Study: Key findings
1. European Carotid Surgery Study [42]: In addition to degrees of carotid artery stenosis, angiographic plaque surface irregularity was associated with increased risk of ipsilateral ischemic stroke in symptomatic carotid artery stenosis
2. Academic Medical Centers Consortium data source [43]: Among members of the Academic Medical Centers Consortium from which 100 carotid endarterectomies from each site were randomly selected during the years 1988–1990, the rate of postoperative stroke or death was not significantly impacted by the presence or absence of angiographically recognized ulceration or intraluminal thrombus among asymptomatic patients
3. NASCET [44]: Among symptomatic carotid artery stenosis patients, ipsilateral irregular or ulcerated plaque detected by angiography predicted 30-day perioperative stroke or death
4. Case series data source [45]: In a case-based series, morphologic plaque characteristics based on color duplex ultrasonography determination included echolucent plaques and progressive lesions that affected symptom occurrence
5. Review of the vascular biology of the symptomatic carotid plaque [46]: Unstable plaques were characterized by surface ulceration and plaque rupture in both symptomatic and asymptomatic plaques, thinning of the fibrous cap, and infiltration of the cap by macrophages and T cells
6. Registry data source [47]: Complex carotid ulcers were associated with a higher risk of subsequent stroke in asymptomatic, non-stenosing carotid artery bifurcation lesions
7. ACAS and NASCET data source [48]: Symptomatic patients more commonly had carotid artery ulceration regardless of the side of carotid symptoms, and thrombus was associated with plaque ulceration and symptom laterality
8. Oxford Plaque Study [49]: In patients with symptomatic carotid artery stenosis, with increasing age plaque calcification and size of the large lipid core increased, the fibrous tissue decreased, and lymphocyte infiltration and inflammation decreased
9. Participants of cohort studies/trials at a single academic center [50]: Among persons with carotid stenosis >50 %, occlusion or unstable carotid plaque who had TCD monitoring for 1 h within 48 h of clinical presentation, Power M-mode TCD identified persons with malignant microembolic signals associated with larger baseline infarcts, a higher occurrence of intraluminal thrombus or ulcerated carotid plaque, and worse clinical outcome
10. Stroke Prevention Clinic of the London Health Sciences Center data source [51]: Among patients with asymptomatic internal carotid artery stenosis ≥60 % based on Doppler evaluation and who had 3D ultrasound, those with ≥3 carotid artery ulcers were more likely to have a stroke or death within 3 years regardless of ulcer side; those with microemboli had a higher risk of stroke or death within 3 years; and the annual ipsilateral stroke rate was only 0.8 %. The authors advocated for medical management until there was development of symptoms, ulcers, or emboli
11. Asymptomatic Carotid Embolic Study (ACES) [52]: Among those asymptomatic patients participating in an international multicenter study of embolic signals and ultrasound plaque morphology, the combination of embolic signal and plaque echolucency morphology provided a greater degree of prediction of ipsilateral stroke risk than either measure alone. The authors advocated possible use of these measures for selection of asymptomatic patients for CEA
Future Directions
Future directions in the field of asymptomatic cerebrovascular disease encompassing primarily carotid artery stenosis will need to address means whereby proper technology assessments of new risk stratification schemes to identify patients who will be best served by CEA and endovascular interventions as compared to medical therapy are carried out. Such proof will require large efficacy and effectiveness data resources, new technology to identify and localize carotid plaque morphology, new risk stratification schemes, and plausible means to successfully apply comprehensive and aggressive medical management options in populations. As it currently stands based on a systematic review and meta-analysis, major CEA studies for asymptomatic carotid artery stenosis may no longer be applicable according to contemporary medical practice, and no major trial has reported a comparison of carotid artery stenting to medical therapy alone [53]. We await the implementation and subsequent results of CREST-2, a US National Institutes of Health funded trial, to address medical therapy compared to CEA and stenting [54].
According to an international meta-analysis of individual participant data of carotid intima-media thickness (c-IMT) progression, after adjustment for multiple factors mean c-IMT of two ultrasound scan recordings remains robustly associated with cardiovascular risk [55]. Furthermore and based on another meta-analysis, advances in neuroimaging have improved the prospects that noninvasive studies could replace conventional cerebral angiography and its inherent risks in the measurement of high-grade (70–99 %) carotid artery diameter stenosis though the accuracy remained uncertain for 50–69 % carotid stenosis [56]. New imaging techniques to localize and identify ruptured and high-risk atherosclerotic plaques, such as 18 F-sodium fluoride positron emission tomography-CT, are now being tested and could provide a new pathway to improve management and treatment of patients at risk for complications from asymptomatic atherosclerosis [57].
Given the aforementioned challenges, asymptomatic intracranial atherosclerosis is probably the most prevalent form of cerebral atherosclerosis and deserves the same attention that asymptomatic carotid artery stenosis receives [58]. Reduction of subclinical brain lesions (silent strokes, white matter disease) within the continuum of asymptomatic cerebrovascular disease could lead to cognitive vitality and better general brain health [59].
References
1.
Committee for the National Institute of Neurological Disorders and Stroke. Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke. 1990;21:637–76.CrossRef
2.
Hachinski V. World Stroke Day 2008. “Little strokes, big trouble”. Stroke. 2008;39:2407–8.CrossRef
3.
Das RR, Seshadri S, Beiser AS, Kelley-Hayes M, Au R, Himali JJ, et al. Prevalence of correlates of silent cerebral infarcts in the Framingham Offspring Study. Stroke. 2008;39:2929–35.CrossRef
4.
Llewellyn DJ, Lang I, Xie J, Huppert F, Melzer D, Langa KM. Framingham stroke risk profile and poor cognitive function: a population-based study. BMC Neurol. 2008;8:12. doi:10.1186/1471-2377-8-12. full article found at: http://www.biomedcentral.com/1471-2377/8/12 (accessed March 2, 2014).CrossRef
5.
Sacco RL, Kasner SE, Broderick SP, Caplan LR, Connors JJ, Culebras A, et al. An updated definition of stroke for the 21st century. A statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44:2064–89.CrossRef
6.
Easton JD, Saver JL, Albers GW, Alberts MJ, Chatuvedi S, Feldmann E, et al. Definition and evaluation of transient ischemic attack. A scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. Stroke. 2009;40:2276–93.CrossRef
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