistant phenotype, this would provide protection against the devastating effects of IRI. Moreover, because the protection does not target a specific etiologic mechanism, this end organ protection could produce a much greater incremental reduction in morbidity than single mechanism strategies such as aspirin and statin use. Such a mechanism was identified in mammalian cells >20 years ago, and emerging clinical evidence suggests that it may significantly reduce morbidity after major vascular surgery. About 25 years ago, it was thought that exposure to successive brief periods of ischemia had a cumulative effect leading to tissue necrosis and organ infarction.12Geft I.L. Fishbein M.C. Ninomiya K. Hashida J. Chaux E. Yano J. et al.Intermittent brief periods of ischemia have a cumulative effect and may cause myocadial necrosis.Circulation. 1982; 66: 1150-1153Crossref PubMed Scopus (199) Google Scholar This prevailing dogma was challenged by several experiments in canine models of myocardial ischemia. Cardiac myocytes exposed to 10 minutes of ischemia sustained intracellular adenosine triphosphate (ATP) and adenine nucleotide depletion, as expected. However, if the same myocytes were exposed to a further 10-minute ischemic insult after 20 minutes of reperfusion, no further depletion occurred. These observations suggested that reperfusion after a brief period of ischemia somehow triggered a mechanism that prevented further loss of intracellular ATP during subsequent repeated ischemic insults.13Reimer K.A. Murry C.E. Yamasawa I. Hill M.L. Four brief periods of ischaemia cause no cumulative ATP loss or necrosis.Am J Physiol. 1986; 251 (H1306-5)PubMed Google Scholar The same group hypothesized that multiple brief ischemic episodes might provide some protection for the heart against damage due to a subsequent prolonged ischemic insult. One group of dogs underwent a single 40-minute circumflex occlusion. A second group underwent four 5-minute-long circumflex occlusions, separated by 5-minute periods of reperfusion, followed by a 40-minute occlusion. The second group had significantly smaller areas of infarcted myocardium on subsequent histologic study. This suggested that brief periods of intermittent ischemia provide protection against a subsequent ischemic insult. However, the effect disappeared when the animals were subjected to 3 hours of occlusion instead of 40 minutes, so the protection was limited to significant but moderate episodes of ischemia.14Murry C.E. Jennings R.B. Reimer K.A. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.Circulation. 1986; 74: 1124-1136Crossref PubMed Scopus (6789) Google Scholar Subsequent work in patients undergoing coronary artery bypass graft surgery confirmed that the mechanism, known as ischemic preconditioning (IPC), is preserved in humans.15Yellon D.M. Alkhulaifi A.M. Pugsley W.B. Preconditioning the human myocardium.Lancet. 1993; 342: 276-277Abstract PubMed Scopus (622) Google Scholar Moreover, it is not confined to cardiac cells: A range of tissues have been successfully preconditioned in animal models, including skeletal muscle,16Carroll C.M. Carroll S.M. Overgoor M.L. Tobin G. Barker J.H. Acute ischemic preconditioning of skeletal muscle prior to flap elevation augments muscle-flap survival.Plast Reconstr Surg. 1997; 100: 58-65Crossref PubMed Scopus (98) Google Scholar, 17Mounsey R.A. Pang C.Y. Boyd J.B. Forrest C. Augmentation of skeletal muscle survival in the latissimus dorsi porcine model using acute ischemic preconditioning.J Otolaryngol. 1992; 21: 315-320PubMed Google Scholar liver,18Clavien P.A. Selzner M. Rudiger H.A. Graf R. Kadry Z. Rousson V. et al.A prospective randomized study in 100 consecutive patients undergoing major liver resection with versus without ischemic preconditioning.Ann Surg. 2003; 238: 843-850Crossref PubMed Scopus (421) Google Scholar, 19Clavien P.A. Yadav S. Sindram D. Bentley R.C. Protective effects of ischemic preconditioning for liver resection performed under inflow occlusion in humans.Ann Surg. 2000; 232: 155-162Crossref PubMed Scopus (418) Google Scholar kidney,20Cochrane J. Williams B.T. Banerjee A. Harken A.H. Burke T.J. Cairns C.B. et al.Ischemic preconditioning attenuates functional, metabolic, and morphologic injury from ischemic acute renal failure in the rat.Ren Fail. 1999; 21: 135-145Crossref PubMed Scopus (93) Google Scholar and brain.21Kato H. Liu Y. Kogure K. Kato K. Induction of 27-kDa heat shock protein following cerebral ischemia in a rat model of ischemic tolerance.Brain Res. 1994; 634: 235-244Crossref PubMed Scopus (142) Google Scholar However, triggering IPC required direct interference with the blood supplies of the target tissues. It was concluded that this factor limited its clinical utility to scenarios where the blood supply is readily accessible, such as open heart surgery. Moreover, this dependence on direct the interference with the blood supply implied that IPC could only provide single-organ protection in most procedures, for example, the myocardium can be protected during open heart surgery but not the kidneys. This resulted in a flurry of small clinical trials in cardiac surgery, but little interest in other surgical fields. Analysis of canine models of cardiac IPC revealed that the infarction area in preconditioned hearts tended to increase in proportion to the left ventricle area at risk and, furthermore, that the distance between the edge of the infarct and the margin of the risk area increased as the risk region decreased. Conversely, this lateral distance remained the same in control hearts as the area at risk increased.22Przyklenk K. Darling C.E. Dickson E.W. Whittaker P. Cardioprotection ‘outside the box’–the evolving paradigm of remote preconditioning.Basic Res Cardiol. 2003; 98: 149-157PubMed Google Scholar These observations were formulated into a mathematic model that suggested that a trigger generated in nonischemic tissue may contribute to the myocardial protection produced by conventional, direct IPC.23Whittaker P. Przyklenk K. Reduction of infarct size in vivo with ischemic preconditioning: mathematical evidence for protection via non-ischemic tissue.Basic Res Cardiol. 1994; 89: 6-15Crossref PubMed Scopus (41) Google Scholar The model implied that ischemia induced in one coronary vascular bed protects the myocardium in another coronary vascular bed. This hypothesis was confirmed in the canine heart, where circumflex territory ischemia protected the left anterior descending artery territory against a subsequent prolonged ischemic insult.24Przyklenk K. Bauer B. Ovize M. Kloner R.A. Whittaker P. Regional ischemic ‘preconditioning' protects remote virgin myocardium from subsequent sustained coronary occlusion.Circulation. 1993; 87: 893-899Crossref PubMed Google Scholar Thus, ischemia in one vascular bed protects tissue in another vascular bed, albeit in the same organ. Gho et al25Gho B.C. Schoemaker R.G. van den Doel M.A. Duncker D.J. Verdouw P.D. Myocardial protection by brief ischemia in noncardiac tissue.Circulation. 1996; 94: 2193-2200Crossref PubMed Scopus (517) Google Scholar hypothesized from this observation that ischemia in a distant vascular bed or organ would protect the heart. They found that mesenteric ischemia reduced myocardial infarction size.25Gho B.C. Schoemaker R.G. van den Doel M.A. Duncker D.J. Verdouw P.D. Myocardial protection by brief ischemia in noncardiac tissue.Circulation. 1996; 94: 2193-2200Crossref PubMed Scopus (517) Google Scholar Renal ischemia produced similar results.26Takaoka A. Nakae I. Mitsunami K. Yabe T. Morikawa S. Inubushi T. et al.Renal ischemia/reperfusion remotely improves myocardial energy metabolism during myocardial ischemia via adenosine receptors in rabbits: effects of “remote preconditioning.”.J Am Coll Cardiol. 1999; 33: 556-564Abstract Full Text Full Text PDF PubMed Scopus (155) Google Scholar The kidneys and to a lesser extent the intestine are vulnerable to damage from even brief periods of ischemia. The blood supply of these organs is also inaccessible in many clinical scenarios, rendering them unfeasible candidates as the remote stimulus for cardioprotection. Skeletal muscle, on the other hand, is relatively resistant to damage from ischemia. Transient lower limb ischemia in animal models reduces myocardial infarction size27Birnbaum Y. Hale S.L. Kloner R.A. Ischemic preconditioning at a distance: reduction of myocardial infarct size by partial reduction of blood supply combined with rapid stimulation of the gastrocnemius muscle in the rabbit.Circulation. 1997; 96: 1641-1646Crossref PubMed Scopus (323) Google Scholar and reperfusion tachyarrhythmias.28Oxman T. Arad M. Klein R. Avazov N. Rabinowitz B. Limb ischemia preconditions the heart against reperfusion tachyarrhythmia.Am J Physiol Heart. 1997; 273: H1707-H1712PubMed Google Scholar Skeletal muscle ischemia can be induced simply by the application of an inflatable cuff or tourniquet, with a negligible risk of iatrogenic injury. It can be performed in patients undergoing any type of operation. The protection is not organ specific, so a patient receives simultaneous protection against IRI in any organ. Thus, remote IPC (RIPC) has the potential to significantly reduce morbidity and mortality in any field of surgery. To date, small clinical trials have been conducted in patients undergoing open heart surgery and open abdominal aortic aneurysm (AAA) repair. The initial results have been encouraging. Huge efforts have been made to elucidate the mechanistic pathways responsible for RIPC, but the details remain unclear. There may be some overlap with the mechanisms of ischemic preconditioning and also postconditioning. Hausenloy and Yellon29Hausenloy D.J. Yellon D.M. Remote ischemic preconditioning: underlying mechanisms and clinical application.Cardiovasc Res. 2008; 79: 377-386Crossref PubMed Scopus (385) Google Scholar recently published a thorough review of the current data on putative mechanistic pathways. Briefly, at present, there are three theories regarding the mechanism:•The neural theory proposes that the remote organ releases endogenous substances such as adenosine and bradykinin that activate a local afferent neural pathway; this, in turn, activates an efferent neural pathway that triggers end organ protection.•The humoral theory suggests that the remote tissue releases adenosine, bradykinin, or some other substance into the bloodstream, which carries it to the end organ where it binds to receptors and triggers the intracellular pathways that mediate protection.•The inflammatory suppression theory suggests that remote organ ischemia suppresses inflammation and apoptosis in cells, reducing the systemic inflammatory response.29Hausenloy D.J. Yellon D.M. Remote ischemic preconditioning: underlying mechanisms and clinical application.Cardiovasc Res. 2008; 79: 377-386Crossref PubMed Scopus (385) Google Scholar RIPC could be of considerable value in major vascular surgery. Ischemia–reperfusion injury is an inherent component of arterial surgery. A single method to protect all vulnerable organs against this ischemia–reperfusion injury would be of great value. RIPC has the added attraction that it can be achieved easily with readily available equipment in all vascular units, without any capital outlay or ongoing costs. Thus, it could be an extremely cost-effective means of reducing perioperative complications. Two trials have examined RIPC in the setting of cardiac surgery. Cheung et al30Cheung M.M. Kharbanda R.K. Konstantinov I.E. Shimizu M. Frndova H. Li J. et al.Randomized controlled trial of the effects of remote ischemic preconditioning on children undergoing cardiac surgery: first clinical application in humans.J Am Coll Cardiol. 2006; 47: 2277-2282Abstract Full Text Full Text PDF PubMed Scopus (447) Google Scholar randomized 37 children undergoing open heart surgery for a variety of cardiac problems to receive four 5-minute cycles of lower limb ischemia as a RIPC stimulus about 5 to 10 minutes before the initiation of cardiopulmonary bypass.30Cheung M.M. Kharbanda R.K. Konstantinov I.E. Shimizu M. Frndova H. Li J. et al.Randomized controlled trial of the effects of remote ischemic preconditioning on children undergoing cardiac surgery: first clinical application in humans.J Am Coll Cardiol. 2006; 47: 2277-2282Abstract Full Text Full Text PDF PubMed Scopus (447) Google Scholar The 17 RIPC patients had significantly less myocardial damage, as indicated by lower concentrations of serum troponin I. That said, both groups exhibited a similar pattern of troponin elevations, with an immediate rise in the first few hours after surgery, tapering off by 24 hours; thus, RIPC reduced but did not eliminate myocardial injury. RIPC also produced a statistically significant reduction in inotrope requirements, although the actual reduction was only on the order of 2 to 3 μgs/kg/min.30Cheung M.M. Kharbanda R.K. Konstantinov I.E. Shimizu M. Frndova H. Li J. et al.Randomized controlled trial of the effects of remote ischemic preconditioning on children undergoing cardiac surgery: first clinical application in humans.J Am Coll Cardiol. 2006; 47: 2277-2282Abstract Full Text Full Text PDF PubMed Scopus (447) Google Scholar Despite the apparent reduction in myocardial damage and inotrope requirements, the length of the postoperative critical care stay was unchanged, with the RIPC group requiring a mean stay of 54.2 ± 40.7 hours compared with 39.5 ± 25.7 hours for the control group.30Cheung M.M. Kharbanda R.K. Konstantinov I.E. Shimizu M. Frndova H. Li J. et al.Randomized controlled trial of the effects of remote ischemic preconditioning on children undergoing cardiac surgery: first clinical application in humans.J Am Coll Cardiol. 2006; 47: 2277-2282Abstract Full Text Full Text PDF PubMed Scopus (447) Google Scholar Hausenloy et al31Hausenloy D.J. Mwamure P.K. Venugopal V. Harris J. Barnard M. Grundy E. et al.Effect of remote ischemic preconditioning on myocardial injury in patients undergoing coronary artery bypass graft surgery: a randomised controlled trial.Lancet. 2007; 370: 575-579Abstract Full Text Full Text PDF PubMed Scopus (540) Google Scholar randomized 57 adults undergoing coronary artery bypass grafting to receive RIPC or not. This time the RIPC stimulus comprised three cycles of 5 minutes of ischemia induced by inflating a blood pressure cuff to 200 mm Hg, followed by 5 minutes reperfusion in the upper limb. RIPC was performed in 27 patients after induction of anesthesia. These patients had a significant reduction in serial postoperative serum troponin T levels compared with the 30 non-RIPC controls. However, no data were provided on clinical end points such as hospital stay or death because this small trial was underpowered to detect any significant differences.31Hausenloy D.J. Mwamure P.K. Venugopal V. Harris J. Barnard M. Grundy E. et al.Effect of remote ischemic preconditioning on myocardial injury in patients undergoing coronary artery bypass graft surgery: a randomised controlled trial.Lancet. 2007; 370: 575-579Abstract Full Text Full Text PDF PubMed Scopus (540) Google Scholar Our unit has conducted the largest clinical trial of RIPC to date, to our knowledge, in the setting of open AAA repair.32Ali Z.A. Callaghan C.J. Lim E. Ali A.A. Nouraei S.A. Varty K. et al.Remote ischaemic preconditioning reduces myocardial and renal injury after elective abdominal aortic aneurysm repair: a randomized controlled trial.Circulation. 2007; 116: I95-I106Crossref Scopus (375) Google Scholar Eighty-two patients undergoing elective open AAA repair were randomized to receive RIPC or not. The RIPC was triggered by clamping each common iliac artery sequentially for 10 minutes, followed by 10 minutes of reperfusion. Cross clamping was performed only once the second leg had been allowed to reperfuse for 10 minutes. No lower limb ischemia developed that required intervention. Significant troponin elevations (>0.2 ng/mL) occurred in 15 of 42 control patients (36%) compared with three of 41 preconditioning patients (7%), a significant reduction (P = .002). Postoperative myocardial injury (serum troponin ≥1.5 ng/mL) and infarction was significantly lower in the RIPC group (2 of 41 patients vs 13 of 42; P = .002). The duration of critical care stay was significantly reduced from a mean of 2 ± 2.3 days in the control group to 1.0 ± 0.2 days for RIPC patients (P = .007). Although the trial was relatively small, the results were very encouraging and suggest that RIPC could significantly reduce the complication burden of major vascular surgery. RIPC could be of benefit in other major vascular procedures. Although less invasive than open aneurysm surgery, endovascular aneurysm repair is still associated with significant mortality and major morbidity of about 4% in randomized series, rising to 17% in nonrandomized series.33Adriaensen M.E. Bosch J.L. Halpern E.F. Hunink M.G. Gazelle G.S. Elective endovascular versus open surgical repair of abdominal aortic aneurysms: systematic review of short-term results.Radiology. 2002; 224: 739-747Crossref PubMed Scopus (113) Google Scholar Recent data from a cohort of almost 10,000 Medicare patients undergoing carotid endarterectomy in the United States suggests that the perioperative mortality is about 1%, the perioperative stroke rate is about 3.3%, and a major cardiac complication (myocardial infarction, unstable angina, pulmonary edema or ventricular tachycardia) develops in 3.9%.34Greenstein A.J. Chassin M.R. Wang J. Rockman C.B. Riles T.S. Tuhrim S. et al.Association between minor and major surgical complications after carotid endarterectomy: results of the New York Carotid Artery Surgery Study.J Vasc Surg. 2007; 46: 1138-1146Abstract Full Text Full Text PDF PubMed Scopus (58) Google Scholar A cerebral preconditioning effect has been observed in patients undergoing neurovascular surgery.35Chan M.T. Boet R. Ng S.C. Poon W.S. Gin T. Effect of ischemic preconditioning on brain tissue gases and pH during temporary cerebral artery occlusion.Acta Neurochir Suppl. 2005; 95: 93-96Crossref PubMed Scopus (36) Google Scholar More recently, Faries et al36Faries P.L. Deruberytis B. Trocciola S. Karwowski J. Kent K.C. Chaer R.A. Ischemic preconditioning during the use of the Percusurge occlusion balloon for carotid angioplasty and stenting.Vascular. 2008; 16: 1-9Crossref PubMed Scopus (16) Google Scholar described an apparent preconditioning effect obtained during carotid artery stenting. Neurologic deficits developed in 10 patients when their internal carotid artery was occluded with a balloon. The symptoms resolved ≤10 minutes of balloon deflation. Subsequent reinflation to allow stenting was not associated with any recurrence of the neurologic symptoms, suggesting that the area of brain at risk was now protected against ischemic injury, at least temporarily.36Faries P.L. Deruberytis B. Trocciola S. Karwowski J. Kent K.C. Chaer R.A. Ischemic preconditioning during the use of the Percusurge occlusion balloon for carotid angioplasty and stenting.Vascular. 2008; 16: 1-9Crossref PubMed Scopus (16) Google Scholar RIPC could significantly reduce the complication burden arising from both endovascular aneurysm repair and carotid endarterectomy. Several randomized trials demonstrate that RIPC can reduce cardiac injury. Although some patients will always sustain severe ischemic insults that RIPC cannot ameliorate, the technique has the capacity to significantly reduce a variety of complications after major vascular surgery. The beneficial effects of RIPC can be achieved by the modification of existing surgical techniques and requires no expensive drugs or equipment. Further large-scale clinical studies are required to establish the value of RIPC in vascular surgery." @default.
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• W2106905206 cites W1982993144 @default.
• W2106905206 cites W1987293815 @default.
• W2106905206 cites W1998582292 @default.
• W2106905206 cites W2004068894 @default.
• W2106905206 cites W2005544435 @default.
• W2106905206 cites W2008162308 @default.
• W2106905206 cites W2010563061 @default.
• W2106905206 cites W2016526884 @default.
• W2106905206 cites W2016965599 @default.
• W2106905206 cites W2021202706 @default.
• W2106905206 cites W2022473516 @default.
• W2106905206 cites W2024352468 @default.
• W2106905206 cites W2026348365 @default.
• W2106905206 cites W2026826353 @default.
• W2106905206 cites W2032715486 @default.
• W2106905206 cites W2033203997 @default.
• W2106905206 cites W2059676011 @default.
• W2106905206 cites W2067185367 @default.
• W2106905206 cites W2077523233 @default.
• W2106905206 cites W2089937026 @default.
• W2106905206 cites W2090530769 @default.
• W2106905206 cites W2128041583 @default.
• W2106905206 cites W2136272230 @default.
• W2106905206 cites W2146217294 @default.
• W2106905206 cites W2146350062 @default.
• W2106905206 cites W2156565707 @default.
• W2106905206 cites W2181891066 @default.
• W2106905206 cites W2185467918 @default.
• W2106905206 cites W2320581131 @default.
• W2106905206 cites W2443248231 @default.
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