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Related Concept Videos

Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Formation of the Platelet Plug01:22

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
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.
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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...
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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Related Experiment Video

Updated: May 31, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

Coated-platelet levels are elevated in patients with transient ischemic attack.

Calin I Prodan1, Andrea S Vincent, George L Dale

  • 1Department of Neurology Service, Veterans Administration Medical Center, Oklahoma City, Oklahoma City, OK, USA. calin-prodan@ouhsc.edu

Translational Research : the Journal of Laboratory and Clinical Medicine
|June 29, 2011
PubMed
Summary

Patients experiencing transient ischemic attacks (TIAs) have higher levels of coated-platelets, a marker linked to stroke risk. This finding suggests TIAs and ischemic strokes share underlying prothrombotic mechanisms.

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Last Updated: May 31, 2026

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Published on: April 2, 2013

Area of Science:

  • Neurology
  • Hematology
  • Cardiovascular Medicine

Background:

  • Transient ischemic attack (TIA) poses a significant risk for subsequent ischemic strokes, creating a clinical management challenge.
  • The ABCD2 score is a tool used to assess short-term stroke risk in TIA patients.
  • Coated-platelets, a specific type of procoagulant platelet, are implicated in ischemic stroke and intracerebral hemorrhage.

Purpose of the Study:

  • To investigate whether coated-platelet production is elevated in patients with TIA compared to healthy controls.
  • To explore the relationship between coated-platelet levels and the ABCD2 score in TIA patients.

Main Methods:

  • A pilot study involving 60 TIA patients and 60 controls.
  • Measurement of coated-platelet levels in both groups.
  • Correlation analysis between coated-platelet levels and ABCD2 scores in TIA patients.

Main Results:

  • Coated-platelet levels were significantly higher in TIA patients (38.4 ± 15.1%) compared to controls (31.0 ± 13.2%), with P = 0.005.
  • A significant positive linear correlation was found between ABCD2 scores and coated-platelet levels in TIA patients (P = 0.0003, r = 0.45).

Conclusions:

  • Elevated coated-platelet levels in TIA patients support the hypothesis that TIA and ischemic stroke are part of a disease spectrum.
  • These findings suggest shared prothrombotic processes underlie both TIA and ischemic stroke.