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9 results

  • Chapter 21 - Cervical Artery Dissection and Cerebral Vasculitis

  • from Part V - Prevention
  • Edited by Jeffrey L. Saver, Graeme J. Hankey, University of Western Australia, Perth
  • Book:
    Stroke Prevention and Treatment
    Published online:
    15 December 2020
    Print publication:
    10 December 2020, pp 450-462

  • Summary

    Cervical artery dissection (CAD) is characterized by an intramural haematoma due to a subintimal tear and accounts for up to 25% of ischaemic strokes in young and middle-aged adults. Data regarding intravenous thrombolysis and endovascular thrombectomy in CAD are scarce and observational – both are reasonably safe and probably recommended. Based on observational evidence, antithrombotic therapy is used to prevent first or recurrent cerebral ischaaemic events in acute or subacute CAD, and event rates are low with either antiplatelet or anticoagulant therapy. The long-term rate of recurrent cerebral ischaemic events or bleeding complications in CAD patients is small while under antithrombotic treatment. Cerebral vasculitis treatment is based on observational series. When primary angiitis of the central nervous system is confirmed by biopsy, a combination of glucocorticoids and cyclophosphamide should be started. Rituximab may be used in patients who are intolerant of cyclophosphamide. In atypical, non-biopsy-proven cases, treatment should be adapted to the severity of neurological involvement. For giant cell arteritis, initial high-dose prednisolone is recommended, beginning a slow taper after 2–4 weeks and continuing at a low dose for 1–2 years. Treatment of p-ANCA-positive and -negative systemic vasculitis with cerebral involvement includes induction corticosteroid therapy followed by addition of cyclophosphamide or other glucocorticoid-sparing drugs.

  • Preclinical studies of RUC-4, a novel platelet αIIbβ3 antagonist, in non-human primates and with human platelets

  • Spandana Vootukuri, Jihong Li, Mark Nedelman, Craig Thomas, Jiang-Kang Jiang, Mariana Babayeva, Barry S. Coller
  • Journal:
    Journal of Clinical and Translational Science / Volume 3 / Issue 2-3 / June 2019
    Published online by Cambridge University Press:
    28 June 2019, pp. 65-74
    • Article
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  • Introduction:

    We are developing the novel αIIbβ3 antagonist, RUC-4, for subcutaneously (SC)-administered first-point-of-medical-contact treatment for ST segment elevation myocardial infarction (STEMI).

    Methods:

    We studied the (1) pharmacokinetics (PK) of RUC-4 at 1.0, 1.93, and 3.86 mg/kg intravenous (IV), intramuscular (IM), and SC in non-human primates (NHPs); (2) impact of aspirin on RUC-4 IC50 in human platelet-rich plasma (PRP); (3) effect of different anticoagulants on the RUC-4 IC50 in human PRP; and (4) relationship between αIIbβ3 receptor blockade by RUC-4 and inhibition of ADP-induced platelet aggregation.

    Results:

    (1) All doses of RUC-4 were well tolerated, but animals demonstrated variable temporary bruising. IM and SC RUC-4 reached dose-dependent peak levels within 5–15 minutes, with T1/2 s between 0.28 and 0.56 hours. Platelet aggregation studies in NHPs receiving IM RUC-4 demonstrated >80% inhibition of the initial slope of ADP-induced aggregation with all three doses 30 minutes post-dosing, with subsequent dose-dependent loss of inhibition over 4–5 hours. (2) The RUC-4 IC50 for ADP-induced platelet aggregation was unaffected by aspirin treatment (40±9 nM vs 37±5 nM; p = 0.39). (3) The RUC-4 IC50 was significantly higher in PRP prepared from D-phenylalanyl-prolyl-arginyl chloromethyl ketone (PPACK)-anticoagulated blood compared to citrate-anticoagulated blood using either thrombin receptor activating peptide (TRAP) (122±17 vs 66±25 nM; p = 0.05; n = 4) or ADP (102±22 vs 54±13; p<0.001; n = 5). (4) There was a close correspondence between receptor blockade and inhibition of ADP-induced platelet aggregation, with aggregation inhibition beginning with ~40% receptor blockade and becoming nearly complete at >80% receptor blockade.

    Discussion:

    Based on these results and others, RUC-4 has now progressed to formal preclinical toxicology studies.

  • Efficacy of platelet transfusion for acute intracerebral hemorrhage among patients on antiplatelet therapy

  • Onyinyechi Eke, Mercedeh Shanechi, Michael Gottlieb
  • Journal:
    Canadian Journal of Emergency Medicine / Volume 20 / Issue S2 / October 2018
    Published online by Cambridge University Press:
    14 February 2018, pp. S78-S81
    Print publication:
    October 2018
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  • Clinical question

    In patients taking antiplatelet therapy, does a platelet transfusion after acute spontaneous primary intracerebral hemorrhage reduce the risk of death or dependence?

    Article chosen

    Baharoglu MI, Cordonnier C, Al-Shahi Salman R, et al. Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral hemorrhage associated with antiplatelet therapy (PATCH): a randomized, open-label, phase 3 trial. Lancet 2016;387(10038):2605-13.

    Study objective

    The primary objective of this study was to investigate whether a platelet transfusion with standard care, compared with standard care alone, reduced death or dependence after intracerebral hemorrhage associated with antiplatelet therapy use.

  • Safety of Early Pharmacological Thromboprophylaxis after Subarachnoid Hemorrhage

  • Part of
  • Airton Leonardo de Oliveira Manoel, David Turkel-Parrella, Menno Germans, Ekaterina Kouzmina, Priscila da Silva Almendra, Thomas Marotta, Julian Spears, Simon Abrahamson
  • Journal:
    Canadian Journal of Neurological Sciences / Volume 41 / Issue 5 / September 2014
    Published online by Cambridge University Press:
    30 October 2014, pp. 554-561
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  • Objective

    The recent guidelines on management of aneurysmal subarachnoid hemorrhage (aSAH) advise pharmacological thromboprophylaxis (PTP) after aneurysm obliteration. However, no study has addressed the safety of PTP in the aSAH population. Therefore, the aim of this study was to assess the safety of early PTP after aSAH.

    Methods

    Retrospective cohort of aSAH patients admitted between January 2012 and June 2013 in a single high-volume aSAH center. Traumatic SAH and perimesencephalic hemorrhage patients were excluded. Patients were grouped according to PTP timing: early PTP group (PTP within 24 hours of aneurysm treatment), and delayed PTP group (PTP started > 24 hours).

    Results

    A total of 174 SAH patients (mean age 56.3±12.5 years) were admitted during the study period. Thirty-nine patients (22%) did not receive PTP, whereas 135 patients (78%) received PTP after aneurysm treatment or negative angiography. Among the patients who received PTP, 65 (48%) had an external ventricular drain. Twenty-eight patients (21%) received early PTP, and 107 (79%) received delayed PTP. No patient in the early treatment group and three patients in the delayed PTP group developed an intracerebral hemorrhagic complication. Two required neurosurgical intervention and one died. These three patients were on concomitant PTP and dual antiplatelet therapy.

    Conclusions

    The initiation of PTP within 24 hours may be safe after the treatment of a ruptured aneurysm or in angiogram-negative SAH patients with diffuse aneurysmal hemorrhage pattern. We suggest caution with concomitant use of PTP and dual antiplatelet agents, because it possibly increases the risk for intracerebral hemorrhage.

  • Case 25 - Postoperativenormal perfusion pressure breakthrough

  • from Section I - Neuroanesthesia
  • Edited by George A. Mashour, Ehab Farag
  • Book:
    Case Studies in Neuroanesthesia and Neurocritical Care
    Published online:
    03 May 2011
    Print publication:
    03 February 2011, pp 83-84

  • Summary

    The increasing use of coronary artery angioplasty with deployment of stents for treatment of coronary artery disease poses several dilemmas for perioperative management. These conflicting requirements are manifested most acutely in the management of patients with neurovascular disease. This chapter presents a case study of a 51-year-old female with a past medical history of ischemic heart disease, hypertension, and undifferentiated autoimmune disease with interstitial lung involvement, as an example. The presence of coronary stents in patients undergoing neurosurgical procedures warrants specific consideration prior to anesthesia. It is necessary to balance the risks of stent thrombosis, and the subsequent risk of myocardial infarction, arrhythmia, or cardiac arrest, against the risks of hemorrhage during or after a neurosurgical procedure. There is currently an irresolvable conflict between the risks of with holding and continuing antiplatelet agents in the perioperative period.

  • Chapter 35 - Poisoning

  • from Section III: - Organ dysfunction and management
  • Edited by Fang Gao Smith, University of Warwick
  • Edited in association with Joyce Yeung
  • Book:
    Core Topics in Critical Care Medicine
    Published online:
    06 July 2010
    Print publication:
    22 April 2010, pp 275-283

  • Summary

    Patients with acute coronary syndrome (ACS) are classified into ST segment elevation myocardial infarction (MI), and non-ST segment elevation MI. An ECG should be obtained on admission and the ST segments are monitored. Patients with ST segment depression have a poorer prognosis when compared with patients with T wave abnormalities. An elevation in biomarkers indicates myocardial necrosis. The preferred biomarker is cardiac troponin (I or T) which has a sensitivity of 100% 6 hours after the onset of MI. Creatine kinase CK-MB is the best alternative when troponin is either unsuitable or not available. This chapter discusses management of ST-elevation ACS using percutaneous coronary intervention (PCI) or fibrinolysis, heparin, antiplatelet therapy, rescue PCI, and surgical revascularization. Non-ST-elevation ACS management strategy is based on low-risk patients, and intermediate and high risk patients. Oxygen and pain relief are given to all the patients along with an antiemetic agent in adjunctive therapy.

  • 4 - Hematological processes in emboli formation

  • from Background
  • Edited by Jonathan Gillard, University of Cambridge, Martin Graves, University of Cambridge, Thomas Hatsukami, University of Washington, Chun Yuan, University of Washington
  • Book:
    Carotid Disease
    Published online:
    03 December 2009
    Print publication:
    07 December 2006, pp 45-58

  • Summary

    This chapter outlines the hemostatic response to vascular damage in the carotid artery and considers the endogenous hemostatic factors that may determine the likelihood of embolization in patients. It discusses the mechanisms involved in thrombus formation and stabilization. Platelets provide a reinforced loop in the generation of a thrombus, providing a source of thrombin to recruit new platelets and propagate clot formation. The mechanism of stabilization of a thrombus by P-selectin appears to be partly stabilization of platelet-platelet aggregates but mostly through recruitment of leucocytes via interaction of P-selectin with PSGL-1. Many factors are involved in forming a stable thrombus and consequently there are many candidates for regulating the risk of embolization. Antiplatelet and antithrombotic therapies are of benefit in limiting the growth of thrombus within the carotid vessel. In particular, adenosine diphosphate (ADP) seems to have a very specific role in regulating embolization.

  • 12 - Prevention of coronary heart disease in women

  • from Part III - Disease prevention
  • Edited by Jo Ann Rosenfeld, The Johns Hopkins University
  • Book:
    Women's Health in Mid-Life
    Published online:
    21 August 2009
    Print publication:
    25 March 2004, pp 209-224

  • Summary

    Cardiovascular disease (CVD) is the major cause of death in women in the USA and in the UK. The actual value of the risk factors is used to predict coronary heart disease (CHD) risk more accurately. Primary prevention should focus on the major risk factors of passive and active smoking, systolic and diastolic hypertension, elevated serum total and low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, diabetes, physical inactivity, and obesity. The pillars of secondary prevention are antiplatelet therapy, beta-blockers, angiotensin-converting enzyme inhibitors (ACEIs), statins, cardiac rehabilitation, a Mediterranean diet, and folic acid. Future heart attacks are prevented by the prevention of atherosclerosis or plaque formation in the coronary arteries and by the stabilization and regression of existing plaque through lifestyle modification and medication. Women must take personal preventive action to prevent CHD death and disability by working to prevent plaque formation, and promote stabilization of existing atherosclerotic disease.