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Vascular and Endovascular Surgery Unit San Paolo Hospital Civitavecchia, Rome, Italy G.Marcucci CAROTID PLAQUES AND CEREBRAL EMBOLISM.

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Presentation on theme: "Vascular and Endovascular Surgery Unit San Paolo Hospital Civitavecchia, Rome, Italy G.Marcucci CAROTID PLAQUES AND CEREBRAL EMBOLISM."— Presentation transcript:

1 Vascular and Endovascular Surgery Unit San Paolo Hospital Civitavecchia, Rome, Italy G.Marcucci CAROTID PLAQUES AND CEREBRAL EMBOLISM

2 G.Marcucci Skip to main content Log on / register BioMed Central homeBioMed Central home | Journals A-Z | Feedback | Support | My detailsJournals A-ZFeedbackSupportMy details Home |ome Browse articles |articles Search | Weblinks | Submit article |cle My Cardiovascular Ultrasound | Ultrasound About Cardiovascular Ultrasound Top Abstract Background Methods Results Discussion Conclusion Competing interests Authors' contributions References on Google Scholar on PubMed Central Cardiovascular Ultrasound Volume 4 Viewing options: Abstract Full text PDF (332KB)PDF Associated material: Readers' comments Pre-publication history PubMed record Related literature: Articles citing this article Other articles by authors Related articles/pages Tools: Download citation(s) Download XML to a friend Order reprints Post a comment Post to: Citeulike Connotea Facebook Twitter Research Christina Petersen, Patricia B Peçanha, Lucia Venneri, Emilio Pasanisi, Lorenza Pratali and Eugenio Picano CNR, Institute of Clinical Physiology, Pisa, Italy author corresponding author Cardiovascular Ultrasound 2006, 4:16doi: / The electronic version of this article is the complete one and can be found online at: Received:11 January 2006 Accepted:24 March 2006 Published:24 March 2006 © 2006 Petersen et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background Carotid plaque severity and morphology can affect cardiovascular prognosis. We evaluate both the importance of echographically assessed carotid artery plaque geometry and morphology as predictors of death in hospitalised cardiological patients. Methods 541 hospitalised patients admitted in a cardiological division (age = 66 ± 11 years, 411 men), have been studied through ultrasound Duplex carotid scan and successively followed-up for a median of 34 months. Echo evaluation assessed plaque severity and morphology (presence of heterogeneity and profile). Results 361 patients showed carotid stenosis (67% with 70% stenosis, 4% with near occlusion and 2% with total occlusion). During the follow-up period, there were 83 all-cause deaths (15% of the total population). Using Cox's proportional hazard model, age (RR 1.06, 95% CI 1.03–1.09, p = 0.000), ejection fraction > 50% (RR = 0.62, 95% CI 0.4–0.96, p = 0.03), treatment with statins (RR = 0.52, 95% CI 0.29– 0.95, p = 0.34) and the presence of a heterogeneous plaque (RR 1.6; 95% CI, 1.2 to 2.14, p = 0.002) were independent predictors of death. Kaplan – Meier survival estimates have shown the best outcome in patients without plaque, intermediate in patients with homogeneous plaques and the worst outcome in patients with heterogeneous plaques (90% vs 79% vs 73%, p = ). Conclusion In hospitalised cardiological patients, carotid plaque presence and morphology assessed by ultrasound are independent predictors of death. Background Non-invasive carotid artery ultrasound is a well established and valid method which allows to both visualize and quantify atherosclerotic lesions. Ultrasound and autopsy studies have shown that the presence and extent of carotid atherosclerosis correlates with atherosclerosis elsewhere in the circulation, including coronary arteries [1-4]. Several studies have found that the presence of carotid stenosis is a strong predictor of death in the general population [5,6]. Moreover, there is evidence that ultrasonographic B-mode characterization of plaque morphology may be useful in the assessment of the vulnerability of the atherosclerotic lesions [7-10]. Atherosclerotic plaque composition appears to be more important than plaque size in determining adverse events [11]. In particular, lipids and haemorrhages are associated with a more active plaque [12,13], which appear to be more vulnerable to rupture. Ultrasonically assessed plaque morphology provides an insight into the plaque composition and structure as shown by both in vitro [14-18] and in vivo [19-23] studies. Echo-lucent carotid plaques are lipid-rich and have a greater potential for clinical complications [7,10]. Heterogeneous plaques have a hypoechoic component and are associated with the presence of intra-plaque haemorrhage, ulceration and lipids, more likely to result in adverse events [8,21,22]. From histopathologic and vascular biologic studies, plaque composition and vulnerability, rather than degree of stenosis, have emerged as crucial factors leading to sudden rupture of the plaque surface, usually with superimposed thrombosis, which underlies the majority of acute occlusions. CAROTID PLAQUES The link between echo plaque structure and prognosis do not appear to be limited to the carotid arteries but may apply to virtually all vascular districts

3 G.Marcucci Heterogeneous plaques have been correlated with the presence of intra-plaque haemorrhage, ulceration and loose stroma containing lipids, cholesterol and proteinaceous deposits Echo-lucency is associated with lipid-rich plaques CAROTID PLAQUES

4 G.Marcucci All of the heterogeneous plaques have a echo-lucent component (lipid, haemorrhage, thrombi) A hypo-echoic appearance can also be associated with intra-plaque haemorrhage, which may be the result of intra-plaque neo- vascularization. CAROTID PLAQUES

5 G.Marcucci

6 G.Marcucci These small, fragile vessels could represent the underlying anatomic and pathologic changes leading to intramural haemorrhages and rupture. Lipid lakes and intra-plaque haemorrhage are more frequently found in vulnerable plaques, with greater potential for evolution and complication, and are the dominant substrate of hypoechoic and heterogeneous plaques CAROTID PLAQUES

7 G.Marcucci Cardiovascular Research 2002; 54:36-41 “VULNERABLE PLAQUE”

8 G.Marcucci atheroembolization results from disruption of endothelial surface and fibrous cap Atheroembolization platelet and erytrocyte aggregation to the subendothelial layer distal embolization of the thrombus and debris from the plaque

9 G.Marcucci CEREBRAL EMBOLIZATION DURING CEA AND CAS Perioperative cerebral embolization during CEA or CAS is a potentially devastting complication It is correlated with: - embolic potential of the plaque - during surgical dissection - during CAS procedure - postoperative embolization (technical problems)

10 G.Marcucci In the course of monitoring CEA’s with TCD ultrasonography, it became apparent that during all stages of this operation, signals identical to the qualities of embolic transients could be noticed Carotid endarterectomy

11 G.Marcucci an association between multiple cerebral microemboli during dissection and new white matter lesions on magnetic resonance images (MRI) of the brain made after surgery However, in the majority of these patients the new MRI lesions were clinically silent JANSEN Stroke, 1994

12 G.Marcucci microemboli that appeared during dissection and particularly during wound closure were statistically significantly associated with permanent cerebral deficits, i.e. intraoperative stroke ACKERSTAFF R. Stroke, 2000 but……

13 G.Marcucci CAS has been criticized on the grounds that the risk of cerebral embolism during the procedure may be greater than CEA Carotid Artery Stenting

14 G.Marcucci CRAWLEY Stroke, 1997 In contrast to coronary and peripheral artery angioplasty and stenting, which have been widely adopted, the concern for cerebral embolisation originally resulted in a understandable reluctance to use these techniques in the carotid artery territory. During these peripheral procedures, the risk of embolisation, estimated by myocardial infarction and clinical distal arterial emboli, ranges from 4% to 5%

15 G.Marcucci true incidence of asymptomatic embolisation may be much higher, and emboli of a size that are asymptomatic in the coronary and peripheral arterial circulations may cause neurological deficits in the cerebral circulation The National Heart LaBIR N Engl J Med, 1988

16 G.Marcucci during stent deployment squeezes plaque material from the vessel wall microembolization

17 G.Marcucci utilization of neuroprotection devices has the potential to reduce the intraprocedural cerebral embolic load and neurological event rate but……

18 G.Marcucci In conclusion, CEA is a safe and effective procedure CAS of the carotid bifurcation is a feasible alternative to CEA, particularly in patients with medical or surgical contraindications to surgery Nevertheless, CAS results in a significant higher cerebral embolic load and the number of clinically silent lesions on MRI is greater than in CEA Our aim is not to prove superiority of one technique over other

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