371 research outputs found

    901-97 Stroke and Long-term Anticoagulant Therapy in 3404 Post-Myocardial Infarction Patients

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    In a randomized, double-blind, placebo controlled trial (ASPECT) we studied 3404 post-myocardial infarction patients who suffered a stroke during long-term anticoagulant therapy. The duration of treatment ranged from 1 day to six years. Three years following randomization, 2% of the patients on anticoagulant therapy had a stroke compared to 4% in placebo.The incidence of stroke analyzed on “intention-to-treat” was 0.7 per 100 patient-years in the anticoagulant group and 1.2 per 100 patient-years in placebo, a hazard ratio (HR) of 0.60 with a 95% confidence interval (Cl) of 0.40 to 0.90, a 40% reduction in the risk of stroke in the anticoagulated group. A total of 19 intracranial bleeding was observed. The risk of hemorrhages was 8 times greater for anticoagulated patients compared to placebo. Eight of the 17 bleedings were fatal in the anticoagulant group and no fatal hemorrhages occurred in placebo. A total of 15 cerebral infarctions occurred in the anticoagulated group and 43 in placebo. Of the 14 hemorrhagic strokes, 6 were within INR 3.0–4.0 and 8 with an INR>4.0, Of the 7 non-hemorrhagic strokes, 2 were at INR<2, 3 within INR 3.0–4.0, 1 at INR>4.0, and no measurement was available in one patient. The total number of patients who died or were severely disabled as a result of cerebral stroke amounted to 13 in the anticoagulated group, compared to 18 in placebo.ConclusionThe results of the ASPECT trial indicated that long-term anticoagulant therapy substantially reduced the risk of stroke in post-myocardial infarction patients. The increased risk of bleeding complications associated with anticoagulant therapy was offset by a marked reduction in ischemic events

    Secondary prevention after cerebral ischaemia of presumed arterial origin: is aspirin still the touchstone?

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    Patients who have had a transient ischaemic attack or nondisabling ischaemic stroke of presumed arterial origin have an annual risk of death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction that ranges between 4% and 11% without treatment. In the secondary prevention of these vascular complications the use of aspirin has been the standard treatment for the past two decades. Discussions about the dose of aspirin have dominated the issue for some time, although there is no convincing evidence for any difference in effectiveness in the dose range of 30-1300 mg/day. A far greater problem is the limited degree of protection offered by aspirin: the accumulative evidence from trials with aspirin alone and only for cerebrovascular disease of presumed arterial origin as qualifying event indicates that a dose of aspirin of at least 30 mg/day prevents only 13% of serious vascular complications

    The CODECS study:COgnitive DEficits in Cerebellar Stroke

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    Part of the extra-pyramidal system, the cerebellum is more and more recognized by its non-motor functions known as the cerebellar cognitive affective syndrome. Several studies have identified disturbances specifically in executive and attentional functions after focal cerebellar lesions. However, most studies were performed in small and heterogeneous patient groups. Furthermore, there is a substantial variation in the methodology of assessment. Here, we present the results of a large and homogeneous cohort of patients with isolated uniform cerebellar lesions. After three months post-stroke all patients underwent structural neuroimaging to confirm an isolated lesion and were given neuropsychological testing. The results show that cerebellar lesions relate to mild but long-term cognitive impairment in a broad spectrum of neurocognitive functions compared to normative values. These findings confirm involvement of the cerebellum in cognitive processing and supports the theory of ‘dysmetria of thought’ based upon uniform cerebellar processing in multiple cognitive domains. This study highlights the following results: 1-Cognitive impairments after isolated cerebellar stroke is confirmed in several cognitive domains. 2-Semantic and phonemic fluency are most affected in cerebellar stroke patients. 3-Verbal deficits show an age-independent long term effect post-stroke and should be studied further in depth. 4-Cognitive disorders after cerebellar stroke are more prominent in women than men.</p

    Holter monitoring in patients with transient and focal ischemic attacks of the brain

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    The results of Holter monitoring in 100 patients with transient and focal cerebral ischemia were studied retrospectively. Atrial fibrillation (AF) was found in five patients compared with two from a group of 100 age and sex-matched control patients. Four of these had a previous history of AF or showed AF on the standard electrocardiogram. Episodic forms of sick sinus syndrome, which have also been related to cerebral embolism, were found in 32 of the TIA patients against 13 of the controls (p less than 0.0025). Sick sinus syndrome was of the bradyarrhythmia-tachyarrhythmia type in 14 of the TIA patients and in three of the controls (p less than 0.01). The relationship between TIAs and transient sinus node dysfunction could not be explained by concomitant heart disease. It is not yet clear whether the relationship is causal or indirect

    Visit-to-visit blood pressure variability and the risk of stroke in the Netherlands:A population-based cohort study

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    BACKGROUND: Apart from blood pressure level itself, variation in blood pressure has been implicated in the development of stroke in subgroups at high cardiovascular risk. We determined the association between visit-to-visit blood pressure variability and stroke risk in the general population, taking into account the size and direction of variation and several time intervals prior to stroke diagnosis. METHODS AND FINDINGS: From 1990 to 2016, we included 9,958 stroke-free participants of the population-based Rotterdam Study in the Netherlands. This is a prospective cohort study including participants aged 45 years and older. Systolic blood pressure (SBP) variability was calculated as absolute SBP difference divided by mean SBP over 2 sequential visits (median 4.6 years apart). Directional SBP variability was defined as SBP difference over 2 visits divided by mean SBP. Using time-varying Cox proportional hazards models adjusted for age, sex, mean SBP, and cardiovascular risk factors, hazard ratios (HRs) for stroke up to January 2016 were estimated per SD increase and in tertiles of variability. We also conducted analyses with 3-, 6-, and 9-year intervals between variability measurement and stroke assessment. These analyses were repeated for diastolic blood pressure (DBP). The mean age of the study population was 67.4 ± 8.2 years and 5,776 (58.0%) were women. During a median follow-up of 10.1 years, 971 (9.8%) participants had a stroke, including 641 ischemic, 89 hemorrhagic, and 241 unspecified strokes. SBP variability was associated with an increased risk of hemorrhagic stroke (HR per SD 1.27, 95% CI 1.05–1.54, p = 0.02) and unspecified stroke (HR per SD 1.21, 95% CI 1.09–1.34, p < 0.001). The associations were stronger for all stroke subtypes with longer time intervals; the HR for any stroke was 1.29 (95% CI 1.21–1.36, p < 0.001) at 3 years, 1.47 (95% CI 1.35–1.59, p < 0.001) at 6 years, and 1.38 (95%CI 1.24–1.51, p < 0.001) at 9 years. For DBP variability, we found an association with unspecified stroke risk. Both the rise and fall of SBP and the fall of DBP were associated with an increased risk for unspecified stroke. Limitations of the study include that, due to an average interval of 4 years between visits, our findings may not be generalizable to blood pressure variability over shorter periods. CONCLUSIONS: In this population-based study, we found that visit-to-visit blood pressure variation was associated with an increased risk of unspecified and hemorrhagic stroke, independent of direction of variation or mean blood pressure

    Quantitative Gait Impairments in Patients With Stroke or Transient Ischemic Attack: A Population-Based Approach

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    BACKGROUND AND PURPOSE: Gait is a complex process involving various cortical and subcortical brain regions. An acute stroke or transient ischemic attack (TIA) may disrupt white and gray matter integrity and, therefore, affect gait in patients without evident neurological signs. We determined whether patients with stroke and TIA experience subtle changes in global gait and several independent gait domains. METHODS: In the population-based Rotterdam Study, 4456 participants (median age, 65 years; 55% women) underwent detailed quantitative gait assessment (GAITRite) between 2009 and 2016. We summarized 30 gait parameters into a global gait score and 7 mutually independent gait domains. First, we assessed the association between prior stroke or TIA and global and domain-specific gait using linear regression models adjusted for age, sex, vascular risk factors, and cognition. Subsequently, we repeated the analysis stratified by the presence of different neurological symptoms in a subgroup of participants with ischemic stroke after study entry. RESULTS: Compared with participants without prior stroke, patients with stroke had a worse global gait (SD, -0.49 [95% CI, -0.64 to -0.34]), especially in the gait domains Pace, Phases, and Turning. The detrimental effect of stroke on gait was amplified in participants with worse cognition. No gait differences were found between participants with and without prior TIA. Ischemic stroke patients without lower limb weakness, loss of coordination, or visuospatial problems still had a worse gait compared with participants without stroke. Stratification by different stroke symptoms showed that different gait domains were affected in each group. CONCLUSIONS: Prior stroke without neurological signs that affect gait is still associated with gait difficulties compared with individuals without stroke. Our study suggests that stroke not only has a direct impact on gait through neurological impairments but also includes an indirect effect possibly through disruption of gray and white matter integrity and accelerated neurodegeneration
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