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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.

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Intravenous Thrombolysis at Primary Stroke Centers Versus Comprehensive Stroke Centers: Analysis From the AcT Trial.

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Asundexian for Secondary Stroke Prevention.

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MRI measurement of the delayed secondary ischaemic injury following endovascular thrombectomy: results from the REPERFUSE-NA1 study.

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Recombinant factor VIIa versus placebo for spontaneous intracerebral haemorrhage within 2 h of symptom onset (FASTEST): a multicentre, double-blind, randomised, placebo-controlled, phase 3 trial.

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Related Experiment Video

Updated: Jun 24, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

Hyperfibrinogenemia and functional outcome from acute ischemic stroke.

Gregory J del Zoppo1, David E Levy, Warren W Wasiewski

  • 1Harborview Medical Center, University of Washington, Seattle, WA 98104, USA. grgdlzop@u.washington.edu

Stroke
|March 21, 2009
PubMed
Summary

Elevated fibrinogen levels are linked to poorer functional outcomes after ischemic stroke. Lowering fibrinogen may improve recovery in acute stroke patients.

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A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
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A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

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Last Updated: Jun 24, 2026

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model
09:42

A Fibrin-Enriched and tPA-Sensitive Photothrombotic Stroke Model

Published on: June 4, 2021

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia
09:35

A Mouse Model of Hemorrhagic Transformation Induced by Acute Hyperglycemia Combined with Transient Focal Ischemia

Published on: November 15, 2024

Area of Science:

  • Neurology
  • Cardiovascular Medicine
  • Biochemistry

Background:

  • Elevated plasma fibrinogen is correlated with ischemic stroke incidence and mortality.
  • The impact of fibrinogen levels on functional stroke outcome remains largely unknown.

Purpose of the Study:

  • To investigate the association between initial fibrinogen levels and functional outcomes in acute ischemic stroke patients.
  • To analyze data from placebo arms of the Stroke Treatment with Ancrod Trial (STAT) and European Stroke Treatment with Ancrod Trial (ESTAT).

Main Methods:

  • Analysis of placebo data from STAT and ESTAT trials.
  • Fibrinogen levels measured within 3-6 hours of stroke onset and over 5 days.
  • Functional outcomes assessed using Barthel Index scores at 90 days.
  • Multiple logistic regression used to evaluate the association between fibrinogen and outcomes.

Main Results:

  • Fibrinogen levels increased from a median of 340 mg/dL to 376 mg/dL within 24 hours.
  • Good functional outcome decreased with higher initial fibrinogen quartiles in both trials.
  • Patients with fibrinogen <450 mg/dL showed better outcomes, significant in ESTAT (P=0.0006).

Conclusions:

  • Higher initial fibrinogen levels are independently associated with poor functional outcomes in acute ischemic stroke.
  • Further validation with larger datasets is required.
  • Treatments targeting fibrinogen reduction may be beneficial for acute ischemic stroke management.