American Heart Association/American Stroke Association Council on Stroke; Council on Cardiovascular Radiology and Intervention; American Academy of Neurology. Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention: the American Academy of Neurology affirms the value of

Sacco, R.L.; Adams, Robert; Albers, Greg; Alberts, Mark J.; Benavente, Oscar; Furie, Karen L.; Goldstein, Larry B.; Pb, Gorelick; Halperin, Jonathan L.; Harbaugh, Robert E.; Johnston, Steven; Katzan, Irene; Kelly-Hayes, Margaret; Kenton, Edgar J.; Marks, Michael; Schwamm, Lee H; Tomsick, Thomas A.

doi:10.1016/j.ajo.2006.08.012

Cited by 589 publications

(1,052 citation statements)

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“…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]. In a previous study, we observed a ruptured and thrombotic plaque in 74% of patients with ipsilateral stroke and in 100% of patients treated within 2 months from symptoms onset [1].…”

Section: Introductionmentioning

confidence: 76%

“…The following risk factors were evaluated: hypertension, diabetes mellitus, cigarette smoking (former smokers who had stopped smoking for <5 years were considered as smokers and patients who had not smoked for >5 years were considered as nonsmokers), hypercholesterolemia, elevated triglyceridemia (TG), low HDL-cholesterol (HDL-C), abdominal obesity (patients with a waist circumference ≥102 cm in men or ≥88 cm in women [5]). In addition, we evaluated the presence of metabolic syndrome and the Framingham risk score [17].…”

Section: Risk Factorsmentioning

confidence: 99%

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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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Section: Introductionmentioning

confidence: 76%

Section: Risk Factorsmentioning

confidence: 99%

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

et al. 2011

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“…Additional information recorded included a history of diabetes or end stage renal disease as previous research has noted abnormal coated-platelet levels in these conditions, 9,18 and cardioembolism as the source of stroke due to potential differences in recurrence rates between cardioembolic and noncardioembolic strokes. [19][20][21] Stroke recurrence was defined as a new neurologic deficit with sudden onset occurring after study enrollment and 424 hours after the initial diagnosis of stroke with symptoms lasting 424 hours and not due to edema, mass effect, brain shift syndrome, hemorrhagic transformation, or secondary to a procedure. 19,20,22,23 The diagnosis of recurrent ischemic stroke was established by a neurologist.…”

Section: Materials and Methods Subjectsmentioning

confidence: 99%

Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Prodan

Stoner

Cowan

et al. 2012

J Cereb Blood Flow Metab

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Coated-platelets are procoagulant platelets observed upon dual-agonist stimulation with collagen and thrombin. Coated-platelet levels are elevated in patients with nonlacunar (large-vessel) ischemic stroke and decreased in patients with spontaneous intracerebral hemorrhage as compared with controls. The purpose of this study was to investigate a possible relationship between coated-platelet levels and stroke recurrence in patients with nonlacunar ischemic stroke. We assayed coated-platelet levels in 190 consecutive patients with nonlacunar stroke who were followed for up to 12 months; 20 subjects experienced recurrent stroke. Subjects were categorized into tertiles of coated-platelet levels. The distributions of time-to-recurrent stroke were estimated for each tertile using cumulative incidence curves and compared statistically using a log-rank test. The cumulative incidence of recurrent stroke at 12 months differed among the coated-platelet tertiles: 2% for the first tertile (lowest coated-platelet levels), 18% for the second tertile, and 17% for the third tertile (overall log-rank test, P ¼ 0.019). These data suggest that higher levels of coated-platelets, measured shortly after a nonlacunar stroke, are associated with an increased incidence of stroke recurrence. This observation offers an additional tool for identifying patients at highest risk for stroke recurrence following a nonlacunar (large-vessel) infarct.

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“…In recent years, tremendous efforts have been placed in conducting randomized clinical trials to better understand the efficacy and safety of each antiplatelet agent and the comparison between each, so that a systematic approach of selection of antiplatelet agents could be established. These trials form our current evidence-based approach of antiplatelet therapies for secondary stroke prevention [4,5]. In this article, we will review and discuss the following topics: 1) the mechanisms of action of different antiplatelet agents currently approved for stroke prevention, 2) the clinical trials that have led to the development of the evidence-based practice in antiplatelet agents for secondary stroke prevention, 3) the efficacy of antiplatelet agents for secondary stroke prevention in different stroke subtypes (i.e., large artery atherosclerosis and small vessel lacunar infarct), 4) the significance of antiplatelet resistance, and 5) future directions on clinical trial design for antiplatelet agents in secondary stroke prevention.…”

Section: Antiplatelet Agents In Secondary Stroke Preventionmentioning

confidence: 99%

“…Aspirin also produced a reduction of 9 per 1000 of further stroke or death (427 [8.2%] aspirin vs 516 [9.1%] control, 2P<0.001). Based on these data, the current recommendation of immediate use of aspirin for prevention of early stroke recurrence was established [5].…”

Section: Aspirinmentioning

confidence: 99%

Antiplatelet Agents for Stroke Prevention

Yip

Benavente

2011

Neurotherapeutics

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Stroke is one of the leading causes of disability and death. Ischemic stroke is a syndrome with heterogeneous mechanisms and multiple etiologies, rather than a singularly defined disease. Approximately one third of ischemic strokes are preceded by another cerebrovascular ischemic event. Stroke survivors are at high risk of vascular events (i.e., cerebrovascular and cardiovascular events), particularly during the first several months after the ischemic event. The use of antiplatelet agents remains the fundamental component of secondary stroke prevention. Based on the available data, antiplatelet agents should be used for patients with noncardioembolic stroke. The use of combination therapy (aspirin plus clopidogrel) has not been proven to be effective or safe to use for prevention of early stroke recurrence or in long-term treatment. There is no convincing evidence that any of the available antiplatelet agents are superior for a given stroke subtype. Currently, the uses of aspirin, clopidogrel, or aspirin combined with extended release dipyridamole are all valid alternatives after an ischemic stroke or transient ischemic attack. However, to maximize the effects of these agents, the treatment should be initiated as early as possible and be continued on a lifelong basis.

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Cited by 589 publications

References 0 publications

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

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

Higher Coated-Platelet Levels are Associated with Stroke Recurrence following Nonlacunar Brain Infarction

Antiplatelet Agents for Stroke Prevention

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