Leukocyte-platelet aggregates in acute and subacute ischemic stroke
L Marquardt1, C Anders, F Buggle
1Department of Neurology, Klinikum Ludwigshafen, Ludwigshafen, Germany.
Cerebrovascular Diseases (Basel, Switzerland)
|July 18, 2009
Summary
Leukocyte-platelet aggregates, particularly granulocyte-platelet aggregates, are elevated after ischemic stroke, indicating prothrombotic and inflammatory processes. Monocyte-platelet aggregates show a transient increase in the acute phase.
Area of Science:
- Hematology
- Neurology
- Immunology
Background:
- Leukocyte-platelet aggregates (LPAs) are sensitive markers of platelet activation.
- Previous studies linked LPAs to coronary heart disease.
- This study investigates LPA levels post-ischemic stroke.
Observation:
- Flow cytometry assessed granulocyte-, monocyte-, and lymphocyte-platelet aggregates.
- Serial measurements were taken on days 1, 2, 3, 5, 7, 10, and 90 post-stroke.
- 45 ischemic stroke patients and 30 healthy controls were included.
Findings:
- Granulocyte-platelet aggregates were increased from day 1 to 10 post-stroke, but not at day 90.
- Monocyte-platelet aggregates increased significantly on day 2 only.
- Lymphocyte-platelet aggregates showed no significant changes.
Implications:
- Different leukocyte subtypes exhibit distinct LPA kinetics after ischemic stroke.
- Persistent granulocyte-platelet aggregates suggest ongoing prothrombotic and inflammatory activity.
- Transient monocyte-platelet aggregates may indicate an acute response to cerebral ischemia.
Related Concept Videos
01:22Formation 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...
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...
01:15Ischemic 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.
01:18Structure and Function of Platelets
The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...
01:16Clot 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.
01:29Hemorrhagic 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...
01:15Ischemic 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...