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Han, Moon-Ku, Dong-Wha Kang, Byung-Woo Yoon, and Jae-Kyu Roh. "Vascular Territorial Classification and Etiologies of Acute MCA Infarct by Diffusion-Weighted MRI." Stroke 32, suppl_1 (January 2001): 346. http://dx.doi.org/10.1161/str.32.suppl_1.346-d.
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P42 Background and Purpose - The purpose of this study is to classify infarct subtypes of middle cerebral artery distribution (MCA) seen on diffusion-weighted MRI (DWI) and investigate infarct mechanisms and etiologies of MCA infarct subtypes. Method - We analysed 187 consecutive patients with acute MCA infarct who were studied by DWI/MRA within the first 4 days of stroke onset between 1997 and 1999, and stroke mechanism was determinedaccording to the criteria of the Trial of Org 10172 in Acute Stroke Treatment (TOAST). Infarct patterns from 128 patients except for lacunar infarcts (patients) were classified by the two types of multiple infarcts and large single infarcts: 2 types of multipleinfarcts; subcortical/cortical and cortical/cortical infarcts, 3 types of large single infarcts; subcortical, cortical and large infarcts including cortical and subcortical lesions Results -TOAST diagnostic subtypes were 78 large vessel strokes, 22 cardioembolic strokes, 59 lacune strokes, 4 other strokes, and 26strokes of unknown cause. We identified multiple infarcts (MI) in 41 patients: subcortical/cortical, 29 including 14 MCA disease (p=0.03); cortical/cortical, 7 including 6 ICA disease (p=0.005), and 87 large single infarcts (SI): subcortical, 32 including 13 MCA disease (p=0.02); cortical, 5 including 3 cardioembolism (p=0.03); large infarcts (cortical/subcortical), 50. There was no difference of etiologies among large infarcts (cortical/subcortical) in SI. Conclusion -MCA disease is the most important cause of subcortical and cortical multiple infarcts, and subcortical single infarcts. ICA disease is most frequent cause of cortical multiple infarcts and cardioembolism is more common cause in cortical single infarcts. We conclude that our classificationof MCA Infarct patterns using early DWI in acute ischemic stroke is useful to identify the causes of stroke according to subtypes and to consider the clinical decisions of etiologic investigations and to decide the early treatment modality in acute ischemic stroke.
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Kumar, Abhay, Robert Brown, Rajat Dhar, Tomoko Sampson, Colin P. Derdeyn, Christopher J. Moran, and Michael N. Diringer. "Early vs Delayed Cerebral Infarction After Aneurysm Repair After Subarachnoid Hemorrhage." Neurosurgery 73, no. 4 (June 19, 2013): 617–23. http://dx.doi.org/10.1227/neu.0000000000000057.
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Abstract BACKGROUND: Cerebral infarction is a major contributor to poor outcome after subarachnoid hemorrhage (SAH). Although usually considered a complication of delayed cerebral ischemia, infarcts may also occur early, in relation to initial brain injury or aneurysm-securing procedures. OBJECTIVE: We analyzed the relative frequency and volume of early vs delayed infarcts after SAH and their relationship to hospital outcome. METHODS: Retrospective review of consecutive patients admitted with aneurysmal SAH over 4 years who had follow-up brain imaging 7 days or later after admission. Imaging 24 to 48-hours after aneurysm-securing procedures was reviewed to classify infarcts seen on final imaging as early or delayed. Infarct volumes were measured by perimeter tracing and infarct burden calculated for each patient. RESULTS: Of 250 eligible patients, 205 had follow-up imaging; infarcts were present in 61 patients. Of these, 29 had early infarcts, 16 had delayed infarcts, and 5 had both early and delayed infarcts. Eleven patients with infarcts did not undergo postprocedure computed tomography; these were presumptively classified as having late infarcts. Early and delayed infarcts contributed equally to infarct burden. Early infarcts were associated with aneurysm clipping (odds ratio: 4.2, 95% confidence interval: 1.8-9.5 compared with coiling), whereas delayed infarcts were almost always seen in association with angiographic vasospasm (odds ratio: 3.3, 95% confidence interval: 1.5-7.3). Patients with early as well as late infarcts, especially those with infarct burden more than 30 cm3 had worse hospital discharge disposition. CONCLUSION: Early infarction occurs frequently after SAH and contributes as much as delayed cerebral ischemia to infarct burden and hospital outcome. Efforts to better understand and modify contributors to early infarction appear warranted.
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Skriver, E. B., and T. S. Olsen. "Repeated Computed Tomography in Lacunar Infarcts of the Brain." Acta Radiologica 30, no. 1 (January 1989): 1–6. http://dx.doi.org/10.1177/028418518903000101.
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This prospective and consecutive study of 74 patients with completed stroke elucidates occurrence, localization and evolution of lacunar infarcts on repeated CT examinations. Twenty patients had large infarcts (diameter >3 cm), 25 medium-sized infarcts (diameter ≥1.5 cm – ≤ 3 cm), and 16 had lacunar infarcts (diameter <1.5 cm). In 13 patients no infarct was seen. The lacunar infarcts were characterized by delayed appearance on CT, low incidence of fog effect, and infrequent presence of contrast enhancement. In 9 of the 16 patients (56%) the lacunar infarct could be identified on the first CT, performed approximately 3 days after the stroke. In 2 patients the infarct was first revealed on the second (2 weeks post stroke) and in 5 on the third CT (6 months post stroke). The delayed appearance might be due to a partial volume effect. Early development of fog effect may also be considered. As contrast enhancement was observed in only 8 per cent of the patients with lacunar infarcts on CT, and in 70 per cent of the entire group of patients in our series with ischemic infarcts, contrast enhancement seemed to be a function of lesion size.
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Pfeffer, J. M., M. A. Pfeffer, P. J. Fletcher, and E. Braunwald. "Progressive ventricular remodeling in rat with myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 5 (May 1, 1991): H1406—H1414. http://dx.doi.org/10.1152/ajpheart.1991.260.5.h1406.
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Ventricular dilatation may have important prognostic implications for the survival of patients with left ventricular (LV) dysfunction. To determine the manner and extent to which the left ventricle of the rat remodels and dilates after myocardial infarction, we obtained the passive pressure-volume relationships, chamber stiffness constants, and mass during both the early and late phases. In moderate and large infarcts as inflammation and edema developed, LV weight increased then progressively decreased as a thin scar formed, returning to normal values as a result of compensatory hypertrophy of the residual myocardium. LV dilatation occurred in all rats with infarcts but to different extents depending on infarct size and duration. In the early postinfarction phase, pressure-volume relationship was relatively unchanged in all infarct-size groups, except for significant rightward shift in low pressure range for rats with moderate and large infarcts and significant leftward shift in high pressure range for rats with small infarcts. During resolution of the inflammatory response, LV dilatation occurred in all infarct groups in relation to infarct size. As scar formation became complete, LV enlargement did not progress in rats with small infarcts but did so in rats with moderate and large infarcts. LV chamber stiffness remained within the range of normal values during the early phase in all rats with infarcts but decreased significantly during the late phase in rats with moderate and large infarcts in association with the extent of ventricular enlargement. Alterations in the volume-to-mass ratio (V/Vwt) were most marked in the late postinfarction phase, wherein both volume (increased) and mass (decreased, then increased) changed dramatically and V/Vwt progressively increased in rats with large infarcts.
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Nudo, R. J., and G. W. Milliken. "Reorganization of movement representations in primary motor cortex following focal ischemic infarcts in adult squirrel monkeys." Journal of Neurophysiology 75, no. 5 (May 1, 1996): 2144–49. http://dx.doi.org/10.1152/jn.1996.75.5.2144.
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1. Intracortical microstimulation (ICMS) techniques were used to derive detailed maps of distal forelimb movement representations in primary motor cortex (area 4) of adult squirrel monkeys before and a few months after a focal ischemic infarct. 2. Infarcts caused a marked but transient deficit in use of the contralateral hand, as evidenced by increased use of the ipsilateral hand, and reduced performance on a task requiring skilled digit use. 3. Infarcts resulted in a widespread reduction in the areal extent of digit representations adjacent to the lesion, and apparent increases in adjacent proximal representations. 4. We conclude that substantial functional reorganization occurs in primary motor cortex of adult primates following a focal ischemic infarct, but at least in the absence of postinfarct training, the movements formerly represented in the infarcted zone do not reappear in adjacent cortical regions.
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Fomovsky, Gregory M., and Jeffrey W. Holmes. "Evolution of scar structure, mechanics, and ventricular function after myocardial infarction in the rat." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (January 2010): H221—H228. http://dx.doi.org/10.1152/ajpheart.00495.2009.
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The mechanical properties of the healing scar are an important determinant of heart function following myocardial infarction. Yet the relationship between scar structure, scar mechanics, and ventricular function remains poorly understood, in part because no published study has tracked all of these factors simultaneously in any animal model. We therefore studied the temporal evolution of scar structure, scar mechanics, and left ventricular (LV) function in large anterior myocardial infarcts in rats. At 1, 2, 3, and 6 wk after left anterior descending coronary ligation, we examined LV function using sonomicrometry, infarct mechanical properties using biaxial mechanical testing, infarct structure using polarized light microscopy, and scar collagen content and cross-linking using biochemical assays. Healing infarcts in the rat were structurally and mechanically isotropic at all time points. Collagen content increased with time and was the primary determinant of scar mechanical properties. The presence of healing infarcts influenced systolic LV function through a rightward shift of the end-systolic pressure-volume relationship (ESPVR) that depended on infarct size, infarct collagen content, and LV dilation. We conclude that in sharp contrast to previous reports in large animal models, healing infarcts are structurally and mechanically isotropic in the standard rat model of myocardial infarction. On the basis of the regional strain patterns we observed in healing rat infarcts in this study and in healing pig infarcts in previous studies, we hypothesize that the local pattern of stretching determines collagen alignment in healing myocardial infarct scars.
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Mishra, Ajay Kumar, Vanjare Harshad Arvind, Divya Muliyil, Cijoy K. Kuriakose, Anu Anna George, Reka Karuppusami, Ronald Albert Benton Carey, Sunithi Mani, and Samuel George Hansdak. "Cerebrovascular injury in cryptococcal meningitis." International Journal of Stroke 13, no. 1 (April 19, 2017): 57–65. http://dx.doi.org/10.1177/1747493017706240.
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Background Cryptococcal meningitis continues to be one of the common causes of chronic central nervous system infection worldwide. Individuals with cryptococcal meningitis can occasionally present with small vessel vasculitis causing infarcts primarily in the basal ganglia, internal capsule, and thalamus. Literature regarding patterns of cerebrovascular injury among patients with cryptococcal meningitis is scanty, and outcome following these vascular involvements is unknown. Aim To study the clinical profile, imaging findings, and details of vascular territory involved among patients admitted with cryptococcal meningitis and central nervous system infarct in a tertiary care center from India. And to compare the outcomes of patients of cryptococcal meningitis with or without central nervous system infarcts in terms of mortality and morbidity, Methodology A total of 151 patients with microbiologically proven cryptococcal meningitis over a time span of 11 years were retrospectively enrolled into the study. Of these, 66 patients met the inclusion criteria of having appropriate imaging of the brain. The presence of infarct in the imaging was analyzed by two independent radiologists. Patterns of central nervous system involvement and types of vascular injury were ascertained based on radiological parameters. Clinical parameters and outcomes of patients with and without infarcts were compared. Results Twenty (13%) of these patients had evidence of central nervous system infarcts on imaging. The mean age of patients with and without infarcts was 41 years and 38 years, respectively. Male predominance was present among both the groups. The presence of fever, neck stiffness, positive blood culture, and hydrocephalus in central nervous system imaging was similar among patients with or without infarct. Longer duration of illness, low sensorium at the time of presentation, low Glasgow Coma Scale score, presence of meningeal inflammation, cryptococcomas, and basal exudates in imaging were higher in patients with infarct. All the infarcts were of the lacunar type. Sixty percent of the cerebrovascular infarcts were acute in nature, 50% of these being multiple. Unilateral infarcts were seen in 70% of the patients. The most common site of infarct was the basal ganglia, others being distributed over the thalamus, frontal, temporal, parieto-occipital regions in the descending order. The presence of neurovascular involvement in the form of infarcts to the risk of morbidity and mortality had an odds ratio of 9.1 and 2.6, respectively. Conclusion Neurovascular involvement in chronic cryptococcal meningitis is a rare entity. These tend to present as multiple lacunar infarcts. Mortality and morbidity associated with these patients is higher when compared to patients who do not have infarcts. This result suggests that vascular injury plays a role in predicting outcome of patients with cryptococcal meningitis. Future studies are needed to understand the mechanism by which vascular events (infarcts) occur and result in poor outcome.
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Ospel, Johanna M., Petra Cimflova, Martha Marko, Arnuv Mayank, Moiz Hafeez, Mohammed A. Almekhlafi, Michael D. Hill, Andrew M. Demchuk, Bijoy K. Menon, and Mayank Goyal. "Prevalence and Outcomes of Medium Vessel Occlusions With Discrepant Infarct Patterns." Stroke 51, no. 9 (September 2020): 2817–24. http://dx.doi.org/10.1161/strokeaha.120.030041.
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Background and Purpose: The prognosis of medium vessel occlusions (MeVOs), that is, M2/3 middle cerebral artery, A2/3 anterior cerebral artery, and P2/3 posterior cerebral artery occlusions, is generally better compared with large vessel occlusions, since brain ischemia is less extensive. However, in some MeVO patients, infarcts are seen outside the territory of the occluded vessel (MeVO with discrepant infarcts). This study aims to determine the prevalence and clinical impact of discrepant infarct patterns in acute ischemic stroke due to MeVO. Methods: We pooled data of MeVO patients from INTERRSeCT (Identifying New Approaches to Optimize Thrombus Characterization for Predicting Early Recanalization and Reperfusion With IV Alteplase and Other Treatments Using Serial CT Angiography) and PRove-IT (Precise and Rapid Assessment of Collaterals Using Multi-Phase CTA in the Triage of Patients With Acute Ischemic Stroke for IA Therapy)—2 prospective cohort studies of patients with acute ischemic stroke. The combination of occlusion location on baseline computed tomography angiography and infarct location on follow-up computed tomography/magnetic resonance imaging was used to identify MeVOs with discrepant infarct patterns. Two definitions for discrepant infarcts were applied; one was more restrictive and purely based on infarct patterns of the basal ganglia, whereas the second one took cortical infarct patterns into account. Clinical outcomes of patients with versus without discrepant infarcts were summarized using descriptive statistics. Logistic regression was performed to obtain adjusted effect size estimates for the association of discrepant infarcts and good outcome, defined as a modified Rankin Scale score of 0 to 2, and excellent outcome (modified Rankin Scale score 0–1). Results: Two hundred sixty-two patients with MeVO were included in the analysis. The prevalence of discrepant infarcts was 39.7% (definition 1) and 21.0% (definition 2). Patients with discrepant infarcts were less likely to achieve good outcome (definition 1: adjusted odds ratio, 0.48 [95% CI, 0.25–0.91]; definition 2: adjusted odds ratio, 0.47 [95% CI, 0.22–0.99]). When definition 1 was applied, patients with discrepant infarcts were also less likely to achieve excellent outcome (definition 1: adjusted odds ratio, 0.55 [95% CI, 0.31–0.99]; definition 2: adjusted odds ratio, 0.62 [95% CI, 0.31–1.25]). Conclusions: MeVO patients with discrepant infarcts are common, and they are associated with more severe deficits and poor outcomes.
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Cauley, Keith A., Gino J. Mongelluzzo, and Samuel W. Fielden. "Automated Estimation of Acute Infarct Volume from Noncontrast Head CT Using Image Intensity Inhomogeneity Correction." International Journal of Biomedical Imaging 2019 (August 21, 2019): 1–8. http://dx.doi.org/10.1155/2019/1720270.
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Identification of early ischemic changes (EIC) on noncontrast head CT scans performed within the first few hours of stroke onset may have important implications for subsequent treatment, though early stroke is poorly delimited on these studies. Lack of sharp lesion boundary delineation in early infarcts precludes manual volume measures, as well as measures using edge-detection or region-filling algorithms. We wished to test a hypothesis that image intensity inhomogeneity correction may provide a sensitive method for identifying the subtle regional hypodensity which is characteristic of early ischemic infarcts. A digital image analysis algorithm was developed using image intensity inhomogeneity correction (IIC) and intensity thresholding. Two different IIC algorithms (FSL and ITK) were compared. The method was evaluated using simulated infarcts and clinical cases. For synthetic infarcts, measured infarct volumes demonstrated strong correlation to the true lesion volume (for 20% decreased density “infarcts,” Pearson r = 0.998 for both algorithms); both algorithms demonstrated improved accuracy with increasing lesion size and decreasing lesion density. In clinical cases (41 acute infarcts in 30 patients), calculated infarct volumes using FSL IIC correlated with the ASPECTS scores (Pearson r = 0.680) and the admission NIHSS (Pearson r = 0.544). Calculated infarct volumes were highly correlated with the clinical decision to treat with IV-tPA. Image intensity inhomogeneity correction, when applied to noncontrast head CT, provides a tool for image analysis to aid in detection of EIC, as well as to evaluate and guide improvements in scan quality for optimal detection of EIC.
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Ganesh, A., JM Ospel, AT Wilson, M. Goyal, M. Tymianski, and MD Hill. "P.083 Early and 30-day clinical and neuropsychological effects of iatrogenic brain infarcts in the ENACT randomized-controlled trial." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (November 2021): S43. http://dx.doi.org/10.1017/cjn.2021.362.
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Background: Small brain infarcts are often seen on diffusion-weighted MRI(DWI) following surgical/endovascular procedures. Little is known about their clinical effects. We examined the association of iatrogenic infarcts with outcomes in the ENACT(Evaluating Neuroprotection in Aneurysm Coiling Therapy) trial of nerinetide in endovascular aneurysm repair. Methods: In this post-hoc analysis, we used multi-variable models to evaluate the association of presence/number of DWI iatrogenic infarcts with NIHSS(National Institutes of Health Stroke Scale), mRS(modified Rankin Scale), and cognitive/neuropsychological scores(30-minute battery) at 1-4 and 30-days post-procedure. We also related infarct number to a Z-score-derived composite outcome score(quantile regression). Results: Among 185 patients(median age:56,IQR:50-64), 124(67.0%) had iatrogenic infarcts(median:4,IQR:2-10.5). Nerinetide resulted in fewer infarcts. Patients with infarcts had lower Mini-Mental State Exam(MMSE) scores at 2-4 days(median:28 vs 29, adjusted-coefficient[acoef] per additional infarct:-1.11,95%CI:-1.88 to -0.34,p=0.005). Infarct number was associated with worse day-1 NIHSS(aOR for NIHSS≥1:1.07,1.02-1.12,p=0.009), day 2-4 mRS(adjusted common odds-ratio[aOR]:1.05,1.01-1.09,p=0.005) and MMSE(acoef:-0.07,-0.13 to -0.003,p=0.040), 30-day mRS(aOR:1.04,1.01-1.07,p=0.016) and Hopkins Verbal Learning Test scores(acoef:-0.21,-0.39 to -0.03,p=0.020), as well as worse composite scores at 1-4 and 30-days(acoef:-0.09,-0.15 to -0.03,p=0.006). Conclusions: Iatrogenic infarcts were associated with subtle differences in post-procedural(1-4 days) and 30-day outcomes in this middle-aged cohort. Future studies should use batteries of similar/greater granularity to validate optimal measures for short- versus long-term manifestations.
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Garcia-Dorado, D., P. Theroux, M. Desco, J. Solares, J. Elizaga, F. Fernandez-Aviles, J. Alonso, and J. Soriano. "Cell-to-cell interaction: a mechanism to explain wave-front progression of myocardial necrosis." American Journal of Physiology-Heart and Circulatory Physiology 256, no. 5 (May 1, 1989): H1266—H1273. http://dx.doi.org/10.1152/ajpheart.1989.256.5.h1266.
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Histological sections performed 24 h after coronary occlusion in eight pigs displayed compact infarcts extending transmurally with well-defined edges; reconstruction and inspection of the area of necrosis showed a geometric distribution of the infarcts with very irregular, interdigitating edges always in continuity with the main mass of necrosis. Reperfusion in 32 pigs after periods of coronary occlusion of 90, 60, 45, and 30 min exponentially reduced infarct size and transmural extension of the infarct but did not modify its geometry. The two-dimensional size, progression, and geometry of the infarcts could be reproduced by a computer model. In the simulated infarcts, each myocardial cell within the area at risk was represented by a pixel. The algorithm included an inner loop, which determined at random at each iteration a status of reversible or irreversible damage to all pixels. The number of iterations could reproduce infarct of various sizes. With the addition of an index of transmural sensitivity to ischemia, progression of the infarct area could also be reproduced. The only possible means of reproducing the geometry of the infarct was to enter into the program a contiguity condition requiring a direct contact between irreversibly damaged pixels. These observations suggest that the physical interaction between cells is an important determinant of progression of necrosis during coronary occlusion.
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Yaghi, Shadi, Traci M. Bartz, Richard Kronmal, Hooman Kamel, John Gottdiener, W. T. Longstreth, and Mitchell S. V. Elkind. "Left atrial diameter and vascular brain injury on MRI." Neurology 91, no. 13 (August 29, 2018): e1237-e1244. http://dx.doi.org/10.1212/wnl.0000000000006228.
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ObjectiveTo determine the association left atrial diameter (LAD) and vascular brain injury on brain MRI.MethodsWe analyzed data from the Cardiovascular Health Study (CHS), a prospective cohort of community-dwelling adults ≥65 years old. LAD was measured from 2-dimensional transthoracic echocardiograms. Among CHS participants who underwent brain MRI, we examined associations of LAD with brain infarcts and leukoaraiosis. Primary outcomes (number for analysis) were prevalent infarcts (2,327) and degree of leukoaraiosis on initial MRI (2,315). Secondary outcomes were prevalent nonlacunar infarcts (2,327), incident infarcts (939), incident nonlacunar infarcts (1,185), and degree of leukoaraiosis on follow-up MRI adjusted for initial MRI (1,158). Relative risk (RR) and linear regression models were adjusted for demographics, vascular risk factors, and potential confounders.ResultsMean age of the 2,335 participants with initial brain MRI was 72.0 ± 4.8 years; 38.7% were men; and 29.0% participants had prevalent infarcts. In multivariable, fully adjusted models, LAD was associated with prevalent infarcts (RR 1.20, 95% confidence interval [CI] 1.08–1.34) and prevalent nonlacunar infarcts (RR 1.28, 95% CI 1.06–1.54) but not with leukoaraiosis (−0.08, 95% CI −0.17 to 0.07), incident infarcts (RR 1.00, 95% CI 0.78–1.29), nonlacunar infarcts (RR 0.98, 95% CI 0.67–1.42), or worsening leukoaraiosis (−0.04, 95% CI −0.10 to 0.02).ConclusionLAD is independently associated with prevalent brain infarcts, particularly nonlacunar infarcts, but not leukoaraiosis. Larger studies are needed to determine associations with incident infarct risk and whether this risk in patients with left atrial enlargement can be reduced with anticoagulant agents.
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Fandler, Simon, Thomas Gattringer, Daniela Pinter, Lukas Pirpamer, Florian Borsodi, Sebastian Eppinger, Kurt Niederkorn, Christian Enzinger, and Franz Fazekas. "Dysphagia in supratentorial recent small subcortical infarcts results from bilateral pyramidal tract damage." International Journal of Stroke 13, no. 8 (May 18, 2018): 815–19. http://dx.doi.org/10.1177/1747493018778141.
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Background Dysphagia occurs in up to 20% of patients with a recent small subcortical infarct, even when excluding brainstem infarcts. Aim To examine the impact of lesion topography and concomitant cerebrovascular lesions on the occurrence of dysphagia in patients with a single supratentorial recent small subcortical infarct. Methods We retrospectively identified all inpatients with magnetic resonance imaging-confirmed supratentorial recent small subcortical infarcts over a five-year period. Dysphagia was determined by speech-language therapists. Recent small subcortical infarcts were compiled into a standard brain model and compared using lesion probability maps. Furthermore, magnetic resonance imaging scans were reviewed for the combination of both acute and old cerebrovascular lesions. Results A total of 243 patients with a recent small subcortical infarct were identified (mean age 67.9 ± 12.2 years). Of those, 29 had mild and 18 moderate-to-severe dysphagia. Lesion probability maps suggested no recent small subcortical infarct location favoring the occurrence of moderate-to-severe dysphagia. However, patients with moderate-to-severe dysphagia more frequently showed combined damage to both pyramidal tracts by the recent small subcortical infarct and a contralateral old lesion (lacune: 77.8% vs. 19.9%, p < 0.001; lacune or confluent white matter hyperintensities: 100% vs. 57.7%, p < 0.001) than patients without swallowing dysfunction. Comparable results were obtained when analyzing patients with any degree of dysphagia. Conclusions Preexisting contralateral vascular pyramidal tract lesions are closely related to the occurrence of moderate-to-severe dysphagia in patients with supratentorial recent small subcortical infarcts.
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Garg, Anil, and Deepak Agrawal. "Acute arterial infarcts in patients with severe head injuries." Indian Journal of Neurosurgery 01, no. 02 (July 2012): 126–29. http://dx.doi.org/10.4103/2277-9167.102276.
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Abstract To study the incidence, demographic profile, and outcome of patients with severe closed head injuries who develop acute arterial infarcts. Patients with severe head injury (Glasgow coma score (GCS) ≤8) presenting within 8 h of injury in the Department of Neurosurgery over a period of 5 months were enrolled in the study. Patients with penetrating head injury, infarct due to herniation and iatrogenic arterial injuries were excluded from the study. Only arterial infarcts developing within 8 h of injury were included in the study. A computed tomography (CT) head was done on all patients within 8 h of injury and repeated if necessary. Arterial infarct was defined as well-demarcated wedge-shaped hypodensity corresponding to an arterial territory on plain CT of the head. Outcome was assessed using Glasgow outcome score (GOS) at 1 month post-injury or at death (whichever came earlier). Forty-four patients of severe head injury were included in the study during the above period. Of these, four patients (9.1%) had arterial infarcts on the initial CT scan. The male:female ratio was 1:3. The mean age was 54 years (range 3–85 years). Two patients had infarcts in the middle cerebral artery distribution and two in the superior cerebellar artery distribution. Poor outcome (GOS 1–3) was seen in 100% of the patients with arterial infarct compared to 52.5% (n=21) in patients with severe head injury without arterial infarct. A significant percentage of patients with severe head injury have arterial infarcts on admission, which may imply arterial injury. Our study shows that these patients have a poorer prognosis vis-à-vis patient without these findings
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Casolla, Barbara, Gregory Kuchcinski, Maéva Kyheng, Riyad Hanafi, Jean-Paul Lejeune, Didier Leys, Charlotte Cordonnier, and Hilde Hénon. "Infarct Volume Before Hemicraniectomy in Large Middle Cerebral Artery Infarcts Poorly Predicts Catastrophic Outcome." Stroke 51, no. 8 (August 2020): 2404–10. http://dx.doi.org/10.1161/strokeaha.120.029920.
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Background and Purpose: Infarct volumes predict malignant infarcts in patients undergoing decompressive hemicraniectomy (DH) for large middle cerebral artery territory infarcts. The aim of the study was to determine the optimal magnetic resonance imaging infarct volume threshold that predicts a catastrophic outcome at 1 year (modified Rankin Scale score of 5 or death). Methods: We included consecutive patients who underwent DH for large middle cerebral artery infarcts. We analyzed infarct volumes before DH with semi-automated methods on b1000 diffusion-weighted imaging sequences and apparent diffusion coefficient maps. We studied infarct volume thresholds for prediction of catastrophic outcomes, and analyzed sensitivity, specificity, and the area under the curve, a value ≥0.70 indicating an acceptable prediction. Results: Of 173 patients (109 men, 63%; median age 53 years), 42 (24.3%) had catastrophic outcomes. Magnetic resonance imaging b1000 diffusion-weighted imaging and apparent diffusion coefficient infarct volumes were associated to the occurrence of 1-year catastrophic outcome (adjusted odds ratio, 9.17 [95% CI, 2.00–42.04] and odds ratio, 4.18 [95% CI, 1.33–13.19], respectively, per 1 log increase). The optimal volume cutoff of were 211 mL on b1000 diffusion-weighted imaging and 181 mL on apparent diffusion coefficient maps. The 2 methods showed similar sensitivities and specificities and overlapping area under the curve of 0.64 (95% CI, 0.54–0.74). Conclusions: In patients with large middle cerebral artery infarcts, optimal magnetic resonance imaging infarct volume thresholds showed poor accuracy and low specificity to predict 1-year catastrophic outcome, with different b1000 diffusion-weighted imaging and apparent diffusion coefficient thresholds. In the setting of DH, optimal infarct volumes alone should not be used to deny DH, irrespectively of the method used.
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Brown, Robert J., Abhay Kumar, Rajat Dhar, Tomoko R. Sampson, and Michael N. Diringer. "The Relationship Between Delayed Infarcts and Angiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage." Neurosurgery 72, no. 5 (January 10, 2013): 702–8. http://dx.doi.org/10.1227/neu.0b013e318285c3db.
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Abstract BACKGROUND: Delayed cerebral ischemia is common after aneurysmal subarachnoid hemorrhage (aSAH) and is a major contributor to poor outcome. Yet, although generally attributed to arterial vasospasm, neurological deterioration may also occur in the absence of vasospasm. OBJECTIVE: To determine the relationship between delayed infarction and angiographic vasospasm and compare the characteristics of infarcts related to vasospasm vs those unrelated. METHODS: A retrospective review of patients with aSAH admitted from July 2007 through June 2011. Patients were included if they were admitted within 48 hours of SAH, had a computed tomography scan both 24 to 48 hours following aneurysm treatment and ≥7 days after SAH, and had a catheter angiogram to evaluate for vasospasm. Delayed infarcts seen on late computed tomography but not postprocedurally were attributed to vasospasm if there was moderate or severe vasospasm in the corresponding vascular territory on angiography. Infarct volume was measured by perimeter tracing. RESULTS: Of 276 aSAH survivors, 134 had all imaging requisite for inclusion. Fifty-four (34%) had moderate or severe vasospasm, of whom 17 (31%) had delayed infarcts, compared with only 3 (4%) of 80 patients without vasospasm (P < .001). There were a total of 29 delayed infarcts in these 20 patients; 21 were in a territory with angiographic vasospasm, but 8 (28%) were not. Infarct volume did not differ between vasospasm-related (18 ± 25 mL) and vasospasm-unrelated (11 ± 12 mL) infarcts (P = .54), but infarcts in the absence of vasospasm were more likely watershed (50% vs 10%, P = .03). CONCLUSION: Delayed infarcts following aSAH can occur in territories without angiographic vasospasm and are more likely watershed in distribution.
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Sigurdsson, Sigurdur, Thor Aspelund, Olafur Kjartansson, Elias Gudmundsson, Palmi V. Jonsson, Mark A. van Buchem, Vilmundur Gudnason, and Lenore J. Launer. "Cerebrovascular Risk-Factors of Prevalent and Incident Brain Infarcts in the General Population: The AGES-Reykjavik Study." Stroke 53, no. 4 (April 2022): 1199–206. http://dx.doi.org/10.1161/strokeaha.121.034130.
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Background: Studies on the association of cerebrovascular risk factors to magnetic resonance imaging detected brain infarcts have been inconsistent, partly reflecting limits of assessment to infarcts anywhere in the brain, as opposed to specific brain regions. We hypothesized that risk-factors may differ depending on where the infarct is located in subcortical-, cortical-, and cerebellar regions. Methods: Participants (n=2662, mean age 74.6±4.8) from the longitudinal population-based AGES (Age, Gene/Environment Susceptibility)-Reykjavik Study underwent brain magnetic resonance imaging at baseline and on average 5.2 years later. We assessed the number and location of brain infarcts (prevalent versus incident). We estimated the risk-ratios of prevalent (PRR) and incident (IRR) infarcts by baseline cerebrovascular risk-factors using Poisson regression. Results: Thirty-one percent of the study participants had prevalent brain infarcts and 21% developed new infarcts over 5 years. Prevalent subcortical infarcts were associated with hypertension (PRR, 2.7 [95% CI, 1.1–6.8]), systolic blood pressure (PRR, 1.2 [95% CI, 1.1–1.4]), and diabetes (PRR, 2.8 [95% CI, 1.9–4.1]); incident subcortical infarcts were associated with systolic (IRR, 1.2 [95% CI, 1.0–1.4]) and diastolic (IRR, 1.3 [95% CI, 1.0–1.6]) blood pressure. Prevalent and incident cortical infarcts were associated with carotid plaques (PRR, 1.8 [95% CI, 1.3–2.5] and IRR, 1.9 [95% CI, 1.3–2.9], respectively), and atrial fibrillation was significantly associated with prevalent cortical infarcts (PRR, 1.8 [95% CI, 1.2–2.7]). Risk-factors for prevalent cerebellar infarcts included hypertension (PRR, 2.45 [95% CI, 1.5–4.0]), carotid plaques (PRR, 1.45 [95% CI, 1.2–1.8]), and migraine with aura (PRR, 1.6 [95% CI, 1.1–2.2]). Incident cerebellar infarcts were only associated with any migraine (IRR, 1.4 [95% CI, 1.0–2.0]). Conclusions: The risk for subcortical infarcts tends to increase with small vessel disease risk-factors such as hypertension and diabetes. Risk for cortical infarcts tends to increase with atherosclerotic/coronary processes and risk for cerebellar infarcts with a more mixed profile of factors. Assessment of risk-factors by location of asymptomatic infarcts found on magnetic resonance imaging may improve the ability to target and optimize preventive therapeutic approaches to prevent stroke.
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Rao, Vaishnavi L., Michael Mlynash, Søren Christensen, Amarnath Yennu, Stephanie Kemp, Greg Zaharchuk, Jeremy J. Heit, Michael P. Marks, Maarten G. Lansberg, and Gregory W. Albers. "Collateral status contributes to differences between observed and predicted 24-h infarct volumes in DEFUSE 3." Journal of Cerebral Blood Flow & Metabolism 40, no. 10 (May 19, 2020): 1966–74. http://dx.doi.org/10.1177/0271678x20918816.
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We previously demonstrated that in the DEFUSE 3 trial, the union of the baseline core and the 24-h Tmax > 6 s perfusion lesion predicts the infarct volume at 24 h. Presently, we assessed if collateral robustness measured by the hypoperfusion intensity ratio (HIR) and cerebral blood volume (CBV) index accounts for the variance in these predictions. DEFUSE 3 patients underwent MRI/CT perfusion imaging at baseline and 24 h post-randomization. We compared baseline and follow-up HIR and CBV index across subgroups stratified by differences between predicted and observed 24-h infarct volumes. Of 123 eligible patients, 34 with 24-h infarcts larger than predicted had less favorable collaterals at baseline (HIR 0.43 vs. 0.32, p = 0.006; CBV Index 0.78 vs. 0.85, p = 0.001) and 24 h (HIR 0.56 vs. 0.07, p = 0.004; CBV Index 0.47 vs. 0.73, p = 0.006) compared to 71 patients with more accurate infarct volume prediction. Eighteen patients with 24-h infarcts smaller than predicted had similar baseline collateral scores but more favorable 24-h CBV indices (0.81 vs. 0.73, p = 0.040). Overall, patients with 24-h infarcts larger than predicted had evidence of less favorable baseline collaterals that fail within 24 h, while patients with 24-h infarcts smaller than predicted typically had favorable collaterals that persisted for 24 h.
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Lin, Chen, Rajbeer Sangha, Jungwha Lee, Carlos Corado, Anvesh Jalasutram, Neil Chatterjee, Carson Ingo, Timothy Carroll, and Shyam Prabhakaran. "Infarct location is associated with quality of life after mild ischemic stroke." International Journal of Stroke 13, no. 8 (June 29, 2018): 824–31. http://dx.doi.org/10.1177/1747493018783760.
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Background In patients with mild ischemic stroke, small but eloquent infarcts may have devastating effects, particularly on health-related quality of life. Aim This study investigates the association between acute infarct location and three-month health-related quality of life in patients with mild ischemic stroke. Methods We evaluated consecutively enrolled patients from a single center between August 2012 and July 2013. Our primary outcome at three months was impairment in any health-related quality of life domain (upper extremity, lower extremity, executive function, and general concerns) defined by a T-score <45. We analyzed the association between acute infarct locations and impaired health-related quality of life at three months in univariate and multivariable analysis. Results Among 229 patients (mean age 64.9 years, 55% male, 29.7% black, and median initial NIHSS score 1), impaired health-related quality of life was noted in 84 (36.2%) patients at three months. In univariate analysis, patients with subcortical infarcts (56.0% vs. 39.3%, p = 0.02) and brainstem infarcts (21.4% vs. 10.3%, p = 0.02) were more likely to have impaired health-related quality of life. In multivariable analysis, patients with subcortical and/or brainstem infarcts had increased odds of impaired health-related quality of life (adjusted OR 2.54, 95% CI 1.29–5.01, p = 0.01). Conclusions After mild ischemic stroke, subcortical and brainstem infarct locations predict impairment in health-related quality of life.
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Rozen, TD. "Vanishing Cerebellar Infarcts in a Migraine Patient." Cephalalgia 27, no. 6 (June 2007): 557–60. http://dx.doi.org/10.1111/j.1468-2982.2007.01317.x.
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Recent population-based studies have suggested that migraine is a risk factor for the development of infarct-like lesions in the territory of the posterior circulation. These lesions are thought to be true vascular infarcts based on their size, location and magnetic resonance imaging (MRI) characteristics. However, as there are no postmortem studies identifying the pathology of these MRI findings, their true aetiology is unknown. A case patient with migraine is presented, who developed what appeared to be cerebellar infarcts on MRI, but these lesions vanished on repeat imaging 16 days later, questioning their aetiology as vascular ischaemic based infarcts.
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de Blank, Peter M. K., Daniel M. Hayward, Robert Zimmerman, MD, Avrum Pollock, and Janet L. Kwiatkowski. "Transcranial Doppler Ultrasound Velocity, Cerebral Vasculopathy, and Silent Infarcts In Sickle Cell Disease." Blood 116, no. 21 (November 19, 2010): 269. http://dx.doi.org/10.1182/blood.v116.21.269.269.
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Abstract Abstract 269 Background: Approximately one-fourth of children with sickle cell disease (SCD), type SS, show evidence of cerebral ischemia on magnetic resonance imaging (MRI) without overt neurologic symptoms. Children with these silent infarcts have an increased risk of neuropsychological abnormalities and overt stroke. The pathophysiology of silent infarcts is unclear. Elevated transcranial Doppler ultrasound (TCD) velocities in the internal cerebral artery (ICA) and middle cerebral artery (MCA) are associated with an increased risk of overt stroke, but have not been associated previously with silent infarct. However, prior studies of silent infarcts failed to examine the association with anterior cerebral artery (ACA) vessel abnormalities, despite a predominantly frontal distribution of these infarcts. In addition, the relationship of magnetic resonance angiography (MRA) abnormalities to silent infarcts has not been extensively studied, although children with abnormal TCD velocity who also have stenosis or occlusion of vessels by MRA have the highest risk of overt stroke. We hypothesized that elevated ACA velocity and/or significant vasculopathy of the cerebral vessels demonstrated by MRA would be associated with a higher risk of silent stroke. Methods: A retrospective analysis of children followed at our Sickle Cell Center with SCD, type SS or Sb0-thalassemia was performed. Children with TCD (with ACA velocity) and brain MRI/A performed within a year of each other were included. TCD studies performed while on chronic transfusions were excluded. The last eligible MRI/TCD combination was used for patients who had multiple studies. Laboratory values obtained within a year of the MRI also were analyzed. Results: Of the 254 eligible subjects, 54% were male and the mean age was 10.6 ± 5.2 years. Silent infarcts were present in 78/254 (30.7%); the location was frontoparietal in 68%. The mean time-averaged mean of the maximal velocity (TAMMvel) of qualifying STOP vessels (MCA, bifurcation, and ICA) was 139±35cm/s, while the mean TAMMvel of the ACA was 117±34cm/s, which is 84% of the velocity of the other anterior vessels. As previously reported, TAMMvel inversely correlated with age (r=-0.40, p<0.0001) and hemoglobin concentration (r=-0.30, p<0.0001). There was no significant difference in TAMMvel in STOP qualifying vessels (MCA, bifurcation, DICA; 137cm/s vs. 145cm/s, p=0.08) among those with and without silent infarct. However, silent infarcts were associated with abnormal TAMMvel (≥200cm/s, 69/239 with normal/conditional vs. 9/15 with abnormal TAMMvel p=0.01) in these vessels. TAMMvel in the ACA was significantly higher (125 cm/s vs. 113 cm/s, p=0.004) in children with silent infarcts, and elevated ACA TAMMvel (≥170cm/s) was associated with silent infarcts (70/242 with normal vs. 8/12 with elevated velocity, p=0.006). No other single vessel velocity was significantly associated with silent infarct. Abnormal ICA/MCA TAMMvel was associated with stenosis of these vessels by MRA (p<0.001), and abnormal ACA velocities were associated with ACA stenosis by MRA (p<0.001). Further, stenosis by MRA in the ICA/MCA was associated with silent infarct (p<0.006) as were abnormalities of the ACA vessels (p=0.001). Conclusions: Unlike prior studies, we demonstrate a significant association between abnormal ICA/MCA velocity and silent infarcts. We also show an association between ACA velocity and silent infarct, which may in part be due to the predominantly frontoparietal distribution of these lesions. This, together with the association of MRA abnormalities of all three anterior vessels (ICA, MCA, ACA) with silent infarcts suggests a possible role of larger cerebral vessel vasculopathy in the pathophysiology of silent infarcts. This could be due to decreased distal blood flow related to the larger vessel narrowing, embolization of thrombus in larger vessels, or small vessel vasculopathy associated with larger vessel disease. However, mechanisms other than larger vessel vasculopathy are also likely to be involved given that silent infarcts occur in a substantial number of children without elevated TCD velocity or vasculopathy by MRA. Nonetheless, assessment of TCD velocity and MRA abnormalities may help provide information on risk assessment for CNS disease in children with SCD. Disclosures: No relevant conflicts of interest to declare.
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Kusumoto, Keiji, James V. Haist, and Morris Karmazyn. "Na+/H+ exchange inhibition reduces hypertrophy and heart failure after myocardial infarction in rats." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H738—H745. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h738.
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We investigated the effect of sodium/hydrogen exchange inhibition (NHE-1) on hypertrophy and heart failure after coronary artery ligation (CAL) in the rat. Animals were subjected to occlusion (or sham) of the left main coronary artery and immediately administered a control diet or one consisting of the NHE-1 inhibitor cariporide for 13–15 wk. Hearts were separated by small [≤30% of left ventricle (LV)] and large (>30% of LV) infarcts. CAL depressed change in left ventricular increase in pressure over time (LV +dP/d t) in small and large infarct groups by 18.8% ( P < 0.05) and 34% ( P < 0.01), respectively, whereas comparative values for the cariporide groups were 8.7% (not significant) and 23.1% ( P < 0.01), respectively. LV end-diastolic pressure was increased by 1,225% in the control large infarct group but was significantly reduced to 447% with cariporide. Cariporide also significantly reduced the degree of LV dilation in animals with large infarcts. Hypertrophy, defined by tissue weights and cell size, was reduced by cariporide, and shortening of surviving myocytes was preserved. Infarct sizes were unaffected by cariporide, and the drug had no influence on either blood pressure or the depressed inotropic response of infarcted hearts to dobutamine. These results suggest an important role for NHE-1 in the progression of heart failure after myocardial infarction.
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Toriello, A., N. D. Pugliese, F. Izzi, A. Siani, G. Locatelli, and R. Saponiero. "Neuroradiological and Neuropsychological Study of a Callosal Infarct." Neuroradiology Journal 21, no. 6 (December 2008): 830–34. http://dx.doi.org/10.1177/197140090802100613.
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Corpus callosum infarcts are rare, constituing 0.6% of cerebral infarcts, most likely due to a rich blood supply from three main arterial systems. These infarcts may present with slowly evolving and non-localizing neurologic signs and symptoms that suggest the diagnosis of neoplasm rather than infarct. In addition, they may exhibit radiologic features more often associated with neoplasm, such as mass-like enhancement or extension across the midline. We describe a patient with corpus callosum infarct presenting with a non specific ataxia-like gait disorder, speech difficulty and left-side weakness. MR imaging disclosed an ischemic area in the body and splenium of the corpus callosum with extension to the right semiovalis centre. Neuropsychological study revealed constructive apraxia, attention reduction, motor programming and inhibiting control involvement. The atypical clinical presentation suggested involvement of the posterior circulation, while apraxia and attention impairment were in accordance with lesion localization. In-depth neuropsychological study is essential in patients with suspected corpus callosum involvement because the neurological signs and symptoms are confounding. The infarct localization in the body and semiovalis centre is an interesting neuroradiological feature.
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Conforto, Adriana Bastos, Fábio Iuji Yamamoto, Cláudia da Costa Leite, Milberto Scaff, and Suely Kazue Nagahashi Marie. "Facial sensory symptoms in medullary infarcts." Arquivos de Neuro-Psiquiatria 63, no. 4 (December 2005): 947–50. http://dx.doi.org/10.1590/s0004-282x2005000600008.
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OBJECTIVE: To investigate the correlation between facial sensory abnormalities and lesional topography in eight patients with lateral medullary infarcts (LMIs). METHOD: We reviewed eight sequential cases of LMIs admitted to the Neurology Division of Hospital das Clínicas/ São Paulo University between July, 2001 and August, 2002 except for one patient who had admitted in 1996 and was still followed in 2002. All patients were submitted to conventional brain MRI including axial T1-, T2-weighted and Fluid attenuated inversion-recovery (FLAIR) sequences. MRIs were evaluated blindly to clinical features to determine extension of the infarct to presumed topographies of the ventral trigeminothalamic (VTT), lateral spinothalamic, spinal trigeminal tracts and spinal trigeminal nucleus. RESULTS: Sensory symptoms or signs were ipsilateral to the bulbar infarct in 3 patients, contralateral in 4 and bilateral in 1. In all of our cases with exclusive contralateral facial sensory symptoms, infarcts had medial extensions that included the VTT topography. In cases with exclusive ipsilateral facial sensory abnormalities, infarcts affected lateral and posterior bulbar portions, with slight or no medial extension. The only patient who presented bilateral facial symptoms had an infarct that covered both medial and lateral, in addition to the posterior region of the medulla. CONLUSION: Our results show a correlation between medial extension of LMIs and presence of contralateral facial sensory symptoms.
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Moore, Alastair, Harold Goerne, Prabhakar Rajiah, Yuki Tanabe, Sachin Saboo, and Suhny Abbara. "Chronic Infarcts and Mimickers of Infarcts." Radiologic Clinics of North America 57, no. 1 (January 2019): 57–65. http://dx.doi.org/10.1016/j.rcl.2018.08.007.
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Azeemuddin, Muhammad, Muhammad Awais, Fatima Mubarak, Abdul Rehman, and Noor Ul-Ain Baloch. "Prevalence of subarachnoid haemorrhage among patients with cranial venous sinus thrombosis in the presence and absence of venous infarcts." Neuroradiology Journal 31, no. 5 (June 12, 2018): 496–503. http://dx.doi.org/10.1177/1971400918783060.
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Introduction In patients with cranial venous sinus thrombosis, the occurrence of subarachnoid haemorrhage in association with haemorrhagic venous infarcts is a well described phenomenon. However, the presence of subarachnoid haemorrhage in patients with cranial venous sinus thrombosis in the absence of a haemorrhagic venous infarct is exceedingly rare. Methods We retrospectively reviewed charts and scans of all patients who had cranial venous sinus thrombosis confirmed by magnetic resonance venography at our hospital between September 2004 and May 2015. The presence of subarachnoid haemorrhage was ascertained on fluid-attenuated inversion recovery, susceptibility-weighted imaging and/or unenhanced computed tomography scans by a single experienced neuroradiologist. Statistical analysis was performed using the Statistical Package for Social Sciences version 20. Differences in the proportion of haemorrhagic venous infarcts among patients with subarachnoid haemorrhage versus those without subarachnoid haemorrhage were compared using the chi-square test. A P value of less than 0.05 was considered significant. Results A total of 138 patients who had cranial venous sinus thrombosis were included in the study. Seventy-three (52.9%) were women and the median age of subjects was 35 (interquartile range 22–47) years. Venous infarcts and haemorrhagic venous infarcts were noted in 20/138 (14.5%) and 62/138 (44.9%) cases, respectively. Subarachnoid haemorrhage was present in 15/138 (10.9%) cases and, in three cases, subarachnoid haemorrhage occurred in the absence of a venous infarct. Haemorrhagic venous infarcts were more prevalent ( P = 0.021) among patients with subarachnoid haemorrhage (11/15) than in those without subarachnoid haemorrhage (51/123). Conclusion In patients with cranial venous sinus thrombosis, subarachnoid haemorrhage can occur even in the absence of a haemorrhagic venous infarct. The recognition of cranial venous sinus thrombosis as the underlying cause of subarachnoid haemorrhage is important to avoid misdiagnosis and inappropriate management.
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Soepriatna, Arvin H., A. Kevin Yeh, Abigail D. Clifford, Semih E. Bezci, Grace D. O'Connell, and Craig J. Goergen. "Three-dimensional myocardial strain correlates with murine left ventricular remodelling severity post-infarction." Journal of The Royal Society Interface 16, no. 160 (November 2019): 20190570. http://dx.doi.org/10.1098/rsif.2019.0570.
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Heart failure continues to be a common and deadly sequela of myocardial infarction (MI). Despite strong evidence suggesting the importance of myocardial mechanics in cardiac remodelling, many MI studies still rely on two-dimensional analyses to estimate global left ventricular (LV) function. Here, we integrated four-dimensional ultrasound with three-dimensional strain mapping to longitudinally characterize LV mechanics within and around infarcts in order to study the post-MI remodelling process. To induce infarcts with varying severities, we separated 15 mice into three equal-sized groups: (i) sham, (ii) 30 min ischaemia–reperfusion, and (iii) permanent ligation of the left coronary artery. Four-dimensional ultrasound from a high-frequency small animal system was used to monitor changes in LV geometry, function and strain over 28 days. We reconstructed three-dimensional myocardial strain maps and showed that strain profiles at the infarct border followed a sigmoidal behaviour. We also identified that mice with mild remodelling had significantly higher strains in the infarcted myocardium than those with severe injury. Finally, we developed a new approach to non-invasively estimate infarct size from strain maps, which correlated well with histological results. Taken together, the presented work provides a thorough approach to quantify regional strain, an important component when assessing post-MI remodelling.
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Mendez, R. E., J. M. Pfeffer, F. V. Ortola, K. D. Bloch, S. Anderson, J. G. Seidman, and B. M. Brenner. "Atrial natriuretic peptide transcription, storage, and release in rats with myocardial infarction." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 6 (December 1, 1987): H1449—H1455. http://dx.doi.org/10.1152/ajpheart.1987.253.6.h1449.
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To study the role of atrial natriuretic peptide (ANP) in chronic heart failure, ANP synthesis, storage, and release were examined by measuring atrial ANP messenger ribonucleic acid (mRNA) levels and atrial and plasma ANP concentrations in rats with myocardial infarction produced by coronary artery ligation. Three groups were defined as the following: 1) controls, sham-operated, or operated, but noninfarcted; 2) moderate infarcts, involving 5-30% of the left ventricular circumference; and 3) large infarcts (greater than or equal to 30%). In addition, to determine a possible modulation by dietary Na intake on ANP levels in heart failure, plasma immunoreactive ANP (iANP) levels were measured in rats with and without infarcts given low, regular, or high Na intake for 2 wk, by which time all groups were in neutral balance. Plasma iANP levels varied directly with increasing infarct and atrial sizes, irrespective of Na intake. In contrast, atrial ANP concentration varied inversely with increasing infarct size. The ANP mRNA content index, a measure of total atrial ANP mRNA, was significantly increased in rats with large infarcts compared with control rats. These results indicate that in rats with myocardial infarction, the severity of left ventricular dysfunction, as inferred from infarct size, but not chronic Na intake, is the primary determinant of the extent of activation of the ANP system. Elevated circulating ANP levels are maintained through enhanced atrial synthesis and release. ANP may thus play an important role in the hemodynamic and renal adaptations to chronic heart failure.
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West, G. Alexander, Kiarash J. Golshani, Kristian P. Doyle, Nikola S. Lessov, Theodore R. Hobbs, Steven G. Kohama, Martin M. Pike, et al. "A New Model of Cortical Stroke in the Rhesus Macaque." Journal of Cerebral Blood Flow & Metabolism 29, no. 6 (April 22, 2009): 1175–86. http://dx.doi.org/10.1038/jcbfm.2009.43.
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Primate models are essential tools for translational research in stroke but are reportedly inconsistent in their ability to produce cortical infarcts of reproducible size. Here, we report a new stroke model using a transorbital, reversible, two-vessel occlusion approach in male rhesus macaques that produces consistent and reproducible cortical infarcts. The right middle cerebral artery (distal to the orbitofrontal branch) and both anterior cerebral arteries were occluded with vascular clips. Bilateral occlusion of the anterior cerebral artery was critical for reducing collateral flow to the ipsilateral cortex. Reversible ischemia was induced for 45, 60, or 90 mins ( n = 2/timepoint) and infarct volume and neurologic outcome were evaluated. The infarcts were located predominantly in the cortex and increased in size with extended duration of ischemia determined by T2-weighted magnetic resonance imaging. Infarct volume measured by 2,3,5-triphenyl tetrazolium chloride and cresyl violet staining corroborated magnetic resonance imaging results. Neurologic deficit scores worsened gradually with longer occlusion times. A subset of animals ( n = 5) underwent 60 mins of ischemia resulting in consistent infarct volumes primarily located to the cortex that correlated well with neurologic deficit scores. This approach offers promise for evaluating therapeutic interventions in stroke.
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Tokunaga, Keisuke, Go Hashimoto, Tadataka Mizoguchi, Kota Mori, Masahiro Shijo, Juro Jinnouchi, Takahiro Kuwashiro, Masahiro Yasaka, Takanari Kitazono, and Yasushi Okada. "Left Atrial Appendage Flow Velocity and Multiple Infarcts in Cryptogenic Stroke." Cerebrovascular Diseases 50, no. 4 (2021): 429–34. http://dx.doi.org/10.1159/000514672.
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<b><i>Background:</i></b> To validate the hypothesis that cryptogenic stroke with multiple infarcts included embolic stroke due to left atrial appendage (LAA) dysfunction, the present retrospective observational study was aimed to clarify the association between LAA flow velocity (LAA-FV) and multiple infarcts in patients with cryptogenic stroke. <b><i>Methods:</i></b> From consecutive patients with cryptogenic stroke admitted to our hospital within 7 days after onset, patients without brain magnetic resonance imaging (MRI) on admission or without transesophageal echocardiography (TEE) during acute hospitalization were excluded, and the remaining patients were enrolled. Multiplicity of fresh infarcts was assessed using diffusion-weighted images from brain MRI. LAA-FV was defined as LAA peak emptying flow velocity on TEE. <b><i>Results:</i></b> Of 786 enrolled patients, 522 patients (66%) had a single infarct, and the remaining 264 patients (34%) had multiple infarcts. The percentage of multiple infarcts decreased with increasing quartiles of LAA-FV (<i>p</i> for trend <0.001). The adjusted odds ratio for multiple infarcts decreased with increasing quartiles of LAA-FV (adjusted odds ratio in the fourth quartile, 0.39; 95% confidence interval, 0.25–0.60; compared with the first quartile). LAA-FV as a continuous variable was negatively associated with multiple infarcts (adjusted odds ratio per 10 cm/s, 0.87; 95% confidence interval, 0.81–0.92). <b><i>Conclusions:</i></b> Reduced LAA-FV on TEE was associated with multiple infarcts in patients with cryptogenic stroke. The present findings indicate that cryptogenic stroke with multiple infarcts includes embolic stroke due to LAA dysfunction.
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van den Bos, Ewout J., Barend M. E. Mees, Monique C. de Waard, Rini de Crom, and Dirk J. Duncker. "A novel model of cryoinjury-induced myocardial infarction in the mouse: a comparison with coronary artery ligation." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 3 (September 2005): H1291—H1300. http://dx.doi.org/10.1152/ajpheart.00111.2005.
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Mouse myocardial infarction (MI) models are frequently used research tools. The most commonly applied model is coronary artery ligation. However, coronary ligation often gives rise to apical aneurysmatic infarcts of variable size. Other infarct models include cryoinfarction, which produces reproducible infarcts of the anterior wall. Thus far, this model has not been extensively described in mice. Therefore, we developed a murine cryoinfarction model and compared it with coronary ligation. Studies were performed under isoflurane anesthesia with a follow-up of 4 and 8 wk. Cryoinfarction was induced using a 2- or 3-mm cryoprobe. Two-dimensional guided M-mode echocardiography was used to assess fractional shortening and left ventricular (LV) dimensions at baseline and end point. At end point, hemodynamics were assessed using a 1.4-Fr Millar catheter. Pressure-diameter relations were constructed by combining echocardiography and hemodynamic data. Histological and morphometric analyses of infarct and remote areas were performed. At 4 wk, 3-mm cryoinfarction resulted in decreased LV fractional shortening as well as decreased global LV contractility and relaxation, which was comparable with coronary ligation. No adverse remodeling was observed at this time point, in contrast with the ligation model. However, progressive LV remodeling occured between 4 and 8 wk after cryoinfarction with a further decline in hemodynamic parameters and LV pump function. Histologically, cryoinfarction resulted in highly reproducible, transmural, cone-shaped infarcts with reperfusion at the macrovascular level. These results indicate that the cryoinfarction model represents the anterior myocardial infarct with modest adverse remodeling and may thus be representative for infarcts encountered in clinical practice.
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TANG, W. K., YANGKUN CHEN, WYNNIE W. M. LAM, VINCENT MOK, ADRIAN WONG, GABOR S. UNGVARI, Y. T. XIANG, and KA SING WONG. "Emotional incontinence and executive function in ischemic stroke: A case-controlled study." Journal of the International Neuropsychological Society 15, no. 1 (January 2009): 62–68. http://dx.doi.org/10.1017/s1355617708090061.
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AbstractFrontal and basal ganglia infarcts and executive dysfunction are thought to be involved in the pathophysiology of poststroke emotional incontinence (PSEI). The study examined whether patients with PSEI have more frontal and/or basal ganglia infarcts and impairment in executive function. A total of 516 Chinese patients with acute ischemic stroke consecutively admitted to the acute stroke unit of a university-affiliated regional hospital in Hong Kong were screened for PSEI 3 months after the index stroke. According to Kim’s criteria, 39 (7.6%) had PSEI. Thirty-nine stroke patients without PSEI served as matched control group. The PSEI group had significantly more frontal and/or basal ganglia infarcts, had lower Chinese Frontal Assessment Battery scores, required more time to complete the Stroop Test, and made more omission and commission errors in the Go–NoGo test. There was no significant correlation between frontal or basal ganglia infarcts and executive function. The correlation between frontal infarct and severity of PSEI was .420. Further follow-up and functional imaging studies are warranted to explore the relationship between PSEI, brain infarcts, and executive dysfunction. (JINS, 2009, 15, 62–68.)
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Carlsson, M., P. C. Ursell, D. Saloner, and M. Saeed. "Multidetector computed tomography for characterization of calcium deposits in reperfused myocardial infarction." Acta Radiologica 50, no. 4 (May 2009): 396–405. http://dx.doi.org/10.1080/02841850902756540.
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Background: Calcium overload is a major cause of reperfusion myocardial injury. Multidetector computed tomography (MDCT) has been previously used in visualizing coronary artery calcium, but not calcium deposits in reperfused infarction. Purpose: To assess the ability of MDCT to 1) noninvasively visualize and characterize calcium deposits in reperfused infarcts, and 2) monitor regional wall swelling, regional systolic wall thickening, and infarct resorption. Material and Methods: Reperfused myocardial infarcts were created in seven pigs by 2-hour occlusion of the left anterior descending coronary artery (LAD) after coronary catheterization. A 64-slice MDCT scanner was used for non-contrast images to depict calcium deposits. Furthermore, cine and delayed contrast-enhanced (DE) MDCT imaging were acquired to assess the chronological changes (2–4 hours, 1 week, and 8 weeks) in regional wall swelling, systolic wall thickening, and infarct size. Results: Non-contrast MDCT images depicted calcium deposits as “hot-spots.” Attenuation of calcium deposits was greater (89±6 Hounsfield units [HU]) than remote myocardium (36±3 HU; P<0.05). Calcium deposits were not evident at 2–4 hours and were substantially smaller at 8 weeks compared to 1 week. Correlations were found between the extent of calcium deposits, ejection fraction ( R=0.81), and infarction size ( R=0.70). Cine MCDT images demonstrated transient wall swelling (edema formation and resorption) at 2–4 hours and differences in regional systolic wall thickening among infarcted, peri-infarcted, and remote myocardium. Calcium-specific von Kossa stain confirmed the presence of calcium deposits in infarcted myocardium. Conclusion: 64-slice MDCT has the potential to demonstrate the progression and regression of calcium deposits, interstitial edema, and infarction. The presence of calcium deposits was transient and associated with reperfused recent infarction. The extent of calcium deposits was positively correlated with infarction size and negatively with global left-ventricular function.
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Ganesh, Aravind, Mayank Goyal, Alexis T. Wilson, Johanna Maria Ospel, Andrew M. Demchuk, David Mikulis, Julien Poublanc, et al. "Association of Iatrogenic Infarcts With Clinical and Cognitive Outcomes in the Evaluating Neuroprotection in Aneurysm Coiling Therapy Trial." Neurology 98, no. 14 (February 15, 2022): e1446-e1458. http://dx.doi.org/10.1212/wnl.0000000000200111.
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Background and ObjectivesSmall iatrogenic brain infarcts are often seen on diffusion-weighted MRI (DWI) following surgical or endovascular procedures, but there are few data on their clinical effects. We examined the association of iatrogenic infarcts with outcomes in the ENACT (Evaluating Neuroprotection in Aneurysm Coiling Therapy) randomized controlled trial of nerinetide in patients undergoing endovascular repair of intracranial aneurysms.MethodsIn this post hoc analysis, we used multivariable models to evaluate the association of the presence and number of iatrogenic infarcts on DWI with neurologic impairment (NIH Stroke Scale [NIHSS]), functional status (modified Rankin Scale [mRS]), and cognitive and neuropsychiatric outcomes (30-minute test battery) at 1–4 days and 30 days postprocedure. We also related infarct number to a z score–derived composite outcome score using quantile regression.ResultsAmong 184 patients (median age 56 years [interquartile range (IQR) 50–64]), 124 (67.4%) had postprocedural DWI lesions (median 4, IQR 2–10.5). Nerinetide treatment was associated with fewer iatrogenic infarcts but no overall significant clinical treatment effects. Patients with infarcts had lower Mini-Mental State Examination (MMSE) scores at 2–4 days (median 28 vs 29, adjusted coefficient [acoef] −1.11, 95% CI −1.88 to −0.34, p = 0.005). Higher lesion counts were associated with worse day 1 NIHSS (adjusted odds ratio for NIHSS ≥1: 1.07, 1.02–1.12, p = 0.009), day 2–4 mRS (adjusted common odds ratio [acOR] 1.05, 1.01–1.09, p = 0.005), and day 2–4 MMSE (acoef −0.07, −0.13 to −0.003, p = 0.040) scores. At 30 days, infarct number remained associated with worse mRS (acOR 1.04, 1.01–1.07, p = 0.016) and Hopkins Verbal Learning Test (HVLT) delayed recall scores (acoef −0.21, −0.39 to −0.03, p = 0.020). Patients with infarcts trended towards lower 30-day Digit Symbol Substitution Test (DSST) scores (acoef −3.73, −7.36 to −0.10, p = 0.044). Higher lesion count was associated with worse composite outcome scores at both 1–4 days and 30 days (30-day acoef −0.12, 95% CI −0.21 to −0.03, p = 0.008). Among those with infarcts, day 1 NIHSS and day 2–4 mRS correlated with 30-day NIHSS, DSST, HVLT, and mRS scores, whereas day 2–4 MMSE correlated with 30-day NIHSS and DSST scores (Spearman ρ 0.47, p = 0.001).DiscussionIatrogenic brain infarcts were associated with subtle differences in postprocedural (1–4 days) and 30-day outcomes on different measures in this middle-aged cohort, with earlier dysfunction correlating with later differences.Trial Registration InformationClinical trials registration NCT00728182.
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Connelly, C. M., J. A. Leppo, P. W. Weitzman, W. M. Vogel, and C. S. Apstein. "Effect of coronary occlusion and reperfusion on myocardial blood flow during infarct healing." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (August 1, 1989): H365—H374. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h365.
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Coronary occlusion (CO) of 1 h or longer causes transmural myocardial infarction (MI) in the rabbit. We studied how reperfusion of an infarct affected myocardial blood flow (MBF) acutely and after 3 wk of healing. CO was performed in rabbits for 60 or 180 min (n = 22) followed by reperfusion, and MBF to normal and infarcted zones was determined by radioactive microspheres. In a separate series (n = 23), MBF was measured at 21-25 days post-CO in three groups that had either permanent CO or reperfusion after 60 or 180 min of CO. MBF to the infarct was approximately 8 +/- 3% (+/-SE) of normal MBF (3.8 +/- 0.5 ml.min-1.g-1) during 60-180 min of CO but 3 wk later had increased to 33 +/- 6% of normal MBF (P less than 0.005). Reperfusion after 60 or 180 min of CO resulted in 74 +/- 6% and 41 +/- 5% return of normal MBF, respectively, but 3 wk later, MBF had decreased to 25 +/- 5% (P less than 0.001) and 24 +/- 4% (P less than 0.025) of normal MBF, respectively. Thus after 3 wk of postinfarction healing, MBF to the permanently occluded infarcts increased fourfold, whereas MBF decreased by 50% in the reperfused infarcts so that MBF to the scar tissue was comparable among the three groups and was not influenced by acute post-MI reperfusion.
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Prabhakaran, Shyam, David S. Liebeskind, George Cotsonis, Azhar Nizam, Edward Feldmann, Rajbeer S. Sangha, Iszet Campo-Bustillo, and Jose G. Romano. "Predictors of Early Infarct Recurrence in Patients With Symptomatic Intracranial Atherosclerotic Disease." Stroke 52, no. 6 (June 2021): 1961–66. http://dx.doi.org/10.1161/strokeaha.120.032676.
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Background and Purpose: While prior studies identified risk factors for recurrent stroke in patients with symptomatic intracranial atherosclerotic disease, few have assessed risk factors for early infarct recurrence. Methods: We performed a post hoc analysis of the MYRIAD study (Mechanisms of Early Recurrence in Intracranial Atherosclerotic Disease) of intracranial atherosclerotic disease patients with recent (<21 days) stroke/transient ischemic attack, 50% to 99% stenosis and who underwent 6- to 8-week magnetic resonance imaging (MRI) per protocol. Infarct recurrence was defined as new infarcts in the territory of the symptomatic artery on brain MRI at 6 to 8 weeks compared to index brain MRI. Qualifying events and clinical and imaging outcomes were centrally ascertained by 2 independent reviewers. We assessed the association between baseline clinical and imaging variables and recurrent infarct in bivariate models and multivariable logistic regression to identify independent predictors of infarct recurrence. Results: Of 105 enrolled patients in MYRIAD, 89 (84.8%) were included in this analysis (mean age, 64±12 years, 54 [60.7%] were male, and 53 [59.6%] were White). The median time from qualifying event to MRI was 51+16 days, on which 22 (24.7%) patients had new or recurrent infarcts. Younger age (57.7 versus 66.0 years; P <0.01), diabetes (32.6% versus 14.6%, P =0.05), index stroke (31.3% versus 4.6%, P =0.01), anterior circulation location of stenosis (29.7% versus 12.0%, P =0.08), number of diffusion-weighted imaging lesions (>1: 40.0%, 1: 26.9% versus 0: 4.4%, P <0.01), and borderzone infarct pattern (63.6% versus 25.0%, P =0.01) on baseline MRI were associated with new or recurrent infarcts. Age (adjusted odds ratio, 0.93 [95% CI, 0.89–0.98], P <0.01) and number of diffusion-weighted imaging lesions (adjusted odds ratio, 3.24 [95% CI, 1.36–7.71], P <0.01) were independently associated with recurrent infarct adjusting for hypertension, diabetes, and stenosis location (anterior versus posterior circulation). Conclusions: An index multi-infarct pattern is associated with early recurrent infarcts, a finding that might be explained by plaque instability and artery-to-artery embolism. Further investigation of plaque vulnerability in intracranial atherosclerotic disease is needed. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02121028.
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Arba, Francesco, Grant Mair, Stephen Phillips, Peter Sandercock, and Joanna M. Wardlaw. "Improving Clinical Detection of Acute Lacunar Stroke." Stroke 51, no. 5 (May 2020): 1411–18. http://dx.doi.org/10.1161/strokeaha.119.028402.
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Background and Purpose— We aim to identify factors associated with imaging-confirmed lacunar strokes and improve their rapid clinical identification early after symptom onset using data from the IST-3 (Third International Stroke Trial). Methods— We selected patients likely to have lacunar infarcts as those presenting with: Oxfordshire Community Stroke Project lacunar syndrome; a random sample with National Institutes of Health Stroke Scale (NIHSS) score <7; and recent lacunar infarct identified on imaging by IST-3 central blinded expert panel. An independent reviewer rated brain scans of this sample and classified visible infarcts according to type, size, and location. We investigated factors associated with presence of lacunar infarct on a 24 to 48 hour follow-up scan using multivariable logistic regression and calculated sensitivity and specificity of Oxfordshire Community Stroke Project alone and in combination with NIHSS score <7. Results— We included 568 patients (330 lacunar syndrome; 147 with NIHSS score <7; 91 with lacunar infarct on baseline imaging, numbers exclude overlaps between groups), mean (±SD) age, 73.2 (±13.6) years, 316 (56%) males, and median NIHSS score 5 (IQR, 4–8). On 24 to 48 hour scan, 138 (24%) patients had lacunar infarcts, 176 (31%) other infarct subtypes, 254 (45%) no visible infarct. Higher baseline systolic blood pressure (odds ratio, 1.01 [95% CI, 1.01–1.02]) and preexisting lacunes (odds ratio, 2.29 [95% CI, 1.47–3.57) were associated with recent lacunar infarcts. Sensitivity and specificity of lacunar syndrome was modest (58% and 45%, respectively), but adding NIHSS score <7 increased specificity (99%), positive and negative predictive values (97% and 87%, respectively). Conclusions— In patients presenting within 6 hours of stroke onset, adding NIHSS score <7 to Oxfordshire Community Stroke Project lacunar syndrome classification may increase specificity for identifying lacunar stroke early after stroke onset. Our findings may help selection of patients for clinical trials of lacunar stroke and should be validated externally. Registration— URL: http://www.controlled-trials.com/ ; Unique identifier: ISRCTN25765518.
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Berg, J., R. Jablonowski, D. Nordlund, S. Kopic, S. Bidhult, C. G. Xanthis, M. Saeed, K. Solem, H. Arheden, and M. Carlsson. "Decreased atrioventricular plane displacement after acute myocardial infarction yields a concomitant decrease in stroke volume." Journal of Applied Physiology 128, no. 2 (February 1, 2020): 252–63. http://dx.doi.org/10.1152/japplphysiol.00480.2019.
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Acute myocardial infarction (AMI) can progress to heart failure, which has a poor prognosis. Normally, 60% of stroke volume (SV) is attributed to the longitudinal ventricular shortening and lengthening evident in the atrioventricular plane displacement (AVPD) during the cardiac cycle, but there is no information on how the relationship changes between SV and AVPD before and after AMI. Therefore, the aim of this study was to determine how SV depends on AVPD before and after AMI in two swine models. Serial cardiac magnetic resonance imaging was carried out before and 1–2 h after AMI in a microembolization model ( n = 12) and an ischemia-reperfusion model ( n = 14). A subset of pigs ( n = 7) were additionally imaged at 24 h and at 7 days. Cine and late gadolinium enhancement images were analyzed for cardiac function, AVPD measurements and infarct size estimation, respectively. AVPD decreased ( P < 0.05) in all myocardial regions after AMI, with a concomitant SV decrease ( P < 0.001). The ischemia-reperfusion model affected SV to a higher degree and had a larger AVPD decrease than the microembolization model (−29 ± 14% vs. −15 ± 18%; P < 0.05). Wall thickening decreased in infarcted areas ( P < 0.001), and A-wave AVPD remained unchanged ( P = 0.93) whereas E-wave AVPD decreased ( P < 0.001) after AMI. We conclude that AVPD is coupled to SV independent of infarct type but likely to a greater degree in ischemia-reperfusion infarcts compared with microembolization infarcts. AMI reduces diastolic early filling AVPD but not AVPD from atrial contraction. These findings shed light on the physiological significance of atrioventricular plane motion when assessing acute and subacute myocardial infarction. NEW & NOTEWORTHY The link between cardiac longitudinal motion, measured as atrioventricular plane displacement (AVPD), and stroke volume (SV) is investigated in swine after acute myocardial infarction (AMI). This cardiac magnetic resonance study demonstrates a close coupling between AVPD and SV before and after AMI in an experimental setting and demonstrates that this connection is present in ischemia-reperfusion and microembolization infarcts, acutely and during the first week. Furthermore, AVPD is equally and persistently depressed in infarcted and remote myocardium after AMI.
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Dorrance, Anne M., Heather L. Osborn, Roger Grekin, and R. Clinton Webb. "Aldosterone Antagonism and Epidermal Growth Factor in Cerebral Ischemia." Hypertension 36, suppl_1 (October 2000): 723. http://dx.doi.org/10.1161/hyp.36.suppl_1.723-b.
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P166 Two factors that may contribute to the vascular remodeling involved in the pathogenesis of ischemic cerebrovascular disease are aldosterone (aldo) and epidermal growth factor (EGF). Spironolactone (spir) is known to reduce the frequency of hemorrhagic infarcts, its effects on ischemic infarcts are unknown. We have previously shown that the mRNA for EGF and its receptor (EGFR) are increased in the cerebral blood vessels from stroke-prone spontaneously hypertensive rats (SHRSP) compared to Wistar Kyoto (WKY) rats. We hypothesized that this, along with an altered response to aldo would contribute to a larger experimentally induced ischemic cerebral infarct. Six week old male SHRSP and WKY rats were treated with spir (200mg) or placebo for six weeks. Cerebral ischemia was induced by middle cerebral artery occulsion, infarct size was quantified and expressed as percentage of the hemisphere infarcted. RNA was extracted from aorta and RT-PCR was performed for EGF and EGFR. mRNA was quantified by phosphorimage analysis and corrected for GAPDH. Treatment did not affect blood pressure in either group. Aldo antagonism reduced the size of experimentally induced cerebral infarct in SHRSP (51.7±3.6 vs. 22±6.7 % SHRSP vs. SHRSP + spir p<0.05) and WKY rats (14.2±2.1 vs. 3.2±1.5 % WKY vs. WKY + spir p<0.01). Expression of mRNA for EGFR was higher in the aorta of SHRSP compared to WKY (1.09±0.25 vs. 0.17±0.03 p<0.05 SHRSP vs WKY). The same was true for EGF mRNA expression (13.61 ± 3.73 vs 3.80 ± 1.30 p<0.05 SHRSP vs. WKY). Spir treatment reduced the expression of EGFR mRNA in the aorta of SHRSP (1.09±0.25 vs. 0.56±0.11 SHRSP vs. SHRSP + spir p<0.05) but not WKY rats. Spir treatment had no effect on the EGF mRNA expression in either group. Plasma aldo levels were similar for SHRSP and WKY. The reduction in ischemic infarct size is a novel observation. The mechanism by which spir reduces infarcts in SHRSP may be by its reduction in the expression of the EGFR mRNA leading to reduced vascular remodeling. It is possible that locally produced aldo is responsible for the inceased EGFR mRNA as aldo levels were the same for SHRSP and WKY. Interestingly, the mechanism for the reduction in infarct size appears to be different in the WKY rat.
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Yedavalli, Vivek, and Elizabeth Tong. "The Potential Utility of Arterial Spin Labeling in Detecting and Localizing Posterior Circulation Occlusions in Every Day Practice: A Clinical Report of Selected Cases." Journal of Clinical Imaging Science 10 (December 10, 2020): 78. http://dx.doi.org/10.25259/jcis_118_2020.
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Arterial spin labeling (ASL) is a non-contrast, non-invasive method used for the evaluation of cerebral perfusion, which is now increasingly utilized in everyday clinical practice. As a marker of cerebral blood flow at the capillary level, it has particular utility in stroke assessment. One rarer stroke subtype with non-specific symptomatology that can lead to significant morbidity is the posterior circulation (PC) infarct. As with the more common anterior circulation infarcts, ASL has shown benefit in PC infarcts as well, but has not been extensively explored in the literature nor been directly compared to bolus perfusion techniques. This clinical report of selected cases shows the utility of ASL in localization and detection of PC infarcts both in conjunction with and in the absence of bolus perfusion.
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Hart, R. G., and J. D. Easton. "Hemorrhagic infarcts." Stroke 17, no. 4 (July 1986): 586–89. http://dx.doi.org/10.1161/01.str.17.4.586.
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Caplan, L. R., J. D. Schmahmann, C. S. Kase, E. Feldmann, G. Baquis, J. P. Greenberg, P. B. Gorelick, C. Helgason, and D. B. Hier. "Caudate Infarcts." Archives of Neurology 47, no. 2 (February 1, 1990): 133–43. http://dx.doi.org/10.1001/archneur.1990.00530020029011.
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Moulin, Thierry, Thierry Crépin-Leblond, Jean-Luc Chopard, and Julien Bogousslavsky. "Hemorrhagic Infarcts." European Neurology 34, no. 2 (1994): 64–77. http://dx.doi.org/10.1159/000117012.
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Kappelle, L. J., and J. van Gijn. "Lacunar infarcts." Clinical Neurology and Neurosurgery 88, no. 1 (January 1986): 3–17. http://dx.doi.org/10.1016/0303-8467(86)90002-8.
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Leys, D., and J. P. Pruvo. "Spinal infarcts." Revue Neurologique 177, no. 5 (May 2021): 459–68. http://dx.doi.org/10.1016/j.neurol.2020.12.002.
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Berger, Asaf, Garry Tzarfati, Mathias Costa, Marga Serafimova, Akiva Korn, Tali Alfassi, Daniel Aviram, Alon Kashinian, Zvi Ram, and Rachel Grossman. "NCMP-05. THE INCIDENCE AND IMPACT OF POST-OPERATIVE STROKE IN SURGERY FOR LGG." Neuro-Oncology 21, Supplement_6 (November 2019): vi180. http://dx.doi.org/10.1093/neuonc/noz175.751.
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Abstract BACKGROUND Postoperative neurological deficits may outweigh the benefit conferred by maximal resection of gliomas. We evaluated the incidence of ischemic events in patients undergoing surgery for low-grade gliomas (LGG) and the long-term neurological and cognitive sequelae. METHODS Between 2013–2017, 168 patients underwent surgical resection or biopsy for LGG at our center. A full dataset, including pre- and postoperative magnetic resonance imaging (MRI) and long-term clinical evaluation findings, was available for 82 patients (study group). Ischemic complications, overall and progression-free survival, and functional and neurocognitive outcomes were evaluated. RESULTS The immediate postoperative MRI revealed an acute ischemic stroke adjacent to the tumor resection cavity in 19 patients (23%), 13 of whom developed new neurological deficits due to the ischemic event. Infarcts were more common in patients with recurrent tumors, especially those involving the Sylvian fissure (p< 0.05). Surgery for insular gliomas had the strongest association with postoperative infarcts. Survival of patients w/wo a postoperative infarct was the same. The median Karnofsky-Performance Status was lower for the infarct group vs. the non-infarct group at 3 months post-surgery (p=0.016), with a gradual significant improvement for the former over one year (p=0.04). Immediately after surgery, 27% of the patients without infarcts and 58% of those with infarcts experienced a new motor deficit (p=0.037), decreasing to 16% (p=0.028) and 37% (p=0.001), respectively, at one year. Neurocognitive analysis findings before and 3 months after surgery were unchanged, but patients with an infarct had a significant decrease in naming (p=0.04). Confusion during awake craniotomy was a strong predictor of an ischemic stroke. CONCLUSIONS Intraoperative strokes are more prevalent among patients who undergo recurrent surgeries, especially in the insula. Although they do not affect survival, these strokes negatively impact the patients’ activity and performance status, especially during the first 3 postoperative months, with gradual functional improvement over one year.
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Leary, Megan C., and Jeffrey L. Saver. "Incidence of Silent Stroke in the United States." Stroke 32, suppl_1 (January 2001): 363. http://dx.doi.org/10.1161/str.32.suppl_1.363-b.
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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.
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Strouse, John J., Michael Kraut, Lisa M. Williams, Michael R. DeBaun, and James F. Casella. "Low Levels of Apolipoprotein A1 Are Associated with Silent Cerebral Infarcts in Children with Sickle Cell Disease." Blood 114, no. 22 (November 20, 2009): 259. http://dx.doi.org/10.1182/blood.v114.22.259.259.
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Abstract Abstract 259 Background: Cerebral infarct is a frequent complication in children and adults with sickle cell disease (SCD). About 10% of children with sickle cell anemia (HbSS) will have an overt stroke by 18 years of age and another 22% will have “silent” cerebral infarcts by 14 years of age. There is a second peak in the incidence of overt ischemic stroke in adults with SCD. Both silent and overt stroke can be accompanied by cognitive impairment and thereby increased risk of academic failure. Several laboratory parameters have been associated with these complications, including low hematocrit or hemoglobin, high white blood cell count (WBC), and high platelet count, while lactate dehydrogenase (LDH) and apolipoprotein A1 have been associated with pulmonary vasculopathy in adults with SCD. Elevated C-reactive protein (CRP) and the ratio of apolipoprotein B/A1 are associated with increased stroke risk in the general population. We hypothesized that these and other biomarkers might also be important in children with silent cerebral infarction. Methods: We prospectively measured potential biomarkers, including complete blood count, reticulocytes, fetal hemoglobin (HbF), LDH, CRP, and apolipoprotein A1 and B in 73 children with HbSS and 3 with sickle-β0-thalassemia (HbSβ0), in addition to performing brain magnetic resonance imaging (MRI), in a single center ancillary study of the Silent Infarct Transfusion Trial. MRIs were interpreted for the presence or absence of silent cerebral infarcts (FLAIR hyperintensities ≥3 mm in diameter seen in at least two imaging planes without corresponding symptoms or signs of stroke). Groups were compared by Student's t-test or Wilcoxon rank-sum test and associations evaluated by univariate and multivariate logistic regression. Results: Twenty-seven participants (35.5%, 1 with HbSβ0) had silent cerebral infarcts (age 8.9 ± 2.4 years, 59% male) and 49 (65.2%) had normal brain MRIs (age 8.7 ± 2.1, 53% male). The group with SCD and silent cerebral infarcts had significantly lower hemoglobin concentration and apolipoprotein A1 (P=0.01 for both) than children with SCD without silent cerebral infarcts. Apolipoprotein B and the ratio of apolipoprotein B to A1 were similar between groups. By univariate logistic regression, both apolipoprotein A1 [Odds ratio (OR) 0.95 per mg/dl increase, P<0.05] and hemoglobin (OR 0.52 per g/L increase, P<0.05) were associated with silent cerebral infarct; however, in a multivariate model, apolipoprotein A1 (OR 0.96 per mg/dl, P<0.05), but not hemoglobin (OR 0.78 per g/L, P=0.5), was significantly associated with silent cerebral infarct. Discussion and Conclusions: These data suggest a role of apolipoprotein A1 in the pathogenesis of silent cerebral infarct in children with SCD. Apolipoprotein A1 is a plausible marker or risk factor for cerebrovascular disease in SCD, given the association of lower levels with pulmonary hypertension in SCD and increased risk for cererbrovascular and cardiac disease in the general population. This marker should be studied in a larger longitudinal cohort of children at risk for cerebral infarcts. Disclosures: Strouse: General Electric: Equity Ownership. Casella:Boehringer Ingelheim: Honoraria; Cytrex: Research Funding; Ikaria: Research Funding.
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De Pasquale, Carmine G., Andrew D. Bersten, Ian R. Doyle, Phillip E. Aylward, and Leonard F. Arnolda. "Infarct-induced chronic heart failure increases bidirectional protein movement across the alveolocapillary barrier." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2136—H2145. http://dx.doi.org/10.1152/ajpheart.00875.2002.
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Chronic heart failure (CHF) is associated with adaptive structural changes at the alveolocapillary barrier that may be associated with altered protein permeability. Bidirectional protein movement across the barrier was studied in anesthetized rats with infarct-induced CHF by following125I-labeled albumin (125I-albumin) flux into the alveoli and the leakage of surfactant protein (SP)-B from the alveoli into the circulation. Three groups were studied: controls [0% left ventricular (LV) infarction], moderate infarct (25–45% LV infarction), and large infarct (>46% LV infarction). Wet and dry lung weights increased in the large infarct group (both P < 0.001), consistent with increased lung water and solid lung tissue.125I-albumin flux increased across the endothelial ( P < 0.001) and epithelial ( P < 0.01) components of the alveolocapillary barrier in the large infarct group. Plasma SP-B increased 23% with moderate infarcts ( P < 0.05) and 97% with large infarcts ( P < 0.001), independent of alveolar levels. Lavage fluid immune cells ( P < 0.01) and myeloperoxidase activity ( P < 0.05) increased in the large infarct group, consistent with inflammation. Bidirectional protein movement across the alveolocapillary barrier is increased in CHF, and alveolar inflammation may contribute to this pathophysiological defect.
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Hollander, Monika, Michiel L. Bots, Jacqueline Cm Witteman, Peter J. Koudstaal, Diederick E. Grobbee, Albert Hofman, and Monique Mb Breteler. "Plaques in the carotid artery and risk of cerebral infarcts in the elderly; The Rotterdam Study." Stroke 32, suppl_1 (January 2001): 363. http://dx.doi.org/10.1161/str.32.suppl_1.363.
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P132 Background Presence of carotid plaques is associated with increased risk of cerebral infarcts. Whether they directly cause a stroke through embolism or merely are indicators of generalised atherosclerosis is not extensively investigated. We studied this by assessing the association between plaques at different carotid segments and risk of subtypes of cerebral infarcts. Methods Our study is based on 5444 subjects from the Rotterdam Study, a population based cohort study. Subjects were free from previous stroke. Presence of plaques was assessed in 3 segments of both carotid arteries at baseline (1990–1993). A total plaque score reflected the number of locations with plaques (range 0–6). Follow up for stroke was complete until December 31 1997. We calculated the risk of severe plaques (score 5–6) compared to absence of plaques (score 0) by Cox regression, adjusting for age and gender. Furthermore, we analysed the risk of unilateral and bilateral plaques compared to absence of plaques at different segments of the carotid artery. Relative risks (95% CI) are given for subtypes of cerebral infarct. Results In total 224 strokes occurred of whom 130 were ischemic. Severe plaques were present in 7% of the population and associated with an increased risk of lacunar and anterior circulation infarcts (RR 12.0 (2.0–70) and 4.5 (1.6–12.3), respectively). After exclusion of infarcts of presumed cardio-embolic cause the relative risk of anterior circulation infarcts was 9.4 (2.5–35.7). The risk for bilateral plaques was higher than for unilateral plaques when we analysed carotid segments separately. We found no association between severe plaques and risk of posterior circulation infarcts. Conclusion Carotid plaques are associated with increased risk of lacunar and anterior circulation infarcts. Associations were stronger with increasing number of plaques. This suggests that carotid plaques are markers of atherosclerosis on large and small vessel level. Since we found no association with posterior circulation infarcts it seems likely that at least part of the effect is through thrombo-embolism.