Platelet Aggregation - What Is It? Norm, How To Pass?

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Video: Platelet Aggregation - What Is It? Norm, How To Pass?

Video: Platelet Aggregation - What Is It? Norm, How To Pass?
Video: Platelet Adhesion and Aggregation 2023, March
Platelet Aggregation - What Is It? Norm, How To Pass?
Platelet Aggregation - What Is It? Norm, How To Pass?

Platelet aggregation: what is it and what is the norm?

Platelet aggregation is the concentration of certain blood cells (Bizzocero plaques) to repair vascular damage that causes blood loss. Violation of integrity with minor damage to small vessels against the background of normal hemostasis does not threaten with massive blood loss. Minor bleeding, according to many people, stops spontaneously after a short time. Not everyone knows that in this complex process of preventing significant blood loss, a lot depends on platelet aggregation.


  • Platelet aggregation or natural control of bleeding
  • What does platelet aggregation say in a blood test?
  • Norm and deviation during pregnancy
  • Aggregation of platelets with inducers
  • Additional Information
  • Vulnerability of the concentration of cells in the blood

Platelet aggregation or natural control of bleeding

Platelet aggregation
Platelet aggregation

The process of stopping bleeding in the vasculature (capillaries, venules, arterioles) goes through several stages:

  • After damage to the vessel, its spasm occurs, which makes it possible to partially reduce the intensity of bleeding.
  • At the site of trauma to the vascular wall, blood plates are concentrated, which partially cover the defect of the damaged area - platelet adhesion occurs.

  • At the site of the vessel defect, platelets accumulate, forming conglomerates, this is platelet aggregation, the first stage of thrombus formation.
  • As a result of irreversible aggregation, a platelet plug is formed. It is loose, does not hold firmly on the wound, with a slight mechanical effect on it, bleeding resumes.
  • Under the influence of thromboplastin of fibrin filaments, the blood plug acquires density, contracts, the thrombin thrombus is retracted, and blood loss stops.

The picture below shows the stages of blood clot formation:

stages of blood clot formation
stages of blood clot formation

Aggregation of platelets when stopping bleeding is not the final stage of an important process, but this does not make it less important. This phenomenon, which is extremely important in stopping bleeding, has a downside. With increased platelet aggregation, the platelets stick together, even in the absence of bleeding, forming blood clots. These clots, moving through the blood vessels, provoke their blockage, disrupting the blood supply to the organs.

This is how myocardial infarction, pulmonary infarction, kidney infarction, ischemic stroke of the brain occur. In these cases, active therapy with antiplatelet agents is carried out, prescribed for the prevention and treatment of thrombosis.

A seemingly insignificant pathological reaction of spontaneous aggregation of platelets can lead to thromboembolism of the leading arteries, and even to the death of the patient.

What does platelet aggregation say in a blood test?

To study the ability of platelets to aggregate in the laboratory, they create an imitation of natural conditions - the circulation of blood cells in the bloodstream.

This study is carried out on glass with the addition of inducer substances that normally participate in similar reactions in the human body:

  • Adrenalin;
  • Collagen;
  • ADP;
  • Thrombin.

Ristomycin (ristocein), which has no analogues in the human body, is additionally used as an inducer. Each inducer of platelet aggregation has its own normal range, slightly different in different laboratory conditions.

The rate of platelet aggregation depending on the reaction inducer

Method for determining platelet aggregation


Blood test with ADP

30.8 - 77.8

Blood test with adrenaline

35.0 - 92.5

Collagen blood test

46.5 - 93.2

Blood test with ristomycin

58 - 167

For the diagnosis of cardiovascular pathologies, it is of great importance to determine the spontaneous aggregation of platelets, when the plates of blood cells glued together circulate through the circulatory system.

Disturbances in the microcirculation zone:

  • Changes in the vascular walls in the microcirculation zone;
  • The formation of aggregates from platelets, increasing the risk of developing pathology of the heart and blood vessels, serious complications.

Methods for determining the parameters of CAT:

  • Change in the optical density of a suspension of platelets;
  • Visual assessment of platelet aggregation.

In laboratory conditions, to diagnose pathological platelet aggregation, use:

  • Optical aggregometers - register platelet aggregation in plasma;
  • Conductometric Aggregometers - measure the level of aggregation in whole blood.

The data obtained is displayed as a curve on the aggregatogram. The method of laboratory diagnostics of the level of platelet aggregation is reliable, but requires high labor intensity, a large volume of blood plasma.

Norm and deviation during pregnancy

Rate and deviation
Rate and deviation

Deviations from the norm in the level of platelet aggregation in any direction is a sign of pathology. During pregnancy, a blood test is required to determine the risk of blood clots. In the last trimester of pregnancy, the female body prepares for possible blood loss by moderately increasing blood clotting rates. If platelet hyperaggregation is detected, this condition needs to be corrected.

At lower rates, the risk of bleeding increases, at higher rates, the risk of thrombosis increases. For the pregnancy to proceed safely, the platelet aggregation capacity must be located within the normal range - from 30 to 60%.

You can clarify the normal range in the laboratory, where the specialist will report the risk of increased or decreased aggregation intensity, and the likelihood of negative pregnancy complications.

Aggregation of platelets with inducers

According to the standard, for a more accurate diagnosis of the process, a blood test to determine the level of platelet aggregation is carried out with at least 4 inductors.

ADP inductor

ADP inductor
ADP inductor

Diagnostics with ADP allows you to identify a failure of the process in the following diseases and conditions:

  • Ischemia, myocardial infarction;
  • Atherosclerosis;
  • Diabetes;
  • Arterial hypertension;
  • Cerebral circulation disorder;
  • Hyperlipoproteinemia;
  • Hereditary thrombopathy;
  • Thrombocytopathy in hemoblastosis;
  • Taking drugs that inhibit platelet activity.

Diseases that provoke a decrease in the level of platelet aggregation:

  • Essential atrombia - a violation of the functionality of platelets;
  • Wiskott-Aldrich syndrome is a rare genetically determined disease that occurs depending on the sex of the patient, is associated with changes in the size and shape of cells;
  • Glanzman thrombastenia is a genetic disease, expressed in the absence of receptors for fibrinogen and glycoproteins;
  • Thrombocytopathy with uremia;
  • Aspirin-like syndrome - a violation of the second phase of platelet aggregation;
  • Secondary disorders of platelet aggregation in hemoblastosis, hypothyroidism, therapy with antiplatelet agents, NSAIDs, diuretics, antibacterial drugs and agents for lowering blood pressure.

Diseases provoking an increase in the level of platelet aggregation:

  • Activation of the coagulation system during psycho-emotional stress, the formation of immune complexes, taking certain medications;
  • Aspirin resistance;
  • Viscous platelet syndrome: increased level of aggregation, predisposition to adhesion.

Collagen inductor

Going beyond the normative indicators when reacting with collagen is diagnosed in case of violations at the adhesion stage. The decrease in the level of platelet aggregation has the same reason as in the ADP tests. An increase in the level accompanies vasculitis, viscous platelet syndrome.

Inductor with adrenaline

The study of indicators of platelet aggregation capacity in a test with adrenaline is considered the most informative diagnostic method. It fully shows the internal mechanisms of activation, including the "release reaction". A decrease in the normative indicator is typical for similar reasons found in the reaction with ADP and collagen. An increase in the intensity of platelet aggregation is associated with an increased viscosity of platelets, with stress, with the intake of certain drugs.

Ristocetin inductor

The study is carried out when diagnosing von Willebrand syndrome. The study of ristocetin-cofactor activity of platelets helps to reveal the severity of this factor.

All types of diagnostics using aggregation inductors allow an objective assessment of the functionality of platelets. Another purpose of diagnostics is to assess the effectiveness of the use of antiplatelet agents, to help in selecting the dosage of drugs.

Additional Information

Adhesion of platelets, the formation of a hemostatic plug includes complex methods of platelet activation and the following reactions.

What is the role of platelets?

What is the role of platelets
What is the role of platelets

The functions of blood cells in the implementation of vascular-platelet hemostasis:

  • Providing angiotrophic function to maintain the normal structure and functionality of the vascular walls of small venules and arterioles.
  • Ensuring the adhesive-aggregation function, which consists in the concentration of platelets and their adhesion to the damaged basement membrane of the vessel (adhesion), the formation of a hemostatic plug (aggregation), which makes it possible to stop bleeding in a short time.
  • Maintaining spasm of damaged capillaries to prevent increased blood loss.
  • Participation in coagulation processes, in reactions of fibrinolysis.

The adhesion-aggregation function includes adhesion and aggregation of blood cells, discovered by researchers back in the 19th century. A platelet plug is formed before being transported to the site of damage to the basement membrane.

Collagen is the main stimulator of platelet plug attachment, although other components of connective tissue may also perform these functions.

Changes in the appearance and functionality of platelets during bleeding

Appearance changes
Appearance changes

In the event of a vascular injury, the preparation of platelets for response begins long before arriving at the emergency site:

  • They change their shape from flat disc-shaped to spherical, acquire pseudopodia. These processes are designed to bind to each other and attach to the basement membrane of the vessel.
  • Arriving at the scene of the emergency, the blood plates are ready to activate adhesion and aggregation, they attach to the vessel walls in less than 5 seconds.
  • Platelets, located in the space of the circulatory system, are concentrated in conglomerates, numbering 3-20 cells.
  • Conglomerates arriving at the site of injury combine with platelets, which are primarily adhered at the site of exposure of the basement membrane.

All stages of this process are aimed at an intensive increase in the hemostatic plug, which in a short time closes the damage to the vessel and stops bleeding.

Cell concentration as a complex biochemical process

In the process of adhesion and aggregation of platelets, external and internal factors are involved:

  • Energy costs;
  • Reaction stimulants;
  • Rearrangement of cell structure.

For example, platelets cannot perform their functions without glycoprotein, a plasma cofactor for collagen (von Willebrand factor). It is produced in the vascular walls, and platelets, moving through the veins and arteries, deposit it for future use in their granules to be released if necessary.

Cell concentration
Cell concentration

Stimulants of platelet aggregation, included in the activation mode:

  1. Collagen is the most important stimulant.
  2. ADP - in the initial stage of aggregation, is released from the damaged basement membrane of the vascular wall and from erythrocytes in the area of injury, then it is released by platelets that have passed through primary adhesion and activation.
  3. Adrenaline and serotonin - activate platelet membrane enzymes, promote the formation of arachidonic acid and thromboxane, which intensively activate the reaction.
  4. Prostaglandins - when activated, they form thromboxane in smooth muscles, at the last stage of aggregation, they ensure the flow of prostacyclin into the blood, which suppresses the unnecessary activity of platelets.
  5. Thrombin - helps to strengthen and increase the strength of the hemostatic plug.

Focusing on the mechanism of the platelet hemostasis reaction, one can understand the etiology of diseases associated with blood clotting disorders.

Vulnerability of the concentration of cells in the blood

Concentration vulnerability
Concentration vulnerability

Separate endogenous and exogenous factors provoke pathological processes in the mechanism of platelet hemostasis.

The most vulnerable point is the "release reaction", when the platelets do not join and stick together, and a hemostatic plug does not form.

For the high-quality implementation of the blood coagulation process, the presence of proteins is necessary: fibrinogen, albumin, gamma fraction, as well as phospholipid factor, Ca 2+, Mg 2+. Proteins create a "plasma atmosphere" for the full functioning of platelets, but some of the derivatives of protein cleavage can inhibit the aggregation of platelets, especially those obtained during the breakdown of fibrinogen and fibrin.

If all participants in platelet hemostasis perform their functions, the aggregation of these blood cells can stop bleeding, but in large vessels, where blood circulates under high pressure, the hemostatic plug is not able to do this.


The author of the article: Shutov Maxim Evgenievich | Hematologist

Education: In 2013 he graduated from the Kursk State Medical University and received a diploma "General Medicine". After 2 years, completed residency in the specialty "Oncology". In 2016 completed postgraduate studies at the National Medical and Surgical Center named after N. I. Pirogov.

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