Antiplatelet drug

From Wikipedia, the free encyclopedia
  (Redirected from Antiplatelets)
Jump to: navigation, search

An antiplatelet drug (antiaggregant) is a member of a class of pharmaceuticals that decrease platelet aggregation [1] and inhibit thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect.[citation needed]

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

Antiplatelet therapy with one or more of these drugs decreases the ability of blood clot to form by interfering with platelet activation process in primary hemostasis.[2] Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another and to damaged blood vessels endothelium.[2]

Choice of antiplatelet drug[edit]

A 2006 review [3] states: "...low-dose aspirin increases the risk of major bleeding 2-fold compared with placebo. However, the annual incidence of major bleeding due to low-dose aspirin is modest—only 1.3 patients per thousand higher than what is observed with placebo treatment. Treatment of approximately 800 patients with low-dose aspirin annually for cardiovascular prophylaxis will result in only 1 additional major bleeding episode."

Dual antiplatelet therapy[edit]

Often a combination of aspirin plus an ADP/P2Y inhibitor[4] (such as clopidogrel, prasugrel, ticagrelor, or another) is used in order to obtain greater effectiveness than with either agent alone.

Classification[edit]

The class of antiplatelet drugs include:

Usage[edit]

Prevention and treatment of arterial thrombosis

Prevention and treatment of arterial thrombosis is essential in patients with certain medical conditions whereby the risk of thrombosis or thromboembolism may result in disastrous consequences such as heart attack, pulmonary embolism or stroke.[2] Patients who require the use of antiplatelet drugs are: stroke with or without atrial fibrillation, any heart surgery (especially prosthetic replacement heart valve), Coronary Heart Disease such as stable angina, unstable angina and heart attack, patients with coronary stent, Peripheral Vascular Disease/Peripheral Arterial Disease and apical/ventricular/mural thrombus.[2]

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

  • Aspirin and Triflusal irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane - powerful vasoconstrictor that lowers cyclic AMP and initiates the platelet release reaction).
  • Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2
  • Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex
  • Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes:
    • Murine-human chimeric antibodies (e.g., abciximab)
    • Synthetic peptides (e.g., eptifibatide)
    • Synthetic non-peptides (e.g., tirofiban)
  • Epoprostenol is a prostacyclin that is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension.

Thrombolytic therapy is used in myocardial infarction, cerebral infarction, and, on occasion, in massive pulmonary embolism. The main risk is bleeding. Treatment should not be given to patients having had recent bleeding, uncontrolled hypertension or a 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 (PA), tissue-type plasminogen activators (alteplase, tenecteplase) are produced by recombinant technology.

Dental Management of Patients on Antiplatelet Drugs[edit]

Dentists should be aware of the risk of prolonged bleeding time in patients taking antiplatelet drugs when planning dental treatments that are likely to cause bleeding. Therefore, it is important for dentists to know how to assess patient’s bleeding risk and how to manage them.[2]

Assess Bleeding Risk[edit]

Identify the likelihood and risk of dental treatment causing bleeding complications.[2]

Dental procedures unlikely to cause bleeding Dental procedures with low risk of post-operative bleeding complications Dental procedures with high risk of post-operative bleeding complications
Local anaesthesia using aspirating syringe and vasoconstrictor Simple extractions up to 3 teeth with restricted wound size Extractions involving surgery, large wound or more than 3 teeth at once
Basic Periodontal examination (BPE) Incision and drainage of intra-oral swellings Flap raising procedures
Supragingival plaque, calculus, stain removal Six point full periodontal examination Gingival recontouring
Direct or indirect restoration with supragingival margins Root surface debridement and subgingival sclaing Biopsies
Orthograde endodontics Direct or indirect restorations with subgingival margins
Prosthetic procedures
Fitting and adjustment of orthodontic appliances.

Drug toxicity[edit]

Antiplatelet drugs effect may be affected by patient’s medications, current medical conditions, food and supplements taken. Antiplatelet drugs effect may be increased or decreased. An increase in antiplatelet effect would increase the risk of bleeding and results in prolonged or excessive bleeding. A decrease in antiplatelet effect would reduce the risk of bleeding and potentially increase the thromboembolic risk.[2] Drug toxicity also may increased when multiple antiplatelet drugs are used. Gastrointestinal bleeding is a common adverse event seen in many patients.[5]

Medications[edit]

Medications that may increase antiplatelet drugs effect:[2]

  • NSAIDS (e.g: Aspirin, Ibuprofen, Diclofenac, Naproxen)
  • Cytotoxic drugs or drugs associated with bone marrow suppression (e.g: Leflunamide, Hydrochloroquine, Adalimumab, Infliximab, Etanercept, Sulfasalazine, Penicillamine, Gold, Methotrexate, Azathioprine, Mycophenolate)
  • Other anticoagulants or antiplatelet drugs
  • Drugs affecting the nervous system (e.g: Selective serotonin reuptake inhibitors (SSRIs))

Medications that may decrease antiplatelet drugs effect:[2]

  • Carbamazepine
  • Erythromycin
  • Fluconazole
  • Omeprazole

Usage of NSAIDS as part of dental management of patients with vascular disease should be discouraged as NSAIDS has antiplatelet effect. Instead, simple analgesics such as Paracetamol, Co-codamol should be of first choice. If NSAIDS is required, dentist should be aware of the risk of bleeding and minimise treatment length.[2]

Medical Conditions[edit]

Medical conditions that may increase antiplatelet drugs effect:[2]

Chronic renal failure, liver disease, haematological malignancy, recent or current chemotherapy, advanced heart failure, mild forms of inherited bleeding disorders (e.g Haemophilia, Von Willebrand’s disease) and idiopathic thrombocytopenic purpura.

Food and Supplements[edit]

Food and supplements that may increase antiplatelet drugs effect:[2]

St. John’s Wort, Ginkgo biloba, Garlic

Oral Antiplatelet Drugs Available in the UK[2][edit]

Oral Antiplatelet Drugs UK Trade Name Other Names (Non-UK)
Aspirin Nu-Seals, Microprin, caprin Dual with dipyridamole: Asasantin Retard, Molita Modified Release There are numerous brand names for Aspirin
Clopidogrel Plavix, Grepid Iscover
Dipyridamole Persantin, Persantin Retard, Attia Modified Release, Ofcram PR. Dual with aspirin: Asasantin Retard, Molita Modified Release
Prasugrel Efient Effient, Prasita
Ticagrelor Brilique Brilinta, Possia

See also[edit]

References[edit]