Aortic Arch Atheroma Progression and Recurrent Vascular Events in Patients With Stroke or Transient Ischemic Attack

Hinderliter

et al. 2007

Stroke

Self Cite

Background and Purpose-Leukocyte count is an independent predictor of stroke. We investigated the association between leukocyte count and progression of aortic atheroma over 12 months in stroke/transient ischemic attack (TIA) patients. Methods-Consecutive ischemic stroke and transient ischemic attack patients underwent 12-month sequential transesophageal echocardiography and were assessed for total and differential leukocyte counts on admission. Paired aortic plaque images were assessed for several parameters, including changes in grade, intimal-medial thickness (IMT), and cross-sectional area. Multivariate linear and logistic regressions were used to calculate the effect of leukocyte count on the change in aortic atheromas over 12 months. Results-Of the 115 participants (meanϮSD age, 64.6Ϯ11.9 years; 53.1% men; 73.4% white, 24.2% black, and 2.3% Asian), 45 (35%) showed clinically significant progression of aortic atheromas (maximal change in IMT Ͼ0.70 mm over 12 months). The mean admission leukocyte count was higher in the progression group compared with the no-progression group (8.6Ϯ2.2 vs 7.3Ϯ2.2ϫ10 9 /L respectively, Pϭ0.002). Each unit increase in leukocyte count was associated with a 0.26-mm increase in aortic arch IMT over 12 months (Pϭ0.006). After adjustment for other atherosclerosis risk factors, the relation persisted (mean increase in aortic arch IMT per unit increase in leukocyte countϭ0.27 mm, Pϭ0.007). Each unit increase in leukocyte count was associated with an increased risk of significant progression of aortic atheromas (adjusted odds ratioϭ1.33; 95% CI, 1.09 to 1.61). Conclusions-In stroke/transient ischemic attack patients, leukocyte count is independently associated with the progression of aortic atheroma over 12 months (Ͼ0.70 mm), which is associated with cardiovascular risk. (Stroke.

Section: Discussionmentioning

confidence: 99%

“…19 In that prior report, we used the traditional grading system to define significant aortic plaque progression (Ն1 grade over 12 months). Now in this study, using detailed aortic plaque measurements, we were able to define significant progression as an increase in aortic plaque IMT of Ͼ0.70 mm.…”

Section: Discussionmentioning

confidence: 99%

Association of Leukocyte Count With Progression of Aortic Atheroma in Stroke/Transient Ischemic Attack Patients

Hinderliter

et al. 2007

Stroke

Self Cite

“…The risk increases with plaque size [20] and with disease progression [21]. Also, silent ischemic lesions in the cerebral parenchyma and leukoaraiosis are indicators of a higher risk of future symptomatic stroke [22].…”

Section: Patients With Subclinical Arteriosclerosismentioning

confidence: 99%

Patients at High Risk of Cerebrovascular Disease: The REACH Study

et al. 2009

Cerebrovascular disease is one of the leading causes of morbidity and mortality in developed countries. The identification of at-risk individuals is a high priority so that efficacious preventive measures can be implemented. Subjects with the highest risk of cerebrovascular diseases are those who already have had a stroke or a transient ischemic attack, and those with vascular disease in other territories, either in coronary or peripheral arteries. Other subjects at risk are those with cardiac disease, such as atrial fibrillation, those with hypertension, diabetes and smoking habit, as well as individuals with subclinical vascular disease. Although there is considerable evidence for the efficacy of preventive treatment in this population, the percentage of patients receiving optimum treatment is far from ideal. There is a need to implement strategies in the population directed towards increasing awareness of the need to establish healthy habits and adequate preventive pharmacological treatment that could reduce the incidence of this debilitating disease.

“…An atherosclerotic plaque at the aortic arch is frequently observed in patients with ischemic stroke and transient ischemic attack of undetermined etiology, and it is known to be a possible cause of such ischemic events [1,2,3,4,5,6,7]. As a predictor of stroke, transient ischemic attack, and other vascular events, several studies attach great importance to the thickness of the aortic plaque (usually ≥4.0 mm) detected on transesophageal echocardiography (TEE) [3,4,5,6,7], and others pay attention to plaque configurations such as ulcerated change and mobile plaque [1,2,8,9,10,11].…”

Section: Introductionmentioning

confidence: 99%

“…As a predictor of stroke, transient ischemic attack, and other vascular events, several studies attach great importance to the thickness of the aortic plaque (usually ≥4.0 mm) detected on transesophageal echocardiography (TEE) [3,4,5,6,7], and others pay attention to plaque configurations such as ulcerated change and mobile plaque [1,2,8,9,10,11]. In our prospective study involving 283 stroke patients, the presence of an aortic plaque that was both ≥4.0 mm thick and extending to at least one branch of the aortic arch was an independent predictor of stroke recurrence after adjusting for age and hypertension, though plaque ≥4.0 mm thick or extending to any branch was not an independent predictor [6].…”

Section: Introductionmentioning

confidence: 99%

Atheromatous Plaques at the Origin of the Left Subclavian Artery in Patients with Ischemic Stroke

et al. 2010

Background: Atheromatous plaques of the aortic arch that extend to the origin of its branches may cause stroke. The frequency and clinical implications of plaque at the origin of the left subclavian artery (LSCA) in patients with recent ischemic stroke were investigated. Methods: We studied 347 consecutive patients (223 men, 69 ± 12 years) who developed symptomatic ischemic stroke and underwent transesophageal echocardiography (TEE). Results: The origin of the LSCA was identified in 303 of 347 patients (87.3%). Plaque ≧1.0 mm was detected in 108 of the 303 patients (35.6%), ranging between 1.0 and 6.1 mm (median, 2.5 mm). Patients having thicker plaque (≧2.5 mm) were older (p = 0.012) and more commonly took antiplatelets prior to stroke (p = 0.038) than patients with no plaque and those with thinner plaque (<2.5 mm). Of the aortic arch findings detected on TEE, maximum intima-media thickness (IMT) was the highest (p < 0.001) in patients with thicker plaque, and large plaque (≧4.0 mm) (p = 0.017), ulcerative plaques (p < 0.001), and spontaneous echo contrasts (p = 0.001) were identified most commonly in patients with thicker plaque. The frequency of infarcts involving the posterior circulation was similar among the three groups. After multivariate adjustment, maximum IMT of the aortic arch was independently related to thicker plaque at the LSCA origin (OR = 1.24, 95% CI = 1.03–1.51, p = 0.024, per 1-mm increase). Conclusions: Atheromatous plaque at the origin of the LSCA was present in approximately one third of patients with a recent ischemic stroke. High IMT at the aortic arch was independently related to the presence of thick plaque at the LSCA origin. The present study does not support the concept that plaque at the LSCA origin may be associated with posterior circulation infarction.