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Prevention of cardioembolic stroke.

ABSTRACT: Cardiac causes of ischemic stroke lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is atrial fibrillation (AF), which has an increasing incidence with age. AF stroke trials demonstrate that anti-coagulation is superior to anti-platelet therapy in terms of ischemic stroke prevention. Recently, warfarin was compared with dabigatran, an oral, direct thrombin inhibitor, and was found to be at least equally effective in reducing ischemic stroke with less intracranial bleeding risk. Future research is investigating other direct thrombin inhibitors as potential alternatives to warfarin, which has a narrow therapeutic index, requires frequent blood monitoring, has multiple drug interactions, and a higher rate of intracranial bleeding. Other causes of cardioembolic stroke include myocardial infarction, left ventricular thrombus, reduced ejection fraction, valvular abnormalities, and endocarditis. Patent foramen ovale is a common finding on echocardiograms in patients with and without stroke (up to 20% of the population), and it is a controversial source of cryptogenic stroke. The best way to prevent cardioembolic stroke remains early detection and treatment of AF, and treating the underlying stroke mechanism. Cardiac magnetic resonance imaging is an emerging technology and reveals some sources of cardiac embolism missed by echocardiography, and might provide an additional diagnostic tool in investigating cardioembolic stroke.

SUBMITTER: Freeman WD

PROVIDER: S-EPMC3250282 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature

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Prevention of cardioembolic stroke.

Freeman William David WD Aguilar Maria I MI

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics 20110701 3

Cardiac causes of ischemic stroke lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is atrial fibrillation (AF), which has an increasing incidence with age. AF stroke trials demonstrate that anti-coagulation is superior to anti-platelet therapy in terms of ischemic stroke prevention. Recently, warfarin was compared with dabigatran, an oral, direct thrombin inhibitor, and was found ...[more]

PMID: 21638139

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Project description:Background and purposeOral anticoagulation is generally indicated for cardioembolic strokes, but not for other stroke causes. Consequently, subtype classification of ischemic stroke is important for risk stratification and secondary prevention. Because manual classification of ischemic stroke is time-intensive, we assessed the accuracy of automated algorithms for performing cardioembolic stroke subtyping using an electronic health record (EHR) database.MethodsWe adapted TOAST (Trial of ORG 10172 in Acute Stroke Treatment) features associated with cardioembolic stroke for derivation in the EHR. Using administrative codes and echocardiographic reports within Mass General Brigham Biobank (N=13 079), we iteratively developed EHR-based algorithms to define the TOAST cardioembolic stroke features, revising regular expression algorithms until achieving positive predictive value ≥80%. We compared several machine learning-based statistical algorithms for discriminating cardioembolic stroke using the feature algorithms applied to EHR data from 1598 patients with acute ischemic strokes from the Massachusetts General Hospital Ischemic Stroke Registry (2002-2010) with previously adjudicated TOAST and Causative Classification of Stroke subtypes.ResultsRegular expression-based feature extraction algorithms achieved a mean positive predictive value of 95% (range, 88%-100%) across 11 echocardiographic features. Among 1598 patients from the Massachusetts General Hospital Ischemic Stroke Registry, 1068 had any cardioembolic stroke feature within predefined time windows in proximity to the stroke event. Cardioembolic stroke tended to occur at an older age, with more TOAST-based comorbidities, and with atrial fibrillation (82.3%). The best model was a random forest with 92.2% accuracy and area under the receiver operating characteristic curve of 91.1% (95% CI, 87.5%-93.9%). Atrial fibrillation, age, dilated cardiomyopathy, congestive heart failure, patent foramen ovale, mitral annulus calcification, and recent myocardial infarction were the most discriminatory features.ConclusionsMachine learning-based identification of cardioembolic stroke using EHR data is feasible. Future work is needed to improve the accuracy of automated cardioembolic stroke identification and assess generalizability of electronic phenotyping algorithms across clinical settings.

Project description:ObjectiveTo determine whether altered metabolic profiles represent a link between atrial dysfunction and cardioembolic (CE) stroke, and thus whether underlying dysfunctional atrial substrate may contribute to thromboembolism risk in CE stroke.MethodsA total of 144 metabolites were measured using liquid chromatography-tandem mass spectrometry in plasma samples collected within 9 hours of stroke onset in 367 acute stroke patients. Stroke subtype was assigned using the Causative Classification of Stroke System, and CE stroke (n = 181) was compared to non-CE stroke (n = 186). Markers of left atrial dysfunction included abnormal atrial function (P-wave terminal force in lead V1, PTFV1 >4,000 μV·ms), left atrial enlargement on echocardiography, and frank atrial fibrillation on ECG. Stroke recurrence risk was assessed using CHADS2 and CHA2DS2-VASc scores. Associations between metabolites and CE stroke, atrial dysfunction, and stroke recurrence risk were evaluated using logistic regression models.ResultsThree tricarboxylic acid metabolites-succinate (odds ratio [OR] 1.71, 95% confidence interval [CI] 1.36-2.15, p = 1.37 × 10-6), α-ketoglutarate (OR 1.62, 95% CI 1.29-2.04, p = 1.62 × 10-5), and malate (OR 1.58, 95% CI 1.26-1.97, p = 2.57 × 10-5)-were associated with CE stroke. Succinate (OR 1.36, 95% CI 1.31-1.98, p = 1.22 × 10-6), α-ketoglutarate (OR 2.14, 95% CI 1.60-2.87, p = 2.08 × 10-8), and malate (OR 2.02, 95% CI 1.53-2.66, p = 1.60 × 10-7) were among metabolites also associated with subclinical atrial dysfunction. Of these, succinate was also associated with left atrial enlargement (OR 1.54, 95% CI 1.23-1.94, p = 1.06 × 10-4) and stroke recurrence based on dichotomized CHADS2 (OR 2.63, 95% CI 1.68-4.13, p = 3.00 × 10-6) and CHA2DS2-VASc (OR 2.43, 95% CI 1.60-3.68, p = 4.25 × 10-6) scores.ConclusionsMetabolite profiling identified changes in succinate associated with CE stroke, atrial dysfunction, and stroke recurrence, revealing a putative underlying link between CE stroke and energy metabolism.

Project description:BackgroundInflammation contributes to unstable atherosclerotic plaque and stroke. In randomised trials in patients with coronary disease, canukinumab (an interleukin-1B antagonist) and colchicine (a tubulin inhibitor with pleiotropic anti-inflammatory effects) reduced recurrent vascular events.Hypothesis: Anti-inflammatory therapy with low-dose colchicine plus usual care will reduce recurrent vascular events in patients with non-severe, non-cardioembolic stroke and TIA compared with usual care alone.DesignCONVINCE is a multi-centre international (in 17 countries) Prospective, Randomised Open-label, Blinded-Endpoint assessment (PROBE) controlled Phase 3 clinical trial in 3154 participants. The intervention is colchicine 0.5 mg/day and usual care versus usual care alone (antiplatelet, lipid-lowering, antihypertensive treatment, lifestyle advice). Included patients are at least 40 years, with non-severe ischaemic stroke (modified Rankin score ≤3) or high-risk TIA (ABCD2 > 3, or positive DWI, or cranio-cervical artery stenosis) within 72 hours-28 days of randomisation, with qualifying stroke/TIA most likely caused by large artery stenosis, lacunar disease, or cryptogenic embolism. Exclusions are stroke/TIA caused by cardio-embolism or other defined cause (e.g. dissection), contra-indication to colchicine (including potential drug interactions), or incapacity for participation in a clinical trial. The anticipated median follow-up will be 36 months. The primary analysis will be by intention-to-treat.OutcomeThe primary outcome is time to first recurrent ischaemic stroke, myocardial infarction, cardiac arrest, or hospitalisation with unstable angina (non-fatal or fatal).SummaryCONVINCE will provide high-quality randomised data on the efficacy and safety of anti-inflammatory therapy with colchicine for secondary prevention after stroke.ScheduleFirst-patient first-visit was December 2016. Recruitment to complete in 2021, follow-up to complete in 2023.

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Prevention of cardioembolic stroke.

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Prevention of cardioembolic stroke.

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