Publications
162 results found
Hart RG, Sharma M, Mundl H, et al., 2018, Rivaroxaban for stroke prevention after embolic stroke of undetermined source, New England Journal of Medicine, Vol: 378, Pages: 2191-2201, ISSN: 0028-4793
BackgroundEmbolic strokes of undetermined source represent 20% of ischemic strokes and are associated with a high rate of recurrence. Anticoagulant treatment with rivaroxaban, an oral factor Xa inhibitor, may result in a lower risk of recurrent stroke than aspirin.MethodsWe compared the efficacy and safety of rivaroxaban (at a daily dose of 15 mg) with aspirin (at a daily dose of 100 mg) for the prevention of recurrent stroke in patients with recent ischemic stroke that was presumed to be from cerebral embolism but without arterial stenosis, lacune, or an identified cardioembolic source. The primary efficacy outcome was the first recurrence of ischemic or hemorrhagic stroke or systemic embolism in a time-to-event analysis; the primary safety outcome was the rate of major bleeding.ResultsA total of 7213 participants were enrolled at 459 sites; 3609 patients were randomly assigned to receive rivaroxaban and 3604 to receive aspirin. Patients had been followed for a median of 11 months when the trial was terminated early because of a lack of benefit with regard to stroke risk and because of bleeding associated with rivaroxaban. The primary efficacy outcome occurred in 172 patients in the rivaroxaban group (annualized rate, 5.1%) and in 160 in the aspirin group (annualized rate, 4.8%) (hazard ratio, 1.07; 95% confidence interval [CI], 0.87 to 1.33; P=0.52). Recurrent ischemic stroke occurred in 158 patients in the rivaroxaban group (annualized rate, 4.7%) and in 156 in the aspirin group (annualized rate, 4.7%). Major bleeding occurred in 62 patients in the rivaroxaban group (annualized rate, 1.8%) and in 23 in the aspirin group (annualized rate, 0.7%) (hazard ratio, 2.72; 95% CI, 1.68 to 4.39; P<0.001).ConclusionsRivaroxaban was not superior to aspirin with regard to the prevention of recurrent stroke after an initial embolic stroke of undetermined source and was associated with a higher risk of bleeding. (Funded by Bayer and Janssen Research and Development; NAVIGATE
Perera KS, Swaminathan B, Veltkamp R, et al., 2018, Frequency and features of embolic stroke of undetermined source in young adults, EUROPEAN STROKE JOURNAL, Vol: 3, Pages: 110-116, ISSN: 2396-9873
Kasner SE, Lavados P, Sharma M, et al., 2018, Characterization of Patients with Embolic Strokes of Undetermined Source in the NAVIGATE ESUS Randomized Trial, JOURNAL OF STROKE & CEREBROVASCULAR DISEASES, Vol: 27, Pages: 1673-1682, ISSN: 1052-3057
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- Citations: 40
Laible M, Schueler S, Veltkamp R, 2018, Preexisting cognitive impairment in intracerebral hemorrhage: Methodological issues Response, ACTA NEUROLOGICA SCANDINAVICA, Vol: 137, Pages: 371-371, ISSN: 0001-6314
Haeusler KG, Groeschel K, Koehrmann M, et al., 2018, Position Paper on Atrial Fibrillation Detection After Ischemic Stroke Working Group Heart and Brain of the German Cardiac Society (DGK) and the German Stroke Society (DSG), AKTUELLE NEUROLOGIE, Vol: 45, Pages: 93-106, ISSN: 0302-4350
Gill D, Sivakumaran P, Aravind A, et al., 2018, Temporal Trends in the Levels of Peripherally Circulating Leukocyte Subtypes in the Hours after Ischemic Stroke, JOURNAL OF STROKE & CEREBROVASCULAR DISEASES, Vol: 27, Pages: 198-202, ISSN: 1052-3057
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- Citations: 21
Charidimou A, Karayiannis C, Song T-J, et al., 2017, Brain microbleeds, anticoagulation, and hemorrhage risk Meta-analysis in stroke patients with AF, NEUROLOGY, Vol: 89, Pages: 2317-2326, ISSN: 0028-3878
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- Citations: 69
Veltkamp R, Purrucker J, 2017, Management of Spontaneous Intracerebral Hemorrhage, CURRENT NEUROLOGY AND NEUROSCIENCE REPORTS, Vol: 17, ISSN: 1528-4042
Purpose of ReviewWe review the current evidence for medical and surgical treatments of spontaneous intracerebral hemorrhage (ICH).Recent FindingsTherapy with hemostatic agents (e.g. factor VIIa and tranexamic acid) if started early after bleeding onset may reduce hematoma expansion, but their clinical effectiveness has not been shown. Rapid anticoagulation reversal with prothrombin concentrates (PCC) plus vitamin K is the first choice in vitamin K antagonist-related ICH. In ICH related to dabigatran, anticoagulation can be rapidly reversed with idarucizumab. PCC are recommended for ICH related to FXa inhibitors, whereas specific reversal agents are not yet approved. While awaiting ongoing trials studying minimally invasive approaches or hemicraniectomy, the role of surgery in ICH remains to be defined. Therapies targeting downstream molecular cascades in order to prevent secondary neuronal damage are promising, but the complexity and multi-phased nature of ICH pathophysiology is challenging. Finally, in addition to blood pressure control, antithrombotic prevention after ICH has to consider the risk of recurrent bleeding as well as the risk of ischemic events.SummaryTreatment of acute ICH remains challenging, and many promising interventions for acute ICH await further evidence from trials.
Korompoki E, Filippidis FT, Nielsen PB, et al., 2017, Long-term antithrombotic treatment in intracranial hemorrhage survivors with atrial fibrillation, NEUROLOGY, Vol: 89, Pages: 687-696, ISSN: 0028-3878
Objective: To perform a systematic review and meta-analysis of studies reporting recurrent intracranial hemorrhage (ICH) and ischemic stroke (IS) in ICH survivors with atrial fibrillation (AF) during long-term follow-up.Methods: A comprehensive literature search including MEDLINE, EMBASE, Cochrane library, clinical trials registry was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. We considered studies capturing outcome events (ICH recurrence and IS) for ≥3 months and treatment exposure to vitamin K antagonists (VKAs), antiplatelet agents (APAs), or no antithrombotic medication (no-ATM). Corresponding authors provided aggregate data for IS and ICH recurrence rate between 6 weeks after the event and 1 year of follow-up for each treatment exposure. Meta-analyses of pooled rate ratios (RRs) were conducted with the inverse variance method.Results: Seventeen articles met inclusion criteria. Seven observational studies enrolling 2,452 patients were included in the meta-analysis. Pooled RR estimates for IS were lower for VKAs compared to APAs (RR = 0.45, 95% confidence interval [CI] 0.27–0.74, p = 0.002) and no-ATM (RR = 0.47, 95% CI 0.29–0.77, p = 0.002). Pooled RR estimates for ICH recurrence were not significantly increased across treatment groups (VKA vs APA: RR = 1.34, 95% CI 0.79–2.30, p = 0.28; VKA vs no-ATM: RR = 0.93, 95% CI 0.45–1.90, p = 0.84).Conclusions: In observational studies, anticoagulation with VKA is associated with a lower rate of IS than APA or no-ATM without increasing ICH recurrence significantly. A randomized controlled trial is needed to determine the net clinical benefit of anticoagulation in ICH survivors with AF.
Marinescu M, Sun L, Fatar M, et al., 2017, Cerebral Microbleeds in Murine Amyloid Angiopathy Natural Course and Anticoagulant Effects, STROKE, Vol: 48, Pages: 2248-2254, ISSN: 0039-2499
Background and Purpose—Cerebral microbleeds (CMBs) predispose patients to intracerebral hemorrhage. Preclinical models to examine the effects of antithrombotic treatments on the development of clinically overt intracerebral hemorrhage are needed. We examined the natural course of CMB development and the effects of long-term anticoagulation with warfarin or dabigatran on cerebral micro- and macrohemorrhage in mice overexpressing the APP23 (amyloid precursor protein).Methods—Repeated susceptibility-weighted magnetic resonance imaging was performed in APP23 mice at the age of 18 and 21 months, respectively. After establishing stable long-term anticoagulation effects of warfarin and dabigatran on number and total volume of CMBs, the outcome parameters were compared with nonanticoagulated control.Results—CMBs were equally located in lobar and deep brain regions, and number and total volume of CMBs increased over time. Anticoagulation with either warfarin or dabigatran did not increase CMBs in APP23 significantly. Mice treated with warfarin numerically had a higher mortality (nonanticoagulated: 31%; dabigatran: 35% versus warfarin: 55%; P=0.21). In postmortem brains of prematurely dying animals warfarin caused significantly more frequently large intracerebral hemorrhage than control and dabigatran.Conclusions—Anticoagulation with warfarin or dabigatran for 3 to 4 months does not promote the formation of CMBs in aged APP23 mice. Nevertheless, warfarin but not dabigatran is associated with a higher risk of extensive intracerebral hemorrhage, suggesting that this model may allow preclinical safety evaluation of antithrombotic therapies.
Rizos T, Bartsch AJ, Johnson TD, et al., 2017, Voxelwise distribution of acute ischemic stroke lesions in patients with newly diagnosed atrial fibrillation: Trigger of arrhythmia or only target of embolism?, PLOS One, Vol: 12, ISSN: 1932-6203
ObjectiveAtrial fibrillation (AF) is frequently detected after ischemic stroke for the first time, and brain regions involved in autonomic control have been suspected to trigger AF. We examined whether specific brain regions are associated with newly detected AF after ischemic stroke.MethodsPatients with acute cerebral infarctions on diffusion-weighted magnetic resonance imaging were included in this lesion mapping study. Lesions were mapped and modeled voxelwise using Bayesian Spatial Generalised Linear Mixed Modeling to determine differences in infarct locations between stroke patients with new AF, without AF and with AF already known before the stroke.Results582 patients were included (median age 68 years; 63.2% male). AF was present in 109/582 patients [(18.7%); new AF: 39/109 (35.8%), known AF: 70/109 (64.2%)]. AF patients had larger infarct volumes than patients without AF (mean: 29.7 ± 45.8 ml vs. 15.2 ± 35.1 ml; p<0.001). Lesions in AF patients accumulated in the right central middle cerebral artery territory. Increasing stroke size predicted progressive cortical but not pontine and thalamic involvement. Patients with new AF had more frequently lesions in the right insula compared to patients without AF when stroke size was not accounted for, but no specific brain region was more frequently involved after adjustment for infarct volume. Controlled for stroke size, left parietal involvement was less likely for patients with new AF than for those without AF or with known AF.ConclusionsIn the search for brain areas potentially triggering cardiac arrhythmias infarct size should be accounted for. After controlling for infarct size, there is currently no evidence that ischemic stroke lesions of specific brain areas are associated with new AF compared to patients without AF. This challenges the neurogenic hypothesis of AF according to which a relevant proportion of new AF is triggered by ischemic brain lesions of particular locations.
Purrucker JC, Rizos T, Haas K, et al., 2017, Coagulation testing in intracerebral hemorrhage related to non-vitamin K antagonist oral anticoagulants, Neurocritical Care, Vol: 27, Pages: 208-213, ISSN: 1556-0961
BACKGROUND: Intracerebral hemorrhage (ICH) is a life-threatening complication of non-vitamin K antagonist oral anticoagulants (NOAC). Little is known about the effect of intensity of anticoagulation on NOAC-ICH. We describe the current use of coagulation testing in the emergency setting and explore associations with baseline size and expansion of hematoma as determined in a previous study. METHODS: Data from the prospective multicenter RASUNOA registry were analyzed. Patients with NOAC-ICH were enrolled between February 2012 and December 2014. Frequency of local test performance of specific (anti-factor Xa tests, diluted thrombin time) and non-specific tests (international normalized ratio (INR), activated partial thromboplastin time (aPTT), thrombin time) was analyzed. The association of anticoagulation intensity at admission with hematoma volume and hematoma expansion was explored. RESULTS: In 61 NOAC-ICH patients enrolled at 21 centers, drug-specific coagulation testing was performed in 16 cases (26%), and only 29% of centers appeared to use drug-specific tests in NOAC-ICH at all. In some cases, INR and aPTT values were normal despite drug concentrations in the peak range. In patients with available drug-specific concentrations, 50% had drug levels in the peak range at admission. Higher intensity of anticoagulation was not associated with higher hematoma volume at admission or with subsequent hematoma expansion. CONCLUSION: Drug-specific tests are only infrequently used in NOAC-ICH. Normal results in non-specific coagulation do not reliably rule out peak range concentrations. Anticoagulation intensity at admission does not predict baseline hematoma volume or subsequent hematoma expansion.
Steiner T, Weitz JI, Veltkamp R, 2017, Anticoagulant-associated intracranial hemorrhage in the era of reversal agents, Stroke, Vol: 48, Pages: 1432-1437, ISSN: 0039-2499
Wilson D, Seiffge DJ, Traenka C, et al., 2017, Outcome of intracerebral hemorrhage associated with different oral anticoagulants, Neurology, Vol: 88, Pages: 1693-1700, ISSN: 0028-3878
Objective: In an international collaborative multicenter pooled analysis, we compared mortality, functional outcome, intracerebral hemorrhage (ICH) volume, and hematoma expansion (HE) between non–vitamin K antagonist oral anticoagulation–related ICH (NOAC-ICH) and vitamin K antagonist–associated ICH (VKA-ICH).Methods: We compared all-cause mortality within 90 days for NOAC-ICH and VKA-ICH using a Cox proportional hazards model adjusted for age; sex; baseline Glasgow Coma Scale score, ICH location, and log volume; intraventricular hemorrhage volume; and intracranial surgery. We addressed heterogeneity using a shared frailty term. Good functional outcome was defined as discharge modified Rankin Scale score ≤2 and investigated in multivariable logistic regression. ICH volume was measured by ABC/2 or a semiautomated planimetric method. HE was defined as an ICH volume increase >33% or >6 mL from baseline within 72 hours.Results: We included 500 patients (97 NOAC-ICH and 403 VKA-ICH). Median baseline ICH volume was 14.4 mL (interquartile range [IQR] 3.6–38.4) for NOAC-ICH vs 10.6 mL (IQR 4.0–27.9) for VKA-ICH (p = 0.78). We did not find any difference between NOAC-ICH and VKA-ICH for all-cause mortality within 90 days (33% for NOAC-ICH vs 31% for VKA-ICH [p = 0.64]; adjusted Cox hazard ratio (for NOAC-ICH vs VKA-ICH) 0.93 [95% confidence interval (CI) 0.52–1.64] [p = 0.79]), the rate of HE (NOAC-ICH n = 29/48 [40%] vs VKA-ICH n = 93/140 [34%] [p = 0.45]), or functional outcome at hospital discharge (NOAC-ICH vs VKA-ICH odds ratio 0.47; 95% CI 0.18–1.19 [p = 0.11]).Conclusions: In our international collaborative multicenter pooled analysis, baseline ICH volume, hematoma expansion, 90-day mortality, and functional outcome were similar following NOAC-ICH and VKA-ICH.
Elkins J, Veltkamp R, Montaner J, et al., 2017, Safety and efficacy of natalizumab in patients with acute ischaemic stroke (ACTION): a randomised, placebo-controlled, double-blind phase 2 trial, Lancet Neurology, Vol: 16, Pages: 217-226, ISSN: 1474-4422
BackgroundIn animal models of acute ischaemic stroke, blocking of the leukocyte-endothelium adhesion by antagonism of α4 integrin reduces infarct volumes and improves outcomes. We assessed the effect of one dose of natalizumab, an antibody against the leukocyte adhesion molecule α4 integrin, in patients with acute ischaemic stroke.MethodsIn this double-blind, phase 2 study, patients with acute ischaemic stroke (aged 18–85 years) from 30 US and European clinical sites were randomly assigned (1:1) to 300 mg intravenous natalizumab or placebo with stratification by treatment window and baseline infarct size. Patients, investigators, and study staff were masked to treatment assignments. The primary endpoint was the change in infarct volume from baseline to day 5 and was assessed in the modified intention-to-treat population. Secondary endpoints were the change in infarct volume from baseline to day 30, and from 24 h to days 5 and 30; the National Institute of Health Stroke Scale (NIHSS) at baseline, 24 h, and at days 5 (or discharge), 30, and 90; and modified Rankin Scale (mRS) and Barthel Index (BI) at days 5 (or discharge), 30, and 90. This trial is registered with ClinicalTrials.gov, number NCT01955707.FindingsBetween Dec 16, 2013, and April 9, 2015, 161 patients were randomly assigned to natalizumab (n=79) or placebo (n=82). Natalizumab did not reduce infarct volume growth from baseline to day 5 compared with placebo (median absolute growth 28 mL [range −8 to 303] vs 22 mL [−11 to 328]; relative growth ratio 1·09 [90% CI 0·91–1·30], p=0·78) or to day 30 (4 mL [−43 to 121] vs 4 mL [−28 to 180]; 1·05 [0·88–1·27], p=0·68), from 24 h to day 5 (8 mL [−30 to 177] vs 7 mL [−13 to 204]; 1·00 [0·89–1·12], p=0·49), and from 24 h to day 30 (−5 mL [−93 to 81] vs −5 mL [−48 to 48]; 0·98 [0&middo
Uhlmann S, Mracsko E, Javidi E, et al., 2017, Genome-wide analysis of the circulating miRNome after cerebral ischemia reveals a reperfusion-induced microRNA cluster, Stroke, Vol: 48, Pages: 762-769, ISSN: 0039-2499
Background and Purpose—Circulating microRNAs (miRNAs) are emerging biomarkers for stroke because of their high stability in the bloodstream and association with pathophysiologic conditions. However, the circulating whole-genome miRNAs (miRNome) has not been characterized comprehensively in the acute phase of stroke.Methods—We profiled the circulating miRNome in mouse models of acute ischemic and hemorrhagic stroke by next-generation sequencing. Stroke models were compared with sham-operated and naive mice to identify deregulated circulating miRNAs. Top-ranked miRNAs were validated and further characterized by quantitative reverse transcription polymerase chain reaction.Results—We discovered 24 circulating miRNAs with an altered abundance in the circulation 3 hours after ischemia, whereas the circulating miRNome was not altered after intracerebral hemorrhage compared with sham-operated mice. Among the upregulated miRNAs in ischemia, the top-listed miR-1264/1298/448 cluster was strongly dependent on reperfusion in different ischemia models. A time course experiment revealed that the miR-1264/1298/448 cluster peaked in the circulation around 3 hours after reperfusion and gradually decreased thereafter.Conclusions—Alteration of the miRNome in the circulation is associated with cerebral ischemia/reperfusion, but not hemorrhage, suggesting a potential to serve as biomarkers for reperfusion in the acute phase. The pathophysiological role of reperfusion-inducible miR-1264/1298/448 cluster, which is located on chromosome X within the introns of the serotonin receptor HTR2C, requires further investigation.
Purrucker JC, Haas K, Wolf M, et al., 2017, Haernorrhagic transformation after ischaemic stroke in patients taking non-vitamin K antagonist oral anticoagulants, Journal of Stroke, Vol: 19, Pages: 67-76, ISSN: 2287-6391
J Stroke > Volume 19(1); 2017 > Article Original ArticleJournal of Stroke 2017;19(1):67-76.Published online: January 31, 2017DOI: https://doi.org/10.5853/jos.2016.00542Haemorrhagic Transformation after Ischaemic Stroke in Patients Taking Non-vitamin K Antagonist Oral AnticoagulantsJan C. Purruckera, Kirsten Haasb, Marcel Wolfc, Timolaos Rizosa, Shujah Khana, Peter Kraftd, Sven Polie, Rainer Dziewasf, Johannes Meyneg, Frederick Palmh, Sebastian Janderi, Markus Möhlenbruchc, Peter U. Heuschmannb,j, Roland Veltkampa,k, on behalf of the, RASUNOA investigatorsaDepartment of Neurology, Heidelberg University Hospital, Heidelberg, GermanybInstitute of Clinical Epidemiology and Biometry, University Würzburg, GermanycDepartment of Neuroradiology, Heidelberg University Hospital, Heidelberg, GermanydDepartment of Neurology, University Hospital Würzburg, Würzburg, GermanyeDepartment of Neurology, Tübingen University, Tübingen, GermanyfDepartment of Neurology, University Hospital Münster, GermanygDepartment of Neurology, University Hospital Schleswig-Holstein, Kiel, GermanyhDepartment of Neurology, Klinikum Ludwigshafen, Ludwigshafen, GermanyiDepartment of Neurology, Heinrich-Heine-University, Medical Faculty, Düsseldorf, GermanyjComprehensive Heart Failure Center, and Clinical Trial Center, University Hospital Würzburg, Würzburg, GermanykDepartment of Stroke Medicine, Imperial College London, London, United GermanyCorrespondence: Roland Veltkamp Department of Stroke Medicine, Imperial College London, Charing Cross Campus, 3 East 6, Fulham Palace Road, London, W6 8RF, United Kingdom Phone: +44-20-33130133, Fax: +44-20-83833309, E-mail: r.veltkamp@imperial.ac.ukReceived June 16, 2016 Revised October 11, 2016 Accepted November 28, 2016Copyright © 2017 Korean Stroke SocietyThis is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://c
Mracsko E, Stegemann-Koniszewski S, Na S-Y, et al., 2017, A mouse model of post-stroke pneumonia induced by intra-tracheal inoculation with Streptococcus pneumoniae, Cerebrovascular Diseases, Vol: 43, Pages: 99-109, ISSN: 1015-9770
Background: Stroke-induced immunodeficiency increases the risk of infectious complications, which adversely affects neurological outcome. Among those, pneumonia affects as many as one third of stroke patients and is the main contributor to mortality in the post-acute phase of stroke. Experimental findings on post-stroke susceptibility to spontaneous pneumonia in mice are contradictory. Here, we established a mouse model inducing standardized bacterial pneumonia and characterized the impaired pulmonary cellular and humoral immune responses after experimental stroke. Methods: Bacterial pneumonia was induced by intra-tracheal inoculation with Streptococcus pneumoniae at different time points after transient middle cerebral artery occlusion (MCAO). Bacterial counts in lungs and blood, histological changes, and cytokine production in the lungs were assessed. Furthermore, we investigated the effect of pneumonia on stroke outcome. Results: Intra-tracheal inoculation resulted in reproducible pneumonia and bacteraemia, and demonstrated post-stroke susceptibility to streptococcal pneumonia developing with a delay of at least 24 h after MCAO. Higher bacterial counts in mice infected 3 days after stroke induction correlated with reduced neutrophil and macrophage infiltration in the lungs and lower levels of pro-inflammatory cytokines in the broncho-alveolar lavage compared to sham-operated animals. Pneumonia increased mortality without affecting brain-infiltrating leukocytes. Conclusions: In this standardized mouse model of post-stroke pneumonia, we describe attenuated leukocyte infiltration and cytokine production in response to bacterial infection in the lungs that has a profound effect on outcome.
Purrucker JC, Haas K, Rizos T, et al., 2016, Coagulation Testing in Acute Ischemic Stroke Patients Taking Non-Vitamin K Antagonist Oral Anticoagulants, Stroke, Vol: 48, Pages: 152-158, ISSN: 0039-2499
Background and Purpose—In patients who present with acute ischemic stroke while on treatment with non–vitamin K antagonist oral anticoagulants (NOACs), coagulation testing is necessary to confirm the eligibility for thrombolytic therapy. We evaluated the current use of coagulation testing in routine clinical practice in patients who were on NOAC treatment at the time of acute ischemic stroke.Methods—Prospective multicenter observational RASUNOA registry (Registry of Acute Stroke Under New Oral Anticoagulants; February 2012–2015). Results of locally performed nonspecific (international normalized ratio, activated partial thromboplastin time, and thrombin time) and specific (antifactor Xa tests, hemoclot assay) coagulation tests were documented. The implications of test results for thrombolysis decision-making were explored.Results—In the 290 patients enrolled, nonspecific coagulation tests were performed in ≥95% and specific coagulation tests in 26.9% of patients. Normal values of activated partial thromboplastin time and international normalized ratio did not reliably rule out peak drug levels at the time of the diagnostic tests (false-negative rates 11%–44% [95% confidence interval 1%–69%]). Twelve percent of patients apparently failed to take the prescribed NOAC prior to the acute event. Only 5.7% (9/159) of patients in the 4.5-hour time window received thrombolysis, and NOAC treatment was documented as main reason for not administering thrombolysis in 52.7% (79/150) of patients.Conclusions—NOAC treatment currently poses a significant barrier to thrombolysis in ischemic stroke. Because nonspecific coagulation test results within normal range have a high false-negative rate for detection of relevant drug concentrations, rapid drug-specific tests for thrombolysis decision-making should be established.
Geraghty O, Korompoki E, Filippidis FT, et al., 2016, Cardiac diagnostic work-up for atrial fibrillation after transient ischaemic attacks in England and Wales: results from a cross-sectional survey, BMJ Open, Vol: 6, ISSN: 2044-6055
Objectives Transient ischaemic attacks (TIAs) are an important precursor of stroke. Atrial fibrillation (AF) is among the most dangerous aetiologies shared between TIAs and strokes. Detection of AF after TIAs is essential for the initiation of oral anticoagulants. We aimed to identify variations in the use of cardiac investigations used to detect AF and cardiac pathology in patients with TIA in the UK.Setting All TIA clinical leads in England and Wales received an invitation by email to participate in an online survey in February 2015. The questionnaire consisted of 36 multiple choice questions covering the domains: (1) general information about stroke units, (2) ECG diagnostics and cardiologic work-up and (3) management of AF.Results 146 survey invitations were sent. The response rate was 40% (n=59). Diagnosis of AF largely depends on medical history and 12-channel ECG which is performed in the vast majority of patients with TIA (>75%) in 94.1% of the TIA services. Many patients with TIA either do not receive 24-hour Holter recording (requested regularly in 42% of the services) or only after considerable delay (>2 weeks). Prolonged event recording is only rarely performed (16%). Only about half of patients with TIA undergo echocardiography. Cranial imaging in patients with TIA is mainly performed as CT (62%). The majority of TIA clinics rapidly initiate anticoagulation in TIA patients with AF (81.6%) preferably using new oral anticoagulants (75.5%).Conclusions Significant variation in the cardiac diagnostic work-up following TIA exists regarding the use of particular detection techniques and the duration of cardiac ECG monitoring. Only limited resources are allocated to cardiac evaluation. In addition to research establishing the optimal ECG technique for patients with TIA, healthcare delivery programmes are needed to ensure proper management to prevent strokes.
Giustino G, Mehran R, Veltkamp R, et al., 2016, Neurologic Outcomes with Embolic Protection Devices in Patients Undergoing Transcatheter Aortic Valve Replacement: A Systematic Review and Meta-Analysis of Randomized Controlled Trials, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 68, Pages: B266-B267, ISSN: 0735-1097
Wilson D, Seiffge D, Traenka C, et al., 2016, Clinical and radiological outcome after Non-vitamin K Oral AntiCoagulant-associated IntraCerebral Haemorrhage (NOAC-ICH) compared to Vitamin K Antagonist-associated IntraCerebral Haemorrhage (VKA-ICH): Multicentre international collaborative pooled analysis, Publisher: SAGE PUBLICATIONS LTD, Pages: S46-S46, ISSN: 1747-4930
Rizos T, Jenetzky E, Beynon C, et al., 2016, Reversing oral anticoagulation in non-traumatic intracerebral hemorrhage with prothrombin complex concentrate - a cohort study on the incidence of adverse events, International Journal of Stroke, Vol: 11, Pages: 95-95, ISSN: 1747-4930
Rizos T, Bartsch AJ, Johnson TD, et al., 2016, Are infarcts in stroke patients with newly diagnosed atrial fibrillation trigger of the arrhythmia or only target of embolism?, International Journal of Stroke, Vol: 11, Pages: 69-69, ISSN: 1747-4930
Giustino G, Mehran R, Veltkamp R, et al., 2016, Neurological outcomes with embolic protection devices in patients undergoing transcatheter aortic valver replacement a systematic review and meta-analysis of randomized controlled trials, JACC: Cardiovascular Interventions, Vol: 9, Pages: 2124-2133, ISSN: 1936-8798
ObjectivesThe aim of this study was to investigate the efficacy and safety of intraprocedural embolic protection (EP) during transcatheter aortic valve replacement (TAVR).BackgroundRandomized controlled trials (RCTs) investigating the efficacy of EP devices during TAVR were relatively underpowered.MethodsA systematic review and study-level meta-analysis was performed of randomized controlled trials that tested the efficacy and safety of EP during TAVR. Trials using any type of EP and TAVR vascular access were included. Primary imaging efficacy endpoints were total lesion volume and number of new ischemic lesions. Primary clinical efficacy endpoints were any deterioration in National Institutes of Health Stroke Scale and Montreal Cognitive Assessment scores at hospital discharge. Primary analyses were performed using the intention-to-treat approach.ResultsFour randomized clinical trials (total n = 252) were included. Use of EP was associated with lower total lesion volume (standardized mean difference −0.65; 95% confidence interval [CI]: −1.06 to −0.25; p = 0.002) and smaller number of new ischemic lesions (standardized mean difference −1.27; 95% CI: −2.45 to −0.09; p = 0.03). EP was associated with a trend toward lower risk for deterioration in National Institutes of Health Stroke Scale score at discharge (risk ratio: 0.55; 95% CI: 0.27 to 1.09; p = 0.09) and higher Montreal Cognitive Assessment score (standardized mean difference 0.40; 95% CI: 0.04 to 0.76; p = 0.03). Risk for overt stroke and all-cause mortality were nonsignificantly lower in the EP group.ConclusionsUse of EP seems to be associated with reductions in imaging markers of cerebral infarction and early clinical neurological effectiveness in patients undergoing TAVR.
Steiner T, Poli S, Huesing J, et al., 2016, Haematoma expansion and vitamin K antagonist reversal - authors' reply, Lancet Neurology, Vol: 15, Pages: 1117-1117, ISSN: 1474-4465
Korompoki E, Del Giudice A, Hillmann S, et al., 2016, Cardiac monitoring for detection of atrial fibrillation after TIA: A systematic review and meta-analysis, International Journal of Stroke, Vol: 12, Pages: 33-45, ISSN: 1747-4930
Background and purposeThe detection rate of atrial fibrillation has not been studied specifically in transient ischemic attack (TIA) patients although extrapolation from ischemic stroke may be inadequate. We conducted a systematic review and meta-analysis to determine the rate of newly diagnosed atrial fibrillation using different methods of ECG monitoring in TIA.MethodsA comprehensive literature search was performed following a pre-specified protocol the PRISMA statement. Prospective observational studies and randomized controlled trials were considered that included TIA patients who underwent cardiac monitoring for >12 h. Primary outcome was frequency of detection of atrial fibrillation ≥30 s. Analyses of subgroups and of duration and type of monitoring were performed.ResultsSeventeen studies enrolling 1163 patients were included. The pooled atrial fibrillation detection rate for all methods was 4% (95% CI: 2–7%). Yield of monitoring was higher in selected (higher age, more extensive testing for arrhythmias before enrolment, or presumed cardioembolic/cryptogenic cause) than in unselected cohorts (7% vs 3%). Pooled mean atrial fibrillation detection rates rose with duration of monitoring: 4% (24 h), 5% (24 h to 7 days) and 6% (>7 days), respectively. Yield of non-invasive was significantly lower than that of invasive monitoring (4% vs. 11%). Significant heterogeneity was observed among studies (I2=60.61%).ConclusionThis first meta-analysis of atrial fibrillation detection in TIA patients finds a lower atrial fibrillation detection rate in TIA than reported for IS and TIA cohorts in previous meta-analyses. Prospective studies are needed to determine actual prevalence of atrial fibrillation and optimal diagnostic procedure for atrial fibrillation detection in TIA.
Laible M, Mohlenbruch M, Horstmann S, et al., 2016, Peri-procedural silent cerebral infarcts after left atrial appendage occlusion, European Journal of Neurology, Vol: 24, Pages: 53-57, ISSN: 1351-5101
Background and purposeTo determine the rate of peri-interventional silent brain infarcts after left atrial appendage occlusion (LAAO).MethodsIn this prospective, uncontrolled single-center pilot study, consecutive patients with atrial fibrillation undergoing LAAO between July 2013 and January 2016 were included. The Amplatzer Cardiac Plug, WATCHMAN or Amulet device was used. A neurological examination and cranial magnetic resonance imaging (MRI) were performed within 48 h before and after the procedure. MRI was evaluated for new diffusion-weighted imaging (DWI) hyperintensities, cerebral microbleeds (CMBs) and white-matter lesions (WMLs).ResultsLeft atrial appendage occlusion was performed in 21 patients (mean age, 73.2 ± 9.5 years). Main reasons for LAAO were previous intracerebral hemorrhage (n = 11) and major systemic bleeding (n = 6). No clinically overt stroke occurred peri-interventionally. After the intervention, one patient had a small cerebellar hyperintensity on DWI (4.8%; 95% confidence interval, 0.0–14.3) that was not present on the MRI 1 day before the procedure. Among 11 patients with available MRI just before LAAO, there were no significant changes in the number of CMBs and the severity of WMLs after LAAO.ConclusionsThis study of peri-interventional MRI in LAAO suggests a low rate of silent peri-procedural infarcts in this elderly population. Confirmation in larger studies is needed.
Wilson D, Charidimou A, Ambler G, et al., 2016, Recurrent stroke risk and cerebral microbleed burden in ischemic stroke and TIA A meta-analysis, Neurology, Vol: 87, Pages: 1501-1510, ISSN: 1526-632X
Objective: To determine associations between cerebral microbleed (CMB) burden with recurrent ischemic stroke (IS) and intracerebral hemorrhage (ICH) risk after IS or TIA.Methods: We identified prospective studies of patients with IS or TIA that investigated CMBs and stroke (ICH and IS) risk during ≥3 months follow-up. Authors provided aggregate summary-level data on stroke outcomes, with CMBs categorized according to burden (single, 2–4, and ≥5 CMBs) and distribution. We calculated absolute event rates and pooled risk ratios (RR) using random-effects meta-analysis.Results: We included 5,068 patients from 15 studies. There were 115/1,284 (9.6%) recurrent IS events in patients with CMBs vs 212/3,781 (5.6%) in patients without CMBs (pooled RR 1.8 for CMBs vs no CMBs; 95% confidence interval [CI] 1.4–2.5). There were 49/1,142 (4.3%) ICH events in those with CMBs vs 17/2,912 (0.58%) in those without CMBs (pooled RR 6.3 for CMBs vs no CMBs; 95% CI 3.5–11.4). Increasing CMB burden increased the risk of IS (pooled RR [95% CI] 1.8 [1.0–3.1], 2.4 [1.3–4.4], and 2.7 [1.5–4.9] for 1 CMB, 2–4 CMBs, and ≥5 CMBs, respectively) and ICH (pooled RR [95% CI] 4.6 [1.9–10.7], 5.6 [2.4–13.3], and 14.1 [6.9–29.0] for 1 CMB, 2–4 CMBs, and ≥5 CMBs, respectively).Conclusions: CMBs are associated with increased stroke risk after IS or TIA. With increasing CMB burden (compared to no CMBs), the risk of ICH increases more steeply than that of IS. However, IS absolute event rates remain higher than ICH absolute event rates in all CMB burden categories.
Hart RG, Sharma M, Mundl H, et al., 2016, Rivaroxaban for secondary stroke prevention in patients with embolic strokes of undetermined source: Design of the NAVIGATE ESUS randomized trial, EUROPEAN STROKE JOURNAL, Vol: 1, Pages: 146-154, ISSN: 2396-9873
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