Incidence Of Silent Infarction Research Articles

Abstract TP213: Arcadia CSI (Cognition And Silent Infarcts): Update

Introduction: Cognitive decline and dementia after stroke is a major public healthcare problem, with dementia risk doubling over time, affecting more than 2M people in the US, with no current treatment. Silent brain infarction has been associated with cognitive decline, especially among those at risk for cardio-embolism. The therapeutic challenge is to prevent the occurrence of silent infarction to mitigate proactively the loss of cognitive function. Methods: The NINDS-funded ARCADIA-CSI is an ancillary study to ARCADIA, a randomized trial comparing apixaban vs aspirin to prevent recurrent clinical stroke in patients with cryptogenic stroke and left atrial cardiopathy. The aim of ARCADIA-CSI is to address whether apixaban might also reduce the incidence of silent infarction and be associated with better cognitive function over time compared to aspirin. Five hundred patients will be enrolled at least 90 days after the ARCADIA index stroke and undergo cognitive assessments at baseline and yearly thereafter using a telephone-based cognitive battery. We are testing the hypothesis that the slope of change in cognitive function is less steep during the follow-up period in patients on apixaban compared to patients on aspirin therapy. We will also collect an initial MRI around the time of the qualifying stroke and a follow-up MRI at the time that the subject completes participation in the ARCADIA parent study to assess the occurrence of new silent infarction. Results: As of August 12, 2021, the study has enrolled 188 subjects from 78 ARCADIA sites which have been green-lighted for enrollment in ARCADIA-CSI. A total of 61 sites have enrolled at least one subject. To date, there is a 95% completion of baseline cognitive exams and 98% completion at the 1-yr follow-up. We have obtained 91% of the clinical scans of the index stroke of which 95% have undergone central reading and interpretation. Conclusion: ARCADIA-CSI is designed to identify the most favorable medical approach to prevent the occurrence of silent infarction and cognitive decline in the setting of secondary stroke prevention. An update will be provided regarding the number of patients enrolled, centers green-lighted, and the completion rates of cognitive assessments, and MRIs obtained and interpreted.

Advances in Vascular Cognitive Impairment

Advances in Vascular Cognitive Impairment

Acoustic inhomogeneity of carotid arterial plaques determined by GHz frequency range acoustic microscopy

Characterization of the structure and composition of carotid arterial plaques is important to predict the risk of embolic and thrombotic events. In clinical echography, echolucent lesions seem to be more associated with stroke than echogenic lesions, and a low grey-scale median is associated with a fivefold increase in the incidence of silent infarcts. In the present study, five fixed human carotid atherosclerotic lesions were observed by GHz-range scanning acoustic microscopy (SAM). The atherosclerotic lesions were characterized by either thickened fibrosis with dense collagen fibers or lipid accumulation with sparse collagen network by optical microscopy. SAM revealed that the fibrosis was classified into type I and III collagen by attenuation of ultrasound (US) and that the sound field of lipid accumulation lesions became inhomogeneous. The results would provide the scientific basis for the images of vulnerable plaques being produced in diagnostic US.

Incidence of Silent Stroke in the United States

P134 Background: Recent estimates of stroke incidence in the US range from 715,000–750,000 annually. These estimates, however, do not reflect silent infarcts and hemorrhages. Since population-based studies have found that prevalence of silent stroke is 10–20 times that of symptomatic, estimates of stroke incidence based solely on symptomatic events may substantially underestimate the annual burden of stroke. Silent strokes contribute to vascular dementia, gait impairment, and other major adverse patient outcomes. Methods: Incidence of silent infarcts for different age strata were derived from two US population-based studies of the prevalence of silent infarct-like lesions on MRI, Atherosclerosis Risk In Communities and Cardiovascular Health Study. Prevalence observations in these studies and age-specific death rates from the US Census Bureau were inputted to calculate silent infarct incidence (method of Leske et al). Similarly, incidence rates of silent hemorrhage at differing ages were extrapolated from population-based prevalence observations employing MR GRE imaging in the Austrian Stroke Prevention Study. Age-specific incidence rates were projected onto age cohorts in the 1998 US population to calculate annual burden of silent stroke. Results: Derived incidence rates per 100,000 of silent infarct ranged from 6400 in the age 50–59 strata to 16400 at ages 75–79. Extrapolated incidence rates of silent hemorrhage ranged from 230 in the age 30–39 strata to 7360 at ages > 80. Incidence rates of both subclinical infarcts and hemorrhage increased exponentially with age. Overall estimated annual US occurrence of silent infarct was 9,039,000, and of silent hemorrhage 2,130,000. Conclusion: In 1998, nearly 12 million strokes occurred in the United States, of which ∼750,000 were symptomatic and over 11 million were subclinical. Among the silent strokes, ∼81% were infarcts and ∼19% hemorrhages. These findings demonstrate that the annual burden of stroke is substantially higher than suggested by estimates based solely on clinically manifest events, and suggest that greater research and clinical resources should be allocated to stroke prevention and treatment.

Asymptomatic carotid lesions and silent cerebral infarction.

Few studies have investigated the relationships between asymptomatic carotid lesions and silent infarcts confirmed on magnetic resonance imaging. A consecutive series of 117 subjects (average age, 62 +/- 9.4 years) who were free from neurological deficit but had at least one established risk factor for stroke were investigated by B-mode carotid ultrasonography and magnetic resonance imaging of the brain. Carotid lesions were evaluated by plaque score, maximum percent stenosis, and the existence of ulcerated lesions. The relations between the carotid lesions and the incidence, size, or localization of the brain lesions were investigated. The incidence of silent infarcts was 42% in all subjects and significantly increased with advancing age (P < .05). Most lesions were smaller than 1 cm in diameter and were usually localized in the subcortical white matter or the basal ganglia. The percentage of subjects with infarcts increased significantly as the plaque score increased (P < .05) or when subjects had high-grade stenosis (P < .05) or ulcerated lesions (P < .01). These relationships were also noted in each decade of age. A higher incidence of larger lesions (> 1 cm) was found in the brain hemisphere ipsilateral to the carotid lesion, particularly in subjects with high-grade stenosis or ulcerated lesions (P < .01). Multivariate analysis indicated significant correlations with silent infarcts for age, hypertension, and plaque score. Both the severity and characteristics of asymptomatic carotid lesions estimated by B-mode ultrasonography were closely related to the appearance of silent infarcts. These results demonstrate that noninvasive assessment of carotid lesions can be useful in predicting the existence of silent cerebral infarction even in patients free from neurological deficits.

Silent cerebral infarction as a form of hypertensive target organ damage in the brain.

The incidence, number, size, and location of silent cerebral infarction on 0.1 T magnetic resonance imaging was investigated in 66 hypertensive patients (63 +/- 9 years old; mean +/- SD) and 42 age-matched normotensive subjects (61 +/- 9 years old) to determine the clinical significance of hypertension in silent cerebral infarction. Cerebrovascular risk factors and the severity of hypertensive changes in other major target organs were also investigated. The incidence of silent infarction in hypertensive patients (47%) tended to be higher than that of normotensive subjects (33%) and increased significantly with advancing age. In hypertensive patients, a significantly higher incidence of silent lesions was noted in patients with hypertensive changes in major target organs (72-73% in patients with organ involvement versus 33-39% in those without). The average number of lesions in hypertensive patients was significantly higher than that in normotensive subjects (6.0 versus 2.1), and the lesions in the hypertensive patients were more frequently detected in the brain areas supplied by perforating arteries than those in normotensive subjects (47% versus 24%). These results clearly demonstrate that silent cerebral infarction is frequently seen in older hypertensive patients, especially when moderate hypertensive changes are noted in major target organs, and suggest that hypertensive arterial changes play a crucial role in the occurrence of silent infarction.