Prevalence of Asymptomatic Carotid Artery Stenosis According to Age and Sex Systematic Review and Metaregression Analysis

Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, GA Utrecht, The Netherlands.
Stroke (Impact Factor: 5.72). 02/2009; 40(4):1105-13. DOI: 10.1161/STROKEAHA.108.532218
Source: PubMed


In the discussion on the value of population-wide screening for asymptomatic carotid artery stenosis (ACAS), reliable prevalence estimates are crucial. We set out to provide reliable age- and sex-specific prevalence estimates of ACAS through a systematic literature review and meta-regression analysis.
We searched PubMed and EmBase until December 2007 for studies that reported the prevalence of ACAS in a population free of symptomatic carotid artery disease. Data were extracted with use of a standardized form on participants' characteristics, assessment method, study quality, and prevalence estimates for moderate (>or=50% stenosis) and severe (>or=70% stenosis) ACAS. Metaregression was used to investigate sources of heterogeneity.
Forty studies fulfilled the inclusion criteria. There was considerable variation among studies with respect to demographics, methods of grading stenosis, and stenosis cutoff point used. The pooled prevalence of moderate stenosis was 4.2% (95% CI, 3.1% to 5.7%). Prevalence of moderate stenosis among people age <70 years was 4.8% (95% CI, 3.1% to 7.3%) in men and 2.2% (95% CI, 0.9% to 4.9%) in women. Among those >or=70 years, prevalence increased to 12.5% (95% CI, 7.4% to 20.3%) in men and to 6.9% (95% CI, 4.0% to 11.5%) in women. Metaregression showed that both age and sex significantly affected the prevalence of moderate stenosis. No contribution of study size, publication year, geographic region, assessment method, and study quality was found. The pooled prevalence of severe stenosis was 1.7% (95% CI, 0.7% to 3.9%).
Prevalence of moderate stenosis increases with age in both men and women, but men at all ages have the higher prevalence estimates. The number of studies that allowed meaningful data synthesis of severe stenosis was limited.

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Available from: Erik Buskens, Sep 18, 2014
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    • "In our population, ICAD was more frequent in males, who were also younger than females, confirming previous data on atherosclerotic disease [8]. The most relevant risk factor for ICAD in our study resulted to be hypertension, followed by hypercholesterolemia; previous reports have shown similar results and aggressive treatment of these risk factors has been shown to reduce the recurrence of ischemic stroke in patients with intracranial stenosis [9] [10]. "
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    ABSTRACT: Stenosis of intracranial arteries are responsible for 30–50% of strokes in Orientals, 11% in Hispanics, 6% in Blacks and only 1% in Caucasians. However, the clinical importance of intracranial stenosis in Whites may have been underestimated.Subjects and methodsWe examined our database registry of all TIA/ischemic stroke Caucasian patients over a two-year period, from January 1st 2009 to December 31st 2010. All patients underwent a complete cervical and intracranial ultrasound assessment, MRA and/or CTA and/or DSA.ResultsAmong 292 patients (males 79.7%; mean age, 71.0 ± 12.8 years), we found 59 (20.2%) subjects harboring at least one intracranial stenosis and 20 (33.9%) patients with 2 stenosis; the total number of intracranial stenosis was 95. Regarding risk factors, hypertension was present in 67.8% of patients, diabetes in 27.1%, smoking in 30.5%, obesity in 10.2%, hypercholesterolemia in 37.3%, previous TIA/stroke in 23.7%, heart disease in 18.6%. Forty-six (77.9%) patients presented with stroke, while 13 (22.1%) with TIA. Concerning the site of stenosis, 50 (52.6%) were located in the anterior circulation [MCA 46 (48.4%), ACA 4 (4.2%)], 45 (47.4%) in the posterior circulation: [PCA 28 (29.5%), BA 11(11.6%), VA 6(6.5%)]; 46 (54.8%) on the right hemisphere, 38 (45.2%) on the left hemisphere.Conclusions In this university hospital-based study among Caucasian patients with acute cerebral ischemia, ultrasound disclosed a higher prevalence of intracranial stenosis than previously thought, suggesting the clinical importance of this condition in White European TIA/stroke patients.
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    ABSTRACT: Carotid atherosclerotic disease is a major cause of stroke, but it may remain clinically asymptomatic. The factors that turn the asymptomatic plaque into a symptomatic one are not fully understood, neither are the subtle effects that a high-grade carotid stenosis may have on the brain. The purpose of this study was to evaluate brain microcirculation, diffusion, and cognitive performance in patients with a high-grade stenosis in carotid artery, clinically either symptomatic or asymptomatic, undergoing carotid endarterectomy (CEA). We wanted to find out whether the stenoses are associated with diffusion or perfusion abnormalities of the brain or variation in the cognitive functioning of the patients, and to what extent the potential findings are affected by CEA, and compare the clinically symptomatic and asymptomatic subjects as well as strictly healthy controls. Coagulation and fibrinolytic parameters were compared with the rate microembolic signals (MES) in transcranial Doppler (TCD) and the macroscopic appearance of stenosing plaques in surgery. Patients (n=92) underwent CEA within the study. Blood samples pertaining to coagulation and fibrinolysis were collected before CEA, and the subjects underwent repeated TCD monitoring for MES. A subpopulation (n= 46) underwent MR imaging and repeated neuropsychological examination (preoperative, as well 4 and 100 days after CEA). In MRI, the average apparent diffusion coefficients were higher in the ipsilateral white matter (WM), and altough the interhemispheric difference was abolished by CEA, the levels remained higher than in controls. Symptomatic stenoses were associated with more sluggish perfusion especially in WM, and lower pulsatility of flow in TCD. All patients had poorer cognitive performance than healthy controls. Cognitive functions improved as expected by learning effect despite transient postoperative worsening in a few subjects. Improvement was greater in patients with deepest hypoperfusion, primarily in executive functions. Symptomatic stenoses were associated with higher hematocrit and tissue plasminogen activator antigen levels, as well as higher rate of MES and ulcerated plaques, and better postoperative improvement of vasoreactivity and pulsatility. In light of the findings, carotid stenosis is associated with differences in brain diffusion, perfusion, and cognition. The effect on diffusion in the ipsilateral WM, partially reversible by CEA, may be associated with WM degeneration. Asymptomatic and symptomatic subpopulations differ from each other in terms of hemodynamic adaptation and in their vascular physiological response to removal of stenosis. Although CEA may be associated with a transient cognitive decline, a true improvement of cognitive performance by CEA is possible in patients with the most pronounced perfusion deficits. Mediators of fibrinolysis and unfavourable hemorheology may contribute to the development of a symptomatic disease in patients with a high-grade stenosis. Kaulavaltimoiden ateroskleroottinen ahtautuminen on tärkeä aivohalvauksen syy, mutta enemmistö ahtaumista ei aiheuta halvausta. Syyt, jotka tekevät kaulavaltimoplakista vaarallisen, tunnetaan puutteellisesti, samoin kuin ne mahdolliset muut vaikutukset, joita tiukalla ahtaumalla voi aivojen kannalta olla. Työn tarkoituksena oli tutkia aivojen perfuusiota eli mikroverenkiertoa, solutason diffuusiota ja kognitiivista suoriutumista potilailla, joiden tiukka kaulavaltimoahtauma poistettiin leikkauksella. Tavoitteina oli selvittää, liittyykö kaulavaltimoita ahtauttavaan tautiin aivojen diffuusion, perfuusion tai kognitiivisten toimintojen muutoksia, ja miten leikkaushoito vaikuttaa näihin ja verisuonten reaktiviteettiin, sekä verrata oireisten ja oireettomien löydöksiä keskenään mukaan lukien veren hyytymiseen ja hyytymän liukenemiseen liittyviä tekijöitä. Potilaiden diffuusio- ja kognitiolöydöksiä verrattiin terveiden henkilöiden arvoihin. Potilaiden kognitiivinen suoriutuminen oli kauttaaltaan alempi kuin täysin terveillä ikätovereilla. Ahtauman puoleisessa aivopuoliskossa todettiin magneettikuvauksella toista puolta korkeammat ns. näennäiset diffuusiovakiot aivojen valkeassa aineessa sekä hitaampi aivoperfuusio, ja nämä poikkeamat korjautuivat leikkauksen jälkeen. Diffuusiovakiot jäivät kuitenkin korkeammiksi kuin terveillä ikätovereilla. Neuropsykologinen suoriutuminen parani potilailla toistomittauksissa kuten terveillä, mutta osalla todettiin väliaikainen kognitiivinen heikkenemä heti leikkauksen jälkeen. Kognitiiviset toiminnot kohenivat pit-källä tähtäimellä enemmän niillä, joilla oli näkyvä aivoperfuusion vajaus ennen leikkausta, ja ensisijaisesti muutos tapahtui toiminnanohjauksessa. Näkyvä perfuusiovajaus oli yleisempää oireita aiheuttaneissa ahtaumissa. Oireilleilla oli myös korkeampi punasolujen tilavuusosuus ja kudosplasminogeenin aktivaattorin antigeeni veressä sekä useammin mikroveritulppia kuvaavia ultraäänisignaaleja aivoverenkierrossa kuin oireettomilla. Tulosten valossa tiukka kaulavaltimoahtauma vaikuttaa aivojen diffuusioon, perfuusioon ja kognitiivisiin toimintoihin kliinisistä oireista riippumattakin. Aivojen valkeaan aineeseen aiheutuva diffuusio muutos on samansuuntainen kuin valkean aineen degeneraatiossa, ja muutos korjaantuu osittain ahtauman kirurgisella hoidolla. Oireiset potilaat eroavat oireettomista hemodynamiikaltaan, ja leikkaus hyödyttää heitä enemmän parantuneen hemodynamiikan ja verisuoniston reaktiivisuuden muodossa. Vaikka potilailla on yleisesti alempi kognitiivinen suoritustaso täysin terveisiin verrattuna ja kirurgiseen hoitoon liittyy pieni ohimenevän kognitiivisen haitan riski, jopa kognitiivinen koheneminen on mahdollista potilailla, joiden perfuusiovajaus on suurin. Veren epäedulliset virtausominaisuudet ja fibrinolyysiin liittyvät tekijät saattavat vaikuttaa oireiden ilmaantumiseen näillä potilailla.
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