The following technologies either use light to measure the amount of opaqueness there is due to clots or non-clotting in platelet-rich plasma or whole blood, or they use the time it takes for clots to form:

Platelet Aggregometry

The VerifyNow Assay is the latest technology in aggregometry.

Whole Blood Aggregometry

Determines how an agonist affects the electrical impedance between two electrodes to cause platelet aggregation.

Light Scattering (LS) Methods

After the administration of an aggregating stimulus, variations in the number of platelet aggregates of various sizes are quantified by particle-counting techniques that use light scattering (LS).

Clot Signature Analyzer

Uses a tube of blood to measure platelet function via platelet “plugs” observed.

Thrombotic Status Analyzer

Measures platelet activation via capillary tube occlusion. The platelet function analyzer measures the drop in flow rate through a capillary tube due to platelet plugs.

High Shear Filterometer

Measures the time it takes for a filter to stop allowing blood through.

Diagnosis of inherited platelet dysfunction can be made from genetic testing and platelet aggregometry.

Other Testing for Platelet Hyperfunction

The end result of platelet hyperfunction is clotting. In this regard, confirmation is done via ultrasound of blood vessels, or when more accuracy is needed, computed tomography (CT) or magnetic resonance imaging (MRI) of arteries or veins suspected to harbor thrombi (clots).

Testing used after Antiplatelet Medicines are begun

Anticoagulation using antiplatelet drugs is challenging, in that the effect must be enough to discourage clot formation but not so much to provoke bleeding. Once antiplatelet medications are begun, it is necessary to do interval testing to ensure the patient’s clotting tendencies fall into the narrow range of what is considered ideal anticoagulation. For this purpose, the following interval blood tests are used:

Complete Blood Count (CBC)

A manual or automated platelet count from a peripheral smear of blood on a slide.

Prothrombin Time (PT)

Measures the time for plasma to clot when exposed to tissue factor.

International Normalized Ratio (INR)

A PT ratio applied to a world-wide standard and measures how well the PT is affected by anticoagulants. It is expressed in the multiples of decreased speeds from normal clotting. The therapeutic goal for anticoagulation is an INR of 2-3 (ideally, 2.5). Because it is an international standard, it is especially useful for travelers.

Activated Partial Thromboplastin Time (aPTT)

Measures the time for plasma to clot after exposure to contact factors.

Treatment of Thrombosis with Antiplatelet Therapy

An overreaction of the clotting process with premature, unprovoked, or exaggerated platelet initiation can be managed using medications that interfere with this, called antiplatelet agents:

• Aspirin: In doses of 50-100 mg/day.

• Non-steroidal anti-inflammatory drugs (NSAIDs): Complications can include upper gastrointestinal bleeding and gastritis.

• Platelet receptor site antagonists: Interfere with platelet activation, P2Y12 receptor blockers (e.g., clopidogrel, prasugrel, ticagrelor), glycoprotein IIb/IIIa inhibitors (e.g., abciximab, tirofiban, eptifibatide).

• Nitrates: Reduces platelet reactivity, adhesion, and aggregation.

• Calcium channel blockers: Reduce platelet aggregation and adhesion.

• Heparin: Reduces platelet adhesion.

• Warfarin: Not a true antiplatelet medication but a vitamin K antagonist, it is used for long term anticoagulation in those who prefer pills or who have recurrent embolic events.

Oral antiplatelet preparations include aspirin, NSAIDs, calcium channel blockers, warfarin, rivaroxaban, apixaban, edoxaban, and dabigatran.

Non-Medical Antiplatelet Treatment

If patients fail to achieve ideal anticoagulation or who have recurrent thrombosis or thromboembolic events, a filter can be placed in the vena cava to catch venous migratory clots before they reach the right-sided heart circulation to the lungs.

Prevention of Platelet Dysfunction

Prevention of platelet dysfunction relies on screening methods involving blood work and platelet function testing in those at risk, such as patients with a strong history of venous thrombosis and pulmonary emboli, stroke, atherosclerosis, and myocardial infarction. A family history positive for platelet dysfunction is a major risk that calls for preventative measures.

Platelet dysfunction may remain dormant until the sudden appearance of venous clots or arterial plaques. Identification of those as risk is the best strategy for preventing venous, arterial, and cardiac thromboembolic disease. Those with an increased tendency toward clotting (i.e., previous thrombosis, strong family history, previous stroke, venous stasis, or atherosclerosis) may benefit from antiplatelet therapy.

Antiplatelet Therapy as Preventative Medicine

Antiplatelet therapy is used to prevent serious complications from many thrombotic and atherosclerotic conditions:

• Coronary artery disease (CAD): Especially those with stents.

• Acute coronary syndromes.

• Previous or current myocardial infarction.

• Atrial fibrillation (AF): Which can throw clots to distal sites that can cause ischemia or tissue death (infarction) in the lungs (from the right atrium), or in the kidneys, liver, spleen, intestines, or other organs (from the left atrium).

• Carotid artery thrombosis (CAT): Ischemic stroke and transient ischemic attack (TIA).

• Pre-operative or perioperative prophylaxis against postoperative pulmonary emboli: “Mini-dose” heparin.

• Prolonged immobilization.

• Severe extremity trauma.

• Chronic deep vein thrombosis (DVT).

• Diabetics with end-organ damage.

• Disseminated intravascular coagulopathy (DIC): An over-clotting phenomenon due to infection, trauma, hemorrhage, surgery, or pregnancy that results in exhausting all of the coagulation factors, ultimately leading to fatal hemorrhage; antiplatelet therapy is given with the intention of stopping the consumption of platelets before all of the coagulation factors are gone.