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Quantity, particle size, and histologic composition of embolic debris collected in a distal protection filter after carotid angioplasty and stenting: Correlation with patient characteristics, timing of carotid artery stenting, and procedural details

2013; Elsevier BV; Volume: 146; Issue: 2 Linguagem: Inglês

10.1016/j.jtcvs.2013.03.024

1097-685X

Jorinde H.H. van Laanen, Joke M. Hendriks, Hence J.M. Verhagen, Heleen M.M. van Beusekom,

Intracranial Aneurysms: Treatment and Complications

The occurrence of distal embolization during carotid artery stenting (CAS) is a major complication. Determining the preoperative risk of embolization may lead to improved patient selection and outcome of CAS. This study examined the quantity, particle size, and histologic composition of embolic debris collected in a distal protection filter and its possible correlation with patient characteristics, timing of CAS, and procedural details. Patients who underwent a CAS procedure during a 17-month period in which a SPIDER Embolic Protection Device (EPD) (ev3 Endovascular Inc, Plymouth, Minn) was used were included. Patient demographics, cardiovascular risk factors, neurologic symptoms, and time interval between symptoms and CAS were retrospectively recorded. CAS was performed according to the standardized protocol in our center as described previously.1Flach H.Z. Ouhlous M. Hendriks J.M. van Sambeek M.R.H.M. Veenland J.F. Koudstaal P.J. et al.Cerebral ischemia after carotid intervention.J Endovasc Ther. 2004; 11: 251-257Crossref PubMed Scopus (115) Google Scholar This protocol also dictates the antiplatelet regimen. Debris was photographed before (Figure 1, A) and after (Figure 1, B) removal from the EPD. Clemex image analysis software (Clemex Technologies Inc, Longueuil, Canada) was used to analyze the number and size of the particles. Consecutive series of paraffin sections were stained with hematoxylin–eosin as a routine stain, resorcin-fuchsin for collagen and elastin, and von Kossa for collagen and calcified tissue to study the particles at different depths. Debris was classified as thrombus (containing platelets, erythrocytes, and fibrin), atheroma (fibrous matrix, cholesterol clefts, and foam cells), and calcified tissue on the basis of morphologic criteria. Data were analyzed using SPSS software (SPSS Statistics 17.0; SPSS Inc, Chicago, Ill). Continuous variables were expressed as median (minimum-maximum) in case normality could not be assumed and compared with nonparametric tests. Demographics of the 55 included patients and details of the 59 treated stenotic lesions in these patients are presented in Table 1.Table 1Patient (n = 55) and lesion (n = 59) characteristicsPatients, n (%)Age, yMean, 67.2 (range, 47-89)Male sex36 (66)Hypertension43 (78)Hypercholesterolemia41 (75)Diabetes9 (16)Cardiac disease13 (24)Chronic renal insufficiency9 (16)Smoking history39 (71)Lesions, n (%)Asymptomatic5 (8.5)Symptomatic54 (91.5) Amaurosis fugax8 (14) Retinal infarction1 (2) Transient ischemic attack28 (48) Stroke17 (29)Onset of symptoms before CAS 0-28 d35 (59) >28 d24 (41)Contralateral occlusion10 (17)Percent stenosis 50%-69%4 (7) 70%-99%55 (93)CAS, Carotid artery stenting. Open table in a new tab CAS, Carotid artery stenting. Macroscopic evaluation detected particles in 44 of the 59 collected filters (75%) (Figure 1). Table 2 represents patient and procedural details of these cases and the number and size of the detected particles. The EPD in patients who smoked showed a significantly lower number of particles compared with nonsmokers (7 vs 14, P = .029). The number of particles was significantly higher when CAS was performed in the first 4 weeks after the qualifying neurologic event (10 vs 4, P = .048).Table 2Patient and procedural characteristics of 44 cases with embolic particles in the Embolic Protection Device and number and size of particlesN = (%)No. of particles, median (min-max)P valueLength of particles, median (min-max)P valueAge (y) mean, 67.6 (47-89) Less than or equal to mean22 (50)8 (1-29).51670 (60-6045).09 Greater than mean22 (50)9 (1-47)609 (79-9423)Sex Male29 (65.9)10 (1-47).98615 (60-9423).31 Female15 (34.1)7 (1-29)728 (79-6771)Hypertension Yes38 (86.4)9.5 (1-31).37684 (60-9423).013 No6 (13.6)3.5 (1-47)474 (129-3681)Hypercholesterolemia Yes30 (68.2)10 (1-24).31653 (60-6771).43 No14 (31.8)5.5 (1-47)621 (79-9423)Diabetes Yes9 (20.5)13 (3-31).5782 (135-9423).018 No35 (79.5)8 (1-47)615 (60-6045)Cardiac disease Yes10 (22.7)9.5 (3-24).83707 (60-6771).17 No34 (77.3)8.5 (1-47)629 (79-9423)Chronic renal insufficiency Yes9 (20.5)8 (1-24).77706 (147-4676).38 No35 (79.5)9 (1-47)636 (60-9423)Smoking history Yes31 (70.5)7 (1-47).029643 (60-9423).42 No13 (29.5)14 (4-29)643 (79-6771)Asymptomatic Yes3 (6.8)3 (1-14).23546 (169-1728).76 No41 (93.2)9 (1-47)645 (60-9423)Symptomatic Amaurosis fugax4 (9.1)4 (1-21).24650 (213-4095).22 Transient ischemic attack23 (52.3)8 (1-31)669 (79-9423) Stroke14 (31.8)11.5 (2-47)606 (60-6771)Onset of symptoms before CAS 0-28 d28 (64)10 (1-47).048653 (60-9423) >28 d16 (36)4 (1-23)615 (135-4676).51Duration CAS <2 h21 (48)8 (1-31).46695 (60-9423).25 ≥2 h23 (52)10 (2-47)603 (79-6045)Predilation Yes40 (91)8.5 (1-47).87630 (60-9423).52 No4 (9)9 (1-19)838 (125-4102)Postdilation Yes41 (93)9 (1-47).89633 (60-9423).14 No3 (7)7 (5-13)881 (160-4676)Stent type Acculink30 (68)8 (1-47).60599 (79-6045).21 Protege7 (16)13 (3-31)714 (60-9423) Other7 (16)10 (4-21)615 (135-4676)CAS, Carotid artery stenting. Open table in a new tab CAS, Carotid artery stenting. Qualitative assessment of histologic sections showed determinable embolic debris in 36 (82%) of the processed filters. Embolic particles consisted of atheromatous debris in 13 cases (36%), thrombus in 16 cases (44%), and calcified tissue in 7 cases (19%) (Figure 2). Atheromatous plaques generated a significantly higher number of particles (median 14, P = .01). Despite the use of protection devices, cerebral embolization has been shown by transcranial Doppler and diffusion-weighted magnetic resonance imaging.2Bonati L.H. Jongen L.M. Haller S. ICSS-MRI study groupNew ischaemic brain lesions on MRI after stenting or endarterectomy for symptomatic carotid stenosis: a substudy of the International Carotid Stenting Study (ICSS).Lancet Neurol. 2010; 9: 353-362Abstract Full Text Full Text PDF PubMed Scopus (480) Google Scholar, 3Timaran C.H. Rosero E.B. Martinez A.E. Ilarraza A. Modrall J.G. Clagett G.P. Atherosclerotic plaque composition assessed by virtual histology intravascular ultrasound and cerebral embolization after carotid stenting.J Vasc Surg. 2010; 52: 1188-1194Abstract Full Text Full Text PDF PubMed Scopus (40) Google Scholar Although most of the clinical implications of detected microemboli remain undefined, association with deterioration in cognitive function 6 months after CAS has been reported.4Altinbas A. van Zandvoort M.J. van den Berg E. Jongen L.M. Algra A. Moll F.L. et al.Cognition after carotid endarterectomy or stenting: a randomized comparison.Neurology. 2011; 77: 1084-1090Crossref PubMed Scopus (74) Google Scholar Currently, no protection device can completely prevent distal embolization. Furthermore, dislodgement of embolic debris can occur during guidewire manipulation and protection device positioning or removal. Determining the risk factors for embolization could lead to a better patient selection, improving outcomes of CAS. Unstable, echolucent atherosclerotic plaques have been associated with increased embolic potential and increased risk of stroke in CAS.5Topakian R. Strasak A.M. Sonnberger M. Haring H.P. Nussbaumer K. Trenkler J. et al.Timing of stenting of symptomatic carotid stenosis is predictive of 30-day outcome.Eur J Neurol. 2007; 14: 672-678Crossref PubMed Scopus (61) Google Scholar This study confirms the increased embolic potential, because we found a significantly higher number of embolic particles when CAS was performed in the first weeks after symptoms and a significantly higher number of particles in atheromatous plaques. Older age, hypertension, hypercholesterolemia, coronary artery disease, symptomatic lesions, number of balloon dilations, and stent diameter have unequivocally been associated with increased embolic potential. In this study, we found only smoking to be negatively correlated with the number of dislodged particles during CAS. A possible explanation for this finding is that plaque composition in smokers differs from nonsmokers because of different etiology, and these plaques could be more stable. Because of the method of histologic processing and section staining, not all filters containing embolic debris appeared in the qualitative analysis. In addition to the small sample size, this is a limitation of this study. The detailed analysis of embolic debris and the findings that lesion characteristics and timing of intervention seem to be the most important factors influencing distal embolization during CAS and contribute to further understanding the mechanism of embolization and better patient selection.