Platelet Antiaggregants: What are they? Uses, Antiplatelet Therapy and Toxicity

They are widely used in the primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease.

An antiplatelet drug (antiplatelet) is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in arterial circulation, where anticoagulants have little effect.

Antiplatelet therapy with one or more of these drugs decreases the ability to form blood clots by interfering with the platelet activation process in primary hemostasis.

Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation, resulting in a decreased tendency for platelets to adhere to each other and to the endothelium of damaged blood vessels.


A 2006 review states:

‘Low-dose aspirin increases the risk of major bleeding twice compared to placebo. However, the annual incidence of major bleeding due to low-dose aspirin is modest – only 1.3 patients per 1,000 times higher than what is seen with placebo treatment.

“Treating approximately 800 patients with low-dose aspirin annually for cardiovascular prophylaxis will result in only 1 additional major bleeding episode.”

Dual antiplatelet therapy

A combination of aspirin plus an ADP / P2Y inhibitor (such as clopidogrel, prasugrel, ticagrelor, or another) is often used to be more effective than either agent alone.


Prevention and treatment of arterial thrombosis

Prevention and treatment of arterial thrombosis are essential in patients with certain medical conditions, so the risk of thrombosis or thromboembolism can have disastrous consequences, such as a heart attack , pulmonary embolism or stroke .

Patients who require the use of antiplatelet drugs are:

  • Patients with a stroke with or without atrial fibrillation .
  • Any heart surgery (especially prostate replacement valve).
  • Coronary heart disease such as stable angina.
  • Heart attack.
  • Patients with coronary stents.
  • Peripheral vascular disease / peripheral arterial disease.

Treatment of established arterial thrombosis includes the use of antiplatelet drugs and thrombolytic therapy. Antiplatelet drugs alter platelet activation at the site of vascular damage crucial for the development of arterial thrombosis.

Aspirin and triflusal irreversibly inhibit the COX enzyme, resulting in reduced platelet production of TXA2 (thromboxane – potent vasoconstrictor that reduces cyclic adenosine monophosphate and initiates the platelet-releasing reaction).

Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic adenosine monophosphate with potentiation of the action of prostacyclin (or PGI2) – it opposes the actions of TXA2.

Clopidogrel affects the adenosine diphosphate-dependent activation of complex IIb / IIIa.

Glycoprotein IIb / IIIa receptor antagonists block a platelet receptor for fibrinogen and von Willebrand factor.

Epoprostenol is a prostacyclin that is used to inhibit platelet aggregation during kidney dialysis (with or without heparin) and is also used in primary pulmonary hypertension.

Thrombolytic therapy is used in myocardial infarction, cerebral infarction, and occasionally in massive pulmonary embolism. The main risk is bleeding.

Treatment should not be given to patients who have had recent bleeding, uncontrolled hypertension or hemorrhagic stroke, or surgery or other invasive procedures within the previous 10 days.

Streptokinase forms a complex with plasminogen, resulting in a conformational change that activates other plasminogen molecules to form plasmin.

Plasminogen activators (PAs), tissue-type plasminogen activators (alteplase, tenecteplase) are produced by recombinant technology.

Dental management of patients with antiplatelet drugs

Dentists should be aware of the risk of prolonged bleeding in patients taking antiplatelet medications when planning dental treatments that can cause bleeding. Therefore, it is important for dentists to know how to assess the patient’s bleeding risk and how to manage it.

Assess the risk of bleeding

Identify the likelihood and risk of dental treatment causing bleeding complications.

Dental procedures are unlikely to cause bleeding
  • Local anesthesia with aspiration syringe and vasoconstrictor.
  • Basic Periodontal Examination (EPB).
  • Supragingival plaque, calculus, stain removal.
  • Direct or indirect restoration with supragingival margins.
  • Orthograde endodontics.
  • Prosthetic procedures.
  • Assembly and adjustment of orthodontic appliances.
Dental procedures with low risk of postoperative bleeding complications
  • Simple extractions of up to 3 teeth with a restricted wound size.
  • Incision and drainage of intraoral swellings.
  • Six-point comprehensive periodontal exam.
  • Debridement of the root surface and subgingival scale.
  • Direct or indirect restorations with subgingival margins.
Dental procedures with high risk of postoperative bleeding complications
  • Extractions involving surgery, a large wound, or more than 3 teeth at a time.
  • Fin lifting procedures.
  • Gingival reconstruction or remodeling.
  • Biopsies.

Drug toxicity

The effect of antiplatelet drugs can be affected by the patient’s medications, current medical conditions, foods, and supplements that are taken. The effect of antiplatelet drugs can increase or decrease.

An increase in the antiplatelet effect would increase the risk of bleeding and cause prolonged or excessive bleeding. A decrease in the antiplatelet effect would reduce the risk of bleeding and possibly increase the risk of thromboembolism.

Drug toxicity can also increase when multiple antiplatelet drugs are used. Gastrointestinal bleeding is a common adverse event seen in many patients.


Drugs that can increase the effect of antiplatelet drugs:

  • Nonsteroidal anti-inflammatory drugs (such as: aspirin, ibuprofen, diclofenac, naproxen ).
  • Cytotoxic drugs or drugs associated with bone marrow suppression (such as: leflunamide, hydrochloroquine, adalimumab, infliximab, etanercept, sulfasalazine, penicillamine, gold, methotrexate , azathioprine, mycophenolate).
  • Other blood thinners or antiplatelet medications.
  • Medicines that affect the nervous system (such as selective serotonin reuptake inhibitors).

Medications that can decrease the effect of antiplatelet drugs:

The use of non-steroidal anti-inflammatory drugs as part of the dental treatment of patients with vascular disease should be discouraged as non-steroidal anti-inflammatory drugs have an antiplatelet effect.

Instead, simple painkillers such as paracetamol, codamol should be the first choice. If non-steroidal anti-inflammatory drugs are required, the dentist must be aware of the risk of bleeding and minimize the duration of treatment.

Medical conditions

Medical conditions that can increase the effect of antiplatelet drugs:

Chronic kidney failure, liver disease, hematologic malignancy, recent or current chemotherapy, advanced heart failure, mild forms of inherited bleeding disorders (eg, hemophilia, Von Willebrand disease), and idiopathic thrombocytopenic purpura.

Food and supplements

Foods and supplements that can increase the effect of antiplatelet drugs:

  • Grass of San Juan.
  • Ginkgo biloba.
  • She.