Embolization During Carotid Artery Stenting

Protect the brain while treating the artery.

By Takao Ohki, MD

Although satisfactory results regarding carotid artery stenting (CAS) have been reported from a number of investigators, concerns about the safety and efficacy of the procedure have been raised, and its general role and comparative value remain unclear.1-3 Among several issues related to CAS, the major concern has been the potential for the procedure to produce embolic particles that may manifest as a neurologic deficit. This article reviews the potential for CAS to produce emboli and presents a rationale for the routine use of cerebral protection devices during CAS.

The main cause of perioperative neurologic deficits following CAS is thought to be embolic particles released from the carotid plaque during balloon dilatation and stent deployment.4 This hypothesis was further confirmed by our study that analyzed the incidence of embolic events following CAS performed in an ex vivo model utilizing human carotid plaques.5 We collected plaques from patients undergoing standard carotid endarterectomy (CEA) procedures. The study demonstrated that embolic particles were consistently produced from all plaques that were stented (Figure 1).

Clinical Evidence
The previously mentioned experimental observations have been further confirmed by clinical studies. The Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) is a randomized, prospective trial comparing the safety and efficacy of CEA with carotid angioplasty, with and without stenting. The preliminary report of this trial focused on the transcranial Doppler results and showed that, on average, balloon angioplasty produced four times the amount of high-intensity signals, which represent embolic particles (including air), compared with CEA (202 ± 119 vs. 52 ± 64).6 However, this dissimilarity has not translated into an overall difference in stoke or death rates between the two arms.7

The Leicester trial, another prospective, randomized trial, also confirmed the fact that CAS generates significantly more embolic particles than CEA.8 This trial was aborted after enrolling only 17 patients because of the unacceptably high stroke death rate following CAS (71%) compared with CEA (0%). Jordan et al have also confirmed these findings regarding embolic events during the two treatment options.9

More recently, Jaeger and Mathias reported on the incidence of silent embolic infarct as detected by diffusion-weighted MRI (DW-MRI) of the brain following CAS.10 These investigators performed DW-MRI of the brain on 67 patients with 70 high-grade stenoses of the carotid artery, before and 24 hours after stent implantation. Symptomatic cerebral embolization occurred during one procedure. DW-MRI showed new ipsilateral ischemic lesions after stent implantation in 20 patients (29%), including the symptomatic patient shown in Figure 2. This study showed additional convincing evidence for the occurrence of embolization during CAS.

Protection Devices Capture Particles
The clinical and experimental observations mentioned led to the development of cerebral protection devices that can capture these particles.11,12 Preliminary studies utilizing cerebral protection devices have confirmed that significant amounts of emboli are released during CAS. Whitlow et al reported their initial results utilizing the PercuSurge GuardWire (Medtronic, Minneapolis, MN) to prevent embolization in 75 CAS procedures.13 Not surprisingly, visible particles consisting of fibrous plaque debris, lipid or cholesterol vacuoles, and calcific plaque fragments were recovered from each case. The number of particles analyzed per patient ranged from 22 to 667 and the mean maximum diameter was 203 ± 256 µm (range, 3.6-5,262 µm).

Despite the fact that there is growing evidence regarding the occurrence of embolization during CAS, the significance of such embolic particles and the need for cerebral protection devices has been a subject of controversy. Many investigators believed that any embolization could not be safe for the brain. However, others thought that unless emboli contributed to clinical events such as stroke, their significance could not be determined and the need for cerebral protection devices remained questionable.

Embolization Associated With Memory Loss
Although it is true that there is no level I evidence to support the clinical effectiveness of cerebral protection devices, there is growing proof that microembolization more often results in clinical sequela. For example, Fearn et al investigated the occurrence of cerebral embolization during CPB with transcranial Doppler and evaluated its significance with careful neuropsychological tests.14 These investigators measured cerebrovascular reactivity in 70 patients before undergoing coronary surgery in which nonpulsatile bypass was used. The surgeons used a transcranial Doppler system throughout the procedure to record middle cerebral artery flow velocity and embolization. A computerized battery of tests measured cognitive function before the operation and 1 week, 2 months, and 6 months after surgery. They detected more than 200 emboli in 40 patients, mainly on aortic clamping and release, when bypass was initiated, and during defibrillation. Cognitive function deteriorated more in patients undergoing CPB than in control patients undergoing urologic procedures. The investigators concluded that emboli were significantly associated with memory loss.

Gaunt et al investigated the clinical significance of microembolization detected by transcranial Doppler ultrasonography. These investigations determined the quantity and character of emboli and correlated them with neurological and psychometric outcome, fundoscopy, automated visual field testing, and computed tomographic brain scans.15 Not surprisingly, the researchers detected embolization in 92% of successfully monitored operations involving 100 consecutive patients undergoing CEA. More than 10 particulate emboli during initial carotid dissection correlated with a significant deterioration in postoperative cognitive function. Overall, 37% of patients undergoing CEA experienced deterioration in cognitive function. Although these studies were carried out in non-CAS procedures, the data show that although embolization may not always result in a stroke, it has a significant negative effect on the brain.

Although the clinical benefit of recovering emboli from the brain has not been proven, the result of the Saphenous Vein Graft Angioplasty Free of Emboli Randomized Trial (SAFER) is relevant.16 This trial randomized 550 patients with degenerated saphenous vein graft following CABG to either PercuSurge GuardWire-protected percutaneous transluminal coronary angioplasty or unprotected PTCA. The 30-day MI rate was 16.5% for the control arm, whereas it was reduced to 8.4% in the protected arm (P<.001). Based on this trial, the PercuSurge GuardWire received FDA approval and is currently considered the standard of care for select patients undergoing PTCA for degenerated coronary saphenous vein grafts. If preventing emboli from reaching the heart is beneficial, we can speculate that it is also beneficial for the brain.

Based on these experimental and clinical observations, many investigators now strongly believe that CAS carries a significant risk for embolic events. Although we do not know the clinical significance of these embolic particles, growing evidence suggests emboli can cause neurological damage. The early results of ongoing clinical trials evaluating the safety and efficacy of CAS in conjunction with protection devices are promising. If these trials prove that protection devices can prevent embolic events without causing excessive problems, they will probably be utilized on a routine basis during CAS.

Takao Ohki, MD, is the Director of the Division of Vascular Surgery and Associate Professor of Surgery at Montefiore Medical Center, Albert Einstein College of Medicine in New York. Dr. Ohki is a consultant for Abbott Vascular, ArteriA Medical Science, Inc., Boston Scientific, and Medtronic. He may be reached at (718) 920-4707; takohki@msn.com.

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