Platelet aggregation is also known as clotting. Platelet adhesion is also an alternative name of it. To better understand the platelet aggregation, you must first know about the platelets. Platelets are tiny disk-shaped blood cells which are also recognized as thrombocytes.

In medical terms, platelet aggregation is defined as the clumping together of platelets in your blood. Platelet aggregation is the portion of a sequence of events for the production of thrombus or clot.

This blood component plays an important role in the process of blood clotting. Platelet aggregation is a crucial part of the clot formation procedure, which avoids bleeding. There are several factors in blood clotting or coagulation. One of these processes includes small cells in the bloodstream which is known as the platelets. Platelets are formed in the bone marrow. It gathers in the area of an injury and bundle together to produce a plug or aggregate. This process helps to reduce the loss of blood and promote healing.

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Causes and Development of Platelet Aggregation

Thrombocytosis is the increased platelet count. It may happen to various illnesses like chronic infections, cancer, and other blood diseases. It can also help to increase blood clot formation. It may happen due to high triglycerides, stress, sodas, caffeine, chocolate, excessive red meat, and others.

Some organic substances can also promote platelet clumping. These substances include ADP, collagen, the catecholamine, fatty acids, and certain immune complexes. Cigarette smoking can also contribute to “hyperactive” platelet formation.

Another cause of platelet aggregation is a high-fat diet. Some possible causes are acute phase protein elevation which is caused by tissue necrosis or allergy, inflammation, a collagen-damaging illness, or an occult disease process that can cause collagen damage or neoplastic changes, and excessive stress level producing biochemical imbalance.

Signs and Symptoms of Platelet Aggregation

According to scientific studies, some of the signs and symptoms of too much platelet aggregation are a capillary blockage, heart problems, poor circulation and blood clots.

Diagnosis and tests

The platelet aggregation test is performed to identify how fine platelets are sticking together to produce blood clots. The test can measure this through the use of platelet antagonist that will initiate clumping in the blood sample of the patient. Platelet is a kind of blood cell that forms blood clots through sticking together. The clot plays an important role in stopping the bleeding if you have injuries and wound. Without platelets, you can bleed to death.

In a platelet aggregation test, a blood sample is examined to monitor how the platelets are divided into the plasma, the liquid part of the blood. Then, a chemical is added to the blood sample to test how fast your platelets clot. The blood sample can get at the office of the doctor or in a medical laboratory. The said test is also known as the platelet aggregometry test or platelet aggregation assay.

To start the test, the technician will use gloves and clean the area around your vein. The blood can be collected through the vein on the front of your arm near the elbow crease or the back of your hand.

Next, the technician uses an elastic band to tie around your upper arm. It will help the blood pool in the vein. In return, the technician can draw blood easily. Then, the technician will insert a needle into your vein and collect blood. In the process, you can feel mild to moderate pain while drawing the blood with the use of a needle. It feels like a burning or prickling sensation. You can reduce the pain by relaxing your arm.

When the technician is done, the needle will be removed, and pressure to the puncture is applied to stop bleeding. You must maintain the pressure on the area to avoid bruising. Lastly, your blood sample will be sent to the laboratory for testing.

Purpose of platelet aggregation test

This test can be requested by your doctor if you are experiencing signs and symptoms of abnormal platelet function, bleeding disorder, as well as low platelet count. Other symptoms also include:

  • Excessive bruising
  • Excessive bleeding
  • Too much menstrual bleeding
  • Bleeding for the gums or nose
  • Blood in the stool or urine

Doctors can also perform this test if your family has a history or record of bleeding problems. Meanwhile, the results of the test helps the doctors determine the cause of bleeding problems. More importantly, the test can also diagnose the following:

  • Genetic disorders like Bernard-Soulier syndrome, Glanzmann’s thrombasthenia, Von Willebrand disease, and platelet storage pool disease
  • Medication side effects that can affect the function of your platelets
  • An autoimmune disorder like systemic lupus erythematosus
  • Uremia that is caused by a kidney disease
  • Myeloproliferative disorders like different types of leukemia

Preparation for the platelet aggregation test

If your doctor told so, you can eat and drink before the test. You can schedule it anytime of the day, unless your doctor gives you specific time. You must not exercise 20 minutes prior to the test. However, several medications can affect the test results. It is therefore necessary for you to inform your doctor of everything that you take before the test. Tell the doctor ahead of time about the over the counter and drug prescriptions. The doctor will inform you if you need to stop taking the drug or change its dosage prior to the test.

Some of the medications that can affect a platelet aggregation test are as follows:

  • Antihistamines
  • Nonsteroidal anti-inflammatory drugs or NSAIDs like aspirin or other combination of drugs with aspirin
  • Antibiotics like penicillin, nitrofurantoin, and cephalosporin
  • Tricyclic antidepressants
  • Theophylline, a medication to relax airway muscles
  • Thienopyridine anti-platelet drugs such as clopidogrel, prasugrel, ticlopidine, and dipyridamole

Treatment and prevention of platelet aggregation

Some substances can reduce the platelet aggregation involve shark liver oil, tocotrienols, curcumin, grape seed extract, gingko biloba, grapes and grape juice, fish oils, Coumadin, testosterone, vitamin E at 300 IU and above, B6 at 150 to 200 mg, garlic, EFAs, gugulipids, and taurine.

Bromelain is also observed to reduce the aggregation of blood platelets. It is an effective fibrinolytic agent which is also important to purify fibrinogen solutions in plasma.

Diagnosis and complications

Extreme platelet aggregation is a potentially serious finding. It can greatly contribute to a cardiovascular disease which is the number one cause of death in the western world. Diabetics and patients having hypercholesterolemia commonly show increased platelet aggregation which can predispose to clotting disorders that may lead to vessel obstructions and vascular thrombus.

Conditions that cause platelet aggregation (clotting)

Too much platelet aggregation is linked with the development of atherosclerosis as well as other cardiovascular complications.

Dangerous factors for Platelet aggregation

A mitral valve prolapse is considered to damage the platelets and increase its aggregation. This work has been proven in many studies. Most blood tests have very low-risk procedures. The platelet aggregation test is only performed for the people with bleeding problems. There is a high risk of extreme bleeding in this process.

So, if you have a bleeding problem, tell the technician to make them prepared for the test. Moreover, it is also significant for you to inform the technician whether you experience fainting, dizziness, and nausea during your last blood test.

Some dangerous factors of blood draw are:

  • Feeing fainting or lightheaded
  • Multiple puncture wounds caused by trouble finding a vein
  • Excessive bleeding
  • Infection in the area of the needle stick
  • Hematoma or the collection of the blood under the skin

Mechanisms of Platelet Aggregation       

Platelet aggregation includes a platelet to platelet adhesion that is important for effective hemostasis. Next, to the initial adhesion of platelets to the area of injury, platelets are activated by agonists like adenosine diphosphate (ADP) and presence of collagen in the area of vascular injury. These agonists activate the platelets through binding them to particular receptors on the platelet surface.

The platelet intracellular calcium increases due to the release from intracellular stores and calcium influx in the plasma membrane. The increased platelet-free calcium concentration leads to various structural and functional changes in the platelets. Your platelet altered from a disc to a spiny sphere and discharged into the lumen of the open canalicular system. This system is the area where they are released to the exterior.

The long membrane projections due to shape-change reaction make the platelets to interact with each other to form aggregates. The main adhesion molecule in the platelet aggregation is the membrane protein GPIIb/IIIa. It is the integrin receptor at high density on platelets. It serves as an inactive form in resting platelets. The receptor-bound fibrinogen serves as the bridge molecule between two GPIIb/IIIa’s for platelet aggregation.

Platelet Aggregation Monitoring

  • Ex Vivo Monitoring: Platelet Aggregometry

There are traditional approaches to monitor the platelet aggregation. Some of these include an exposure of platelets in suspension to different stimuli like ex vivo. Ex vivo is a technique called platelet aggregometry. In the monitoring process, agonists commonly use adenosine diphosphate (ADP), thrombin, collagen, and thromboxane.

Studies are conducted on platelet-rich plasma, or whole blood wherein the platelets are maintained in suspension through stirring. With the exposure on the agonist, the formation of platelet aggregates that result to boost the light transmission through the sample. As a result, the kinetics of the response and aggregation offers a quantitative assessment of platelet aggregation. The Platelet Aggregometry provides information about the platelet function abnormalities in some clinical conditions.

  • In Vivo Monitoring of Platelet Aggregation

While platelet aggregometry provides assessment for platelet aggregation kinetics, it can’t reflect the complexities therein in platelet aggregation in vivo. In vivo monitoring, several intravital video microscopy approaches are used to monitor platelet aggregation on thrombus formation.

The kinetics of platelet aggregation and adhesion can be monitored in real-time with the use of these techniques. These approaches also show the redundancy of various mechanisms responsible for platelet recruitment.

The significance of blood flow in the regulation of platelet aggregation

Rheological of blood flow conditions in the area of vascular injury must be considered in platelet adhesion and aggregation. Platelets are exposed to a large range of hemodynamic conditions in vivo. It ranges from low flow situations in venules and large veins to small arterioles.

The platelets can form stable adhesion contacts on shear conditions that are operating in vivo. These are indispensable for hemostatic plug formation and thrombosis. Experimental systems are made to study the platelet aggregation and adhesion on thrombogenic substrates. The systems allow assessment of platelet aggregation in the flow of the blood, with or without anticoagulant. It also offers the insight about the role of thrombin generation for the regulation of platelet aggregation in various flow rates. The experimental systems are also important for integrin in mediating the platelet aggregation.

Role of membrane tethers in 2-stage platelet aggregation procedure

Membrane tethers have roles for the formation of stable platelet aggregates. The production of discoid platelet aggregates is shear-dependent and mediated through the development of membrane tethers.

The significance of adhesion receptor signals and soluble agonists in regulating platelet aggregation

There is a spatiotemporal signaling relationship between adhesion receptors and soluble agonists for the regulation of platelet and leukocyte activation underflow. One example of this is a leukocyte rolling velocity that is influenced by the cell stimulation level of particular chemokines. The input signals do not happen in isolation and likely to be modified by the signals that emanate from the adhesion receptors themselves.

According to perfusion studies in immobilized VWF, integrin and GPIb appear to elicit distinct, cooperative activating signals. These signals can regulate the platelet translocation dynamics through the reversible activation of integrin.

The models of thrombus development propose a key role for collagen which initiates the activation of platelets in main adherent platelets. Meanwhile, the subsequent propagation of thrombi (platelet aggregation) is mainly driven by agonists generated from the platelet surface like ADP, thrombin, and TXA2.

However, soluble agonists do not recruit platelets to form thrombi, but adhesion receptors do. The role of integrin can derive signals downstream of GPIb that is essential for the initiation of hemostatic plug formation.


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