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Arterial Thrombosis—Diagnosis and Management
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
H. Patrick McNeil, Steven A. Krilis, Colin N. Chesterman
The major use of heparin for the treatment of acute arterial thrombosis is in certain types of stroke, in unstable angina and as adjunctive treatment following thrombolytic therapy to prevent rethrombosis. In stroke, the two major indications are in “progressing stroke” or in strokes due to cardiac emboli.76 There are no studies which prove the efficacy of heparin in “progressing stroke”, but since this syndrome is usually caused by thrombosis of carotid or basilar arteries, there are sound reasons to expect benefits. In the future, tissue plasminogen activator may be more effective in this situation. In stroke due to cardiac emboli, a common cause in aPL-associated syndromes, heparin therapy followed by warfarin has been shown in a number of studies to reduce the risk of further embolization by approximately 66%,76 but cerebral hemorrhage or edema should be excluded by CT scanning, and large infarcts which may become hemorrhagic are generally considered contraindications to anticoagulation.77 Heparin therapy has recently been shown to be highly effective in preventing myocardial infarction and death in unstable angina.78
Venous Thrombosis
Published in Hau C. Kwaan, Meyer M. Samama, Clinical Thrombosis, 2019
Gary E. Raskob, Russell D. Hull
The thrombolytic agents currently available for clinical use are streptokinase and urokinase. Streptokinase, a product of hemolytic streptococci, is antigenic in man and stimulates the production of neutralizing antibodies. Streptokinase complexes with plasminogen to form a plasminogen-streptokinase complex, which then acts on uncomplexed plasminogen to produce plasmin. Urokinase is a naturally occurring activator of plasminogen produced by renal parenchymal cells and is present in human urine. Streptokinase (or urokinase) is more effective than heparin for inducing rapid resolution of recent pulmonary embolism or venous thrombosis.175–186 Newer thrombolytic agents such as tissue plasminogen activator are currently undergoing clinical evaluation; these agents may simplify thrombolytic therapy and prove safer than currently available thrombolytic drugs. (See Chapter 34.)
The heart
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
Thrombolytic agents (tissue plasminogen activator—if employed in the first 1–4 hours following the onset of a myocardial infarction, these drugs may dissolve clots in coronary blood vessels and reestablish blood flow
Temporal course of peripheral inflammation markers and indexes following acute ischemic stroke: prediction of mortality, functional outcome, and stroke-associated pneumonia
Published in Neurological Research, 2022
Ahmet Adiguzel, Ethem Murat Arsava, Mehmet Akif Topcuoglu
A total of 205 patients with acute ischemic stroke, admitted to Hacettepe University Neurology Intensive Care and Stroke Unit for more than 3 days in the last 2 years, were included in the study. The data were collected prospectively, recorded in the departmental database, and processed in a retrospective fashion for this study. Details of our stroke database are described elsewhere [13]. In short, the data is filled directly by a stroke neurologist on a daily basis. All patients undergo transthoracic echocardiography, 24-hour Holter monitoring or continuous bedside cardiac monitoring, cerebral computed tomography (CT), cerebral magnetic resonance (MR) imaging, CT or MR angiography and follow-up neuroimaging. Intravenous tissue plasminogen activator and/or neurointerventional treatments are used per established guidelines. The quality metrics for acute treatment methods and post-acute care were largely followed and included in the database. The Causative Classification of Stroke algorithm was used for etiological classification [14]. The local ethics committee approved the database and protocols.
FlowTriever Retrieval System for the treatment of pulmonary embolism: overview of its safety and efficacy
Published in Expert Review of Medical Devices, 2021
Vivian L. Bishay, Omosalewa Adenikinju, Rachel Todd
Current guidelines recommend ST as first line therapy for high risk PE patients and intermediate high risk patients who decompensate unless otherwise contraindicated. ST can be administered rapidly with regimens of 100 mg over 15 min and 50 mg over 1 min in the most critically ill patients and does not require specialized equipment and set-up. Yet, there are clearly opportunities for alternative therapies that do not utilize lytics. Tissue plasminogen activator is an expensive drug with many patients contraindicated or relatively contraindicated including the elderly, those who have undergone recent surgery and patients with malignancy depending on type and location [8]. These are often the very patients at greatest risk for PE. Administration requires intensive care unit (ICU) monitoring, the most expensive bed in a hospital system, and the morbidity associated with bleeding complications can be costly and increase hospital lengths of stay. Furthermore, the long- term sequelae of residual pulmonary vascular obstruction potentially tied to an undertreatment of PE must also be considered given the treatment and disability costs incurred with long-term adverse PE outcomes.
The effect of cyclosporin a on ischemia-reperfusion damage in a mouse model of ischemic stroke
Published in Neurological Research, 2020
Huajiang Deng, Shuang Zhang, Hongfei Ge, Liang Liu, Luotong Liu, Hua Feng, Ligang Chen
In the present study, we found that CsA may repair BBB injury after cerebral ischemia-reperfusion in mice. We also found significantly increased expression of CypA, p-Akt, NF-κB, and MMP-9 after cerebral ischemia-reperfusion, with CsA inducing the downregulation of CypA, p-Akt, NF-κB, and MMP-9. CsA further inhibits Akt phosphorylation in the PI3K-Akt pathway by inhibiting intracellular CypA, thereby inhibiting NF-κB activation [21], preventing NF-κB from entering the nucleus to participate in the expression of MMP-9 [22], increasing Claudin-5 protein expression [23], and ultimately leading to repairs following BBB damage. The long-term effects of this include benefits to cerebral infarction recovery. This result may be due to the BBB inhibiting the inflammatory response and reducing secondary injury following a brain injury. Prior literature has confirmed that increased BBB repair is conducive to recovery of long-term function after ischemic stroke and reduced stroke recurrence [24]. Furthermore, recombinant tissue plasminogen activator (rt-PA) is effective for the treatment of acute ischemic stroke, but increases cerebral hemorrhage risk. This is mainly because rt-PA down-regulates claudin-5 and ZO-1 expression and impairs BBB structure [25]. CsA may prevent the side effects of rt-PA by repairing BBB damage as we find in the present study. This result provides a theoretical basis for the combined use of CsA and rt-PA treatment of cerebral infarction.