The Symptomatic Carotid Plaque

Golledge, Jonathan; Greenhalgh, Roger M.; Davies, Alun H.

doi:10.1161/01.str.31.3.774

Cited by 385 publications

(298 citation statements)

References 96 publications

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“…Enquanto é provável que poucas formas de acidente vascular cerebral relacionado à estenose carótida extracraniana ocorram por hipoperfusão 11 , na maioria dos casos, o que ocorre é embolização de uma placa aterosclerótica ou oclusão aguda da carótida e propagação do trombo distalmente 12 .…”

Section: Estenose De Carótida Extracranianaunclassified

Estenose de carótida extracraniana

Campos¹,

Filho²

2004

Arq. Bras. Cardiol.

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A estenose de carótida extracraniana é uma importante causa de ataque isquêmico transitório 1 , estando relacionada em 90% dos casos à afecção da bifurcação da carótida comum 2 . Atinge 2 milhões de pessoas nos Estados Unidos 3 e a sua incidência, acima dos 65 anos, segundo o Cardiovascular Health Study, é de 4,2% nos homens e 1,8% nas mulheres 3 . Sua prevalência, conforme dados do estudo Framingham, é de 9% para homens e 7% para mulheres 4 .A aterosclerose da carótida representa ainda, 10 a 20% dos casos de acidente vascular cerebral 1 , que constitui a terceira causa de mortalidade nos Estados Unidos 4,5 , com uma incidência de 700.000 casos por ano e responsável por quatro dos 50 milhões de óbitos anuais no mundo 5 .Portanto, como o ataque isquêmico transitório, muitas vezes, precede o acidente vascular cerebral 2 e a estenose de carótida extracraniana está intimamente relacionada ao ataque isquêmico transitório, é necessária uma abordagem criteriosa e responsável desta entidade a fim de serem evitados graves prejuízos à saúde do paciente.Veja, por exemplo, o caso de um homem branco, de 66 anos com longa história de tabagismo, hipertensão arterial sistêmica não controlada, diabetes mellitus e hiperlipidemia há vários anos, que procurou assistência médica por alguns episódios de paresia em membro superior direito de, aproximadamente, 15 min. Durante o exame físico, o médico percebeu um sopro sobre a carótida esquerda, acrescido da confirmação de seu relato de hipertensão.Como conduzir o caso? -No paciente em questão, fatores de risco cerebrocardiovasculares eram óbvios e exigiam atenção imediata. Incluída na abordagem inicial onde uma investigação neurológica e cardiológica básica é imprescindível, nos deparamos com uma entidade, muito negligenciada na prática clínica, a afecção de carótida.Principais questões na estenose de carótida extracranianaPor quê a estenose de carótida extracraniana é tema tão controverso? Existe relação com a doença arterial coronariana? Como sua fisiopatologia pode explicar as principais complicações? Quando pensar e como diagnosticar a estenose de carótida? Qual o significado de um sopro carotídeo? Em se diagnosticando uma estenose de carótida, qual a conduta terapêutica que obtém melhores resultados?Estenose de carótida é um tema controverso, seria de se esperar? -Um dos grandes problemas na abordagem do paciente com estenose de carótida extracraniana é a existência de muitas controvérsias na sua terapêutica, já que é uma doença que afeta o território arterial macrovascular, tendo relação íntima com a doença arterial coronariana e, como esta, sua etiopatogenia não está totalmente compreendida.Estenose de carótida extracraniana e doença arterial coronariana -Kallikazaros e cols. 6 avaliaram 225 pacientes referidos ao hospital para investigação de dor precordial, sugestivamente isquêmica, submetidos a ultra-sonografia de carótidas e angiografia quantitativa de coronárias, buscando correlacionar a estenose de carótida à doença arterial coronariana e observaram que desses pacientes, 8...

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Section: Estenose De Carótida Extracranianaunclassified

Estenose de carótida extracraniana

Campos¹,

Filho²

2004

Arq. Bras. Cardiol.

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“…The importance of carotid atherosclerosis and related thromboembolic occlusion of a large artery tributary of the brain in the pathogenesis of ischemia and cerebral infarction has been acknowledged for many years [1][2][3][4]. Although the grade of stenosis due to a plaque encroaching the lumen constitutes the major criterion to identify subgroups of patients at high risk of stroke [5,6], results from several studies suggest that plaque rupture and thrombosis represent the most important factor correlated with the onset of symptoms [1,3].…”

Section: Introductionmentioning

confidence: 99%

Asymptomatic carotid plaque rupture with unexpected thrombosis over a non-canonical vulnerable lesion

et al. 2011

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a b s t r a c tObjective: Several studies have demonstrated that carotid plaque rupture and thrombosis represent the most important factors correlated with the onset of acute cerebrovascular symptoms. Nevertheless, ruptured thrombotic plaques have been described also in asymptomatic patients. What still needs to be clarified is why a plaque rupture leads either to an acute ischemic syndrome or, in a minor group of patients, remains asymptomatic. The purpose of this study was to systematically compare the histologic features of thrombotic plaques both in asymptomatic and symptomatic patients in order to identify specific findings that could explain the peculiar clinical behavior that characterizes each of the clinical settings. Methods: A total of 157 thrombotic plaques from 60 asymptomatic patients and 97 with major stroke who consecutively underwent CEA were serially sectioned and studied by histology. Results: A minute cap disruption very frequently characterizes thrombotic plaques of asymptomatic patients and it was always smaller than large ulcers observed in thrombotic symptomatic plaques (651 ± 687 m vs. 4150 ± 3526, p = 0.001). In asymptomatics this typical feature was associated with fewer inflammatory cells (20.1 ± 8.8 vs. 33.9 ± 26.1 cells × hpf, p = 0.001), smaller lipidic-necrotic core (33.9% ± 2.9% vs. 42.0% ± 2.4%; p = 0.04) and larger calcification (16.2 ± 12.8% vs. 8.1 ± 12.2%, p = 0.02). Symptomatic patients with thrombotic plaques showed higher incidence of metabolic syndrome (p = 0.002) and moderate-high Framingham risk scores (p = 0.001) comparing to asymptomatic individuals. Conclusion: The transformation from a stable to a vulnerable plaque is a gradual process in the natural history of the disease and plaque rupture is an event not necessarily occurring at a late phase but also at earlier one. In this case, the rupture will be most likely smaller and clinically asymptomatic.

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“…Rupture of atherosclerotic plaques is crucial in the pathogenesis of acute coronary syndromes and strokes [20,21]. Interactions, within the ICA stenosing plaque, between connective tissue and the cells embedded into the fibrous cap overlying the inner core appear to determine the history of the ICA stenosis: plaque rupture or ulceration, intraplaque haemorrhage and luminal thrombosis are recognized causes of stroke [20,21].…”

Section: Introductionmentioning

confidence: 99%

“…Interactions, within the ICA stenosing plaque, between connective tissue and the cells embedded into the fibrous cap overlying the inner core appear to determine the history of the ICA stenosis: plaque rupture or ulceration, intraplaque haemorrhage and luminal thrombosis are recognized causes of stroke [20,21]. Specific markers to identify in vivo ruptured plaques, or plaques prone to rupture, are not available.…”

Section: Introductionmentioning

confidence: 99%

Genetic control of chemokines in severe human internal carotid artery stenosis

et al. 2008

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Background and purpose: Atherosclerosis is an inflammatory disease. Chemokines and chemokine receptors are known to be involved in atherogenesis. Common single nucleotide polymorphisms (SNPs) affect transcription in response to inflammatory stimuli. The aim of this study was to evaluate the correlations between MCP-1, RANTES, SDF-1, CCR2, and CCR5 gene polymorphisms with increased risk of internal carotid artery (ICA) stenosis. Methods: Hundred and twelve patients, consecutively recruited for ICA occlusive disease, and 282 controls were genotyped for MCP-1-2518G, RANTES-403A, CCR5D32, CCR2 V64I, and SDF-1-801A polymorphisms. Results: The frequency of the SDF-1A allele was significantly different between cases and controls: 0.32 vs. 0.20, respectively (OR 1.81; 95% CI 1.25-2.60; p = 0.007). The frequency of the RANTES-403G allele was significantly higher in patients with stenosis >70% (OR, 2.45; 95% CI 1.12-5.71; p = 0.015). No significant differences were observed with the other polymorphisms. Conclusion:The reported results seem to correlate the polymorphisms of the genes encoding for SDF-1, RANTES with pathogenesis and progression of ICA occlusive disease. Although suggestive, these results need confirmation in prospective cross-sectional studies.

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The Symptomatic Carotid Plaque

Cited by 385 publications

References 96 publications

Estenose de carótida extracraniana

Estenose de carótida extracraniana

Asymptomatic carotid plaque rupture with unexpected thrombosis over a non-canonical vulnerable lesion

Genetic control of chemokines in severe human internal carotid artery stenosis

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