Antiplatelet drug

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An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, 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 classical Vitamin K antagonist anticoagulants have minimal effect. [2]

Contents

Antiplatelet drugs are widely used in primary and secondary prevention of thrombotic disease, especially myocardial infarction and ischemic stroke. [1]

Antiplatelet therapy with one or more of these drugs decreases the ability of blood clots to form 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 decreased tendency of platelets to adhere to one another and to damaged blood vessels' endothelium. [3]

Choice

Antiplatelet medications are one of the primary recommendations for treatment of both stable [4] and unstable [5] ischemic heart disease. Most commonly, aspirin is used as a single medication in cases of uncomplicated stable angina, and in some cases of unstable angina. If a patient does not tolerate aspirin, ADP/P2Y inhibitors may be used as single-drug therapy instead. More severe and complicated cases are treated with dual antiplatelet therapy, or in some cases triple therapy that includes direct oral anticoagulants. [6] Clinicians must make a choice that balances patient risk with the increased risks of bleeding associated with combination therapy. [4] [5]

Dual antiplatelet therapy

Often a combination of aspirin plus an ADP/P2Y inhibitor [7] (such as clopidogrel, prasugrel, ticagrelor, or another) is used to obtain greater effectiveness than with either agent alone. This is known as "dual antiplatelet therapy" (or DAPT). DAPT is used in patients who have or at high risk of developing unstable angina, NSTEMI myocardial infarctions, and other high-risk thrombotic conditions. [5] Dual antiplatelet therapy has been found to significantly reduce rates of heart attacks, strokes, and overall cardiovascular death, but is not used in low-risk patients because it significantly increases the risks of major bleeding. [8]

Classification

Classes of antiplatelet drugs include:

Usage

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. [3] 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. [3]

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.

Management in the perioperative period

Antiplatelet therapy may increase the risk of a bleed during surgery, however, stopping therapy may increase the risk of other thrombotic problems including myocardial infarction. [9] When considering these medications and the risk-benefit ratio in the perioperative period, one must consider the risk of stopping the medication and a clot forming versus the risk of bleeding during or after the surgery if medication is continued. [10] A 2018 Cochrane Review that included five randomized controlled trials found low-certainty evidence to suggest that continuing or discontinuing antiplatelet therapy for a non-cardiac surgery does not make a difference in mortality, major bleeds that require surgery, or ischaemic events. [9] The same review found moderate certainty evidence that continuing or discontinuing therapy also did not have a big difference on the incidence of bleeds requiring a blood transfusion. [9]

Dental management of patients on antiplatelet drugs

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. [3]

Assess bleeding risk

Identify the likelihood and risk of dental treatment causing bleeding complications. [3]

Dental procedures unlikely to cause bleedingDental procedures with low risk of post-operative bleeding complicationsDental procedures with high risk of post-operative bleeding complications
Local anaesthesia using aspirating syringe and vasoconstrictorSimple extractions up to 3 teeth with restricted wound sizeExtractions involving surgery, large wound or more than 3 teeth at once
Basic Periodontal examination (BPE)Incision and drainage of intra-oral swellingsFlap raising procedures
Supragingival plaque, calculus, stain removalSix point full periodontal examinationGingival recontouring
Direct or indirect restoration with supragingival marginsRoot surface debridement and subgingival scalingBiopsies
Orthograde endodonticsDirect or indirect restorations with subgingival margins
Prosthetic procedures
Fitting and adjustment of orthodontic appliances.

Drug toxicity

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 could cause prolonged or excessive bleeding. A decrease in antiplatelet effect would reduce the risk of bleeding, but increase the thromboembolic risk. [3] Drug toxicity may increase when multiple antiplatelet drugs are used. Gastrointestinal bleeding is a common adverse event seen in many patients. [11]

Medications

Medications that may increase antiplatelet drug effect: [3]

Medications that may decrease antiplatelet drug effect: [3]

Use of NSAIDs as part of dental management of patients with vascular disease should be discouraged as NSAIDs have antiplatelet effect. Instead, simple analgesics such as paracetamol or co-codamol should be of first choice. If NSAIDs are required, the risk of bleeding increases with duration of dental treatment. [3]

Medical conditions

Medical conditions that may increase antiplatelet drugs' effect include: [3]

Chronic kidney 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

Food and supplements that may increase antiplatelet drugs' effect: [3]

St. John's wort, ginkgo biloba, garlic.

Oral antiplatelet drugs available in the UK

Oral Antiplatelet DrugsUK Trade NameOther Names (Non-UK)
AspirinNu-Seals, Microprin, caprin Dual with dipyridamole: Asasantin Retard, Molita Modified ReleaseThere are numerous brand names for Aspirin
ClopidogrelPlavix, GrepidIscover
DipyridamolePersantin, Persantin Retard, Attia Modified Release, Ofcram PR. Dual with aspirin: Asasantin Retard, Molita Modified Release
PrasugrelEfientEffient, Prasita
TicagrelorBriliqueBrilinta, Possia

[3]

See also

Related Research Articles

<span class="mw-page-title-main">Aspirin</span> Medication

Aspirin, also known as acetylsalicylic acid (ASA), is a nonsteroidal anti-inflammatory drug (NSAID) used to reduce pain, fever, and/or inflammation, and as an antithrombotic. Specific inflammatory conditions which aspirin is used to treat include Kawasaki disease, pericarditis, and rheumatic fever.

<span class="mw-page-title-main">Angina</span> Chest discomfort due to not enough blood flow to heart muscle

Angina, also known as angina pectoris, is chest pain or pressure, usually caused by insufficient blood flow to the heart muscle (myocardium). It is most commonly a symptom of coronary artery disease.

<span class="mw-page-title-main">Anticoagulant</span> Class of drugs

Anticoagulants, commonly known as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time. Some of them occur naturally in blood-eating animals such as leeches and mosquitoes, where they help keep the bite area unclotted long enough for the animal to obtain some blood. As a class of medications, anticoagulants are used in therapy for thrombotic disorders. Oral anticoagulants (OACs) are taken by many people in pill or tablet form, and various intravenous anticoagulant dosage forms are used in hospitals. Some anticoagulants are used in medical equipment, such as sample tubes, blood transfusion bags, heart–lung machines, and dialysis equipment. One of the first anticoagulants, warfarin, was initially approved as a rodenticide.

<span class="mw-page-title-main">Clopidogrel</span> Antiplatelet medication

Clopidogrel — sold under the brand name Plavix, among others — is an antiplatelet medication used to reduce the risk of heart disease and stroke in those at high risk. It is also used together with aspirin in heart attacks and following the placement of a coronary artery stent. It is taken by mouth. Its effect starts about two hours after intake and lasts for five days.

<span class="mw-page-title-main">Thromboxane</span> Group of lipids

Thromboxane is a member of the family of lipids known as eicosanoids. The two major thromboxanes are thromboxane A2 and thromboxane B2. The distinguishing feature of thromboxanes is a 6-membered ether-containing ring.

<span class="mw-page-title-main">Ticlopidine</span> Chemical compound

Ticlopidine, sold under the brand name Ticlid, is a medication used to reduce the risk of thrombotic strokes. It is an antiplatelet drug in the thienopyridine family which is an adenosine diphosphate (ADP) receptor inhibitor. Research initially showed that it was useful for preventing strokes and coronary stent occlusions. However, because of its rare but serious side effects of neutropenia and thrombotic thrombocytopenic purpura it was primarily used in patients in whom aspirin was not tolerated, or in whom dual antiplatelet therapy was desirable. With the advent of newer and safer antiplatelet drugs such as clopidogrel and ticagrelor, its use remained limited.

<span class="mw-page-title-main">Dipyridamole</span> Anticoagulant drug

Dipyridamole is a nucleoside transport inhibitor and a PDE3 inhibitor medication that inhibits blood clot formation when given chronically and causes blood vessel dilation when given at high doses over a short time.

<span class="mw-page-title-main">Prasugrel</span> Medication used to prevent formation of blood clots

Prasugrel, sold under the brand name Effient in the US, Australia and India, and Efient in the EU) is a medication used to prevent formation of blood clots. It is a platelet inhibitor and an irreversible antagonist of P2Y12 ADP receptors and is of the thienopyridine drug class. It was developed by Daiichi Sankyo Co. and produced by Ube and marketed in the United States in cooperation with Eli Lilly and Company.

<span class="mw-page-title-main">Unstable angina</span> Medical condition

Unstable angina is a type of angina pectoris that is irregular or more easily provoked. It is classified as a type of acute coronary syndrome.

<span class="mw-page-title-main">Eptifibatide</span> Antiplatelet drug

Eptifibatide, is an antiplatelet drug of the glycoprotein IIb/IIIa inhibitor class. Eptifibatide is a cyclic heptapeptide derived from a disintegrin protein found in the venom of the southeastern pygmy rattlesnake. It belongs to the class of the arginin-glycin-aspartat-mimetics and reversibly binds to platelets. Eptifibatide has a short half-life. The drug is the third inhibitor of GPIIb/IIIa that has found broad acceptance after the specific antibody abciximab and the non-peptide tirofiban entered the global market.

P2Y<sub>12</sub> Protein-coding gene in the species Homo sapiens

P2Y12 is a chemoreceptor for adenosine diphosphate (ADP) that belongs to the Gi class of a group of G protein-coupled (GPCR) purinergic receptors. This P2Y receptor family has several receptor subtypes with different pharmacological selectivity, which overlaps in some cases, for various adenosine and uridine nucleotides. The P2Y12 receptor is involved in platelet aggregation and is thus a biological target for the treatment of thromboembolisms and other clotting disorders. Two transcript variants encoding the same isoform have been identified for this gene.

<span class="mw-page-title-main">Bivalirudin</span> Anticoagulant drug

Bivalirudin (Bivalitroban), sold under the brand names Angiomax and Angiox and manufactured by The Medicines Company, is a specific and reversible direct thrombin inhibitor (DTI).

<span class="mw-page-title-main">Coronary stent</span> Medical apparatus implanted into coronary arteries

A coronary stent is a tube-shaped device placed in the coronary arteries that supply blood to the heart, to keep the arteries open in the treatment of coronary heart disease. It is used in a procedure called percutaneous coronary intervention (PCI). Coronary stents are now used in more than 90% of PCI procedures. Stents reduce angina and have been shown to improve survival and decrease adverse events in an acute myocardial infarction.

<span class="mw-page-title-main">Vorapaxar</span> Chemical compound

Vorapaxar is a thrombin receptor antagonist based on the natural product himbacine, discovered by Schering-Plough and developed by Merck & Co.

<span class="mw-page-title-main">Ticagrelor</span> Coronary medication

Ticagrelor, sold under the brand name Brilinta among others, is a medication used for the prevention of stroke, heart attack and other events in people with acute coronary syndrome, meaning problems with blood supply in the coronary arteries. It acts as a platelet aggregation inhibitor by antagonising the P2Y12 receptor. The drug is produced by AstraZeneca.

<span class="mw-page-title-main">Myocardial infarction</span> Interruption of blood supply to a part of the heart

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the coronary arteries of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw. Often it occurs in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat or feeling tired. About 30% of people have atypical symptoms. Women more often present without chest pain and instead have neck pain, arm pain or feel tired. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock or cardiac arrest.

<span class="mw-page-title-main">Cangrelor</span> Chemical compound

Cangrelor, sold under the brand name Kengreal among others, is a P2Y12 inhibitor FDA approved as of June 2015 as an antiplatelet drug for intravenous application. Some P2Y12 inhibitors are used clinically as effective inhibitors of adenosine diphosphate-mediated platelet activation and aggregation. Unlike clopidogrel (Plavix), which is a prodrug, cangrelor is an active drug not requiring metabolic conversion.

Adenosine diphosphate (ADP) receptor inhibitors are a drug class of antiplatelet agents, used in the treatment of acute coronary syndrome (ACS) or in preventive treatment for patients who are in risk of thromboembolism, myocardial infarction or a stroke. These drugs antagonize the P2Y12 platelet receptors and therefore prevent the binding of ADP to the P2Y12 receptor. This leads to a decrease in aggregation of platelets, prohibiting thrombus formation. The P2Y12 receptor is a surface bound protein found on blood platelets. They belong to G protein-coupled purinergic receptors (GPCR) and are chemoreceptors for ADP.

<span class="mw-page-title-main">Reperfusion therapy</span> Restoring blood flow post-heart attack

Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack. Reperfusion therapy includes drugs and surgery. The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis. Surgeries performed may be minimally-invasive endovascular procedures such as a percutaneous coronary intervention (PCI), which involves coronary angioplasty. The angioplasty uses the insertion of a balloon and/or stents to open up the artery. Other surgeries performed are the more invasive bypass surgeries that graft arteries around blockages.

<span class="mw-page-title-main">Management of acute coronary syndrome</span>

Management of acute coronary syndrome is targeted against the effects of reduced blood flow to the affected area of the heart muscle, usually because of a blood clot in one of the coronary arteries, the vessels that supply oxygenated blood to the myocardium. This is achieved with urgent hospitalization and medical therapy, including drugs that relieve chest pain and reduce the size of the infarct, and drugs that inhibit clot formation; for a subset of patients invasive measures are also employed. Basic principles of management are the same for all types of acute coronary syndrome. However, some important aspects of treatment depend on the presence or absence of elevation of the ST segment on the electrocardiogram, which classifies cases upon presentation to either ST segment elevation myocardial infarction (STEMI) or non-ST elevation acute coronary syndrome (NST-ACS); the latter includes unstable angina and non-ST elevation myocardial infarction (NSTEMI). Treatment is generally more aggressive for STEMI patients, and reperfusion therapy is more often reserved for them. Long-term therapy is necessary for prevention of recurrent events and complications.

References

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  2. ↑ García-Ropero Á, Vargas-Delgado AP, Santos-Gallego CG, Badimon JJ (April 2020). "Direct Oral Anticoagulants and Coronary Artery Disease: The Debacle of the Aspirin Era?". Journal of Cardiovascular Pharmacology. 75 (4): 269–275. doi:10.1097/FJC.0000000000000795. PMID   31923049. S2CID   210149420.
  3. 1 2 3 4 5 6 7 8 9 10 11 12 "SDCEP Anticoagulants and Antiplatelets" (PDF). Archived from the original (PDF) on 2017-03-28. Retrieved 2016-03-09.
  4. 1 2 Fihn SD, Gardin JM, Abrams J, Berra K, Blankenship JC, Dallas AP, et al. (American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons) (December 2012). "2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart diseasem". Circulation. 126 (25): e354–e471. doi: 10.1161/CIR.0b013e318277d6a0 . PMID   23166211.
  5. 1 2 3 Wright RS, Anderson JL, Adams CD, Bridges CR, Casey DE, Ettinger SM, et al. (American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the American College of Emergency Physicians, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons) (May 2011). "2011 ACCF/AHA focused update of the Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (updating the 2007 guideline)". Journal of the American College of Cardiology. 57 (19): 1920–1959. doi: 10.1016/j.jacc.2011.02.009 . PMID   21450428.
  6. ↑ Gurbel PA, Fox KA, Tantry US, Ten Cate H, Weitz JI (April 2019). "Combination Antiplatelet and Oral Anticoagulant Therapy in Patients With Coronary and Peripheral Artery Disease". Circulation. 139 (18): 2170–2185. doi: 10.1161/CIRCULATIONAHA.118.033580 . PMID   31034291. S2CID   207592252.
  7. ↑ Lange, RA; Hillis, LD (2013), "The duel between dual antiplatelet therapies", N Engl J Med, 368 (14): 1356–1357, doi:10.1056/NEJMe1302504, PMID   23473370.
  8. ↑ Udell JA, Bonaca MP, Collet JP, Lincoff AM, Kereiakes DJ, Costa F, et al. (January 2016). "Long-term dual antiplatelet therapy for secondary prevention of cardiovascular events in the subgroup of patients with previous myocardial infarction: a collaborative meta-analysis of randomized trials". European Heart Journal. 37 (4): 390–399. doi: 10.1093/eurheartj/ehv443 . PMID   26324537.
  9. 1 2 3 Lewis SR, Pritchard MW, Schofield-Robinson OJ, Alderson P, Smith AF (July 2018). "Continuation versus discontinuation of antiplatelet therapy for bleeding and ischaemic events in adults undergoing non-cardiac surgery". The Cochrane Database of Systematic Reviews. 7 (7): CD012584. doi:10.1002/14651858.CD012584.pub2. PMC   6513221 . PMID   30019463.
  10. ↑ Yeung LY, Sarani B, Weinberg JA, McBeth PB, May AK (2016). "Surgeon's guide to anticoagulant and antiplatelet medications part two: antiplatelet agents and perioperative management of long-term anticoagulation". Trauma Surgery & Acute Care Open. 1 (1): e000022. doi:10.1136/tsaco-2016-000022. PMC   5891708 . PMID   29767644.
  11. ↑ Shehab N, Sperling LS, Kegler SR, Budnitz DS (November 2010). "National estimates of emergency department visits for hemorrhage-related adverse events from clopidogrel plus aspirin and from warfarin". Archives of Internal Medicine. 170 (21): 1926–1933. doi: 10.1001/archinternmed.2010.407 . PMID   21098354.
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