Frequently Asked Questions
The dosing of COUMADIN® (Warfarin Sodium) must be individualized according to patient’s sensitivity to the drug as indicated by the PT/INR. Use of a large loading dose may increase the incidence of hemorrhagic and other complications, does not offer more rapid protection against thrombi formation, and is not recommended. It is recommended that COUMADIN therapy be initiated with a dose of 2 to 5 mg per day with dosage adjustments based on the results of PT/INR determinations. The lower initiation doses should be considered for patients with certain genetic variations in CYP2C9 and VKORC1 enzymes as well as for elderly and/or debilitated patients and patients with potential to exhibit greater than expected PT/INR responses to COUMADIN.
Regular monitoring of INR should be performed on all treated patients.1 Those at high risk of bleeding may benefit from more frequent INR monitoring, careful dose adjustment to desired INR, and a shorter duration of therapy.1 Patients should be instructed about prevention measures to minimize risk of bleeding and to report immediately to physicians signs and symptoms of bleeding (see PRECAUTIONS: Information for Patients).1
REFERENCE
- National Heart Lung Blood Institute Website. Diseases and conditions index: deep vein thrombosis. http://www.nhlbi.nih.gov/health/dci/Diseases/Dvt/DVT_All.html. Accessed October 3, 2008.
COUMADIN® and other coumarin anticoagulants act by inhibiting the synthesis of Vitamin K dependent clotting factors, which include Factors II, VII, IX and X, and the anticoagulant proteins C and S. Half-lives of these clotting factors are as follows: Factor II - 60 hours, VII - 4-6 hours, IX - 24 hours, and X - 48-72 hours.1 The half-lives of proteins C and S are approximately 8 hours and 30 hours, respectively.1 The resultant in vivo effect is a sequential depression of Factor VII, Protein C, Factor IX, Protein S, and Factor X and II activities.2 Vitamin K is an essential cofactor for the post ribosomal synthesis of the Vitamin K dependent clotting factors.2 The vitamin promotes the biosynthesis of γ-carboxyglutamic acid residues in the proteins which are essential for biological activity.1
Warfarin is thought to interfere with clotting factor synthesis by inhibition of the C1 subunit of the Vitamin K epoxide reductase (VKORC1) enzyme complex, thereby reducing the regeneration of Vitamin K1 epoxide.1 The degree of depression is dependent upon the dosage administered and, in part, by the patient's VKORC1 genotype.1 Therapeutic doses of warfarin decrease the total amount of the active form of each Vitamin K dependent clotting factor made by the liver by approximately 30% to 50%.1
An anticoagulation effect generally occurs within 24 hours after drug administration.1 However, peak anticoagulant effect may be delayed 72 to 96 hours.1 The duration of action of a single dose of racemic warfarin is 2 to 5 days.1 The effects of COUMADIN may become more pronounced as effects of daily maintenance doses overlap.1 Anticoagulants have no direct effect on an established thrombus, nor do they reverse ischemic tissue damage.1 However, once a thrombus has occurred, the goal of anticoagulant treatment is to prevent further extension of the formed clot and prevent secondary thromboembolic complications which may result in serious and possibly fatal sequelae.1
REFERENCES
- National Heart Lung Blood Institute Website. Diseases and conditions index: deep vein thrombosis. http://www.nhlbi.nih.gov/health/dci/Diseases/Dvt/DVT_All.html. Accessed October 3, 2008.
- COUMADIN Package Insert.
The amount of Vitamin K1 in food may affect therapy with COUMADIN®. Patients should eat a normal, balanced diet maintaining a consistent amount of Vitamin K1. Drastic changes in dietary habits such as eating large amounts of green leafy vegetables, should be avoided. Patients do not need to eliminate all foods containing Vitamin K1 from their diet.
In general, leafy, green vegetables and certain legumes and vegetable oils contain high amounts of Vitamin K1. Foods that appear to contain low amounts of Vitamin K1 include roots, bulbs, tubers, the fleshy portion of fruits, fruit juices, and other beverages. Likewise, cereal grains and their milled products appear to be low in Vitamin K1.
The most common adverse event and serious risk of oral anticoagulation therapy with COUMADIN (Warfarin Sodium)® is bleeding in any tissue or organ.
Caution should be exercised when herbal products are taken together with COUMADIN®.
The use of herbal products may increase or decrease the effects of COUMADIN®. Patients may want to avoid herbal teas containing tonka beans, melilot (sweet clover), or sweet woodruff, since these products already contain a natural COUMADIN® derivative.
The administration and dosage of COUMADIN® must be individualized for each patient according to the particular patient’s prothrombin time (PT)/International Normalized Ratio (INR) response to the drug. The dosage should be adjusted based upon the patient’s PT/INR.1
Venous Thromboembolism (including deep venous thrombosis [DVT] and pulmonary embolism [PE]): For patients with a first episode of DVT or PE secondary to a transient (reversible) risk factor, treatment with warfarin for 3 months is recommended. For patients with a first episode of idiopathic DVT or PE, warfarin is recommended for at least 6 to 12 months. For patients with two or more episodes of documented DVT or PE, indefinite treatment with warfarin is suggested. For patients with a first episode of DVT or PE who have documented antiphospholipid antibodies or who have two or more thrombophilic conditions, treatment for 12 months is recommended and indefinite therapy is suggested. For patients with a first episode of DVT or PE who have documented deficiency of antithrombin, deficiency of Protein C or Protein S, or the Factor V Leiden or prothrombin 20210 gene mutation, homocystinemia, or high Factor VIII levels (>90th percentile of normal), treatment for 6 to 12 months is recommended and indefinite therapy is suggested for idiopathic thrombosis. The risk-benefit should be reassessed periodically in patients who receive indefinite anticoagulant treatment.2,5 The dose of warfarin should be adjusted to maintain a target INR of 2.5 (INR range, 2.0 to 3.0) for all treatment durations. These recommendations are supported by the 7th ACCP guidelines.3,4,6,7
Atrial Fibrillation: Five clinical trials evaluated the effects of warfarin in patients with non-valvular atrial fibrillation (AF). Meta-analysis findings of these studies revealed that the effects of warfarin in reducing thromboembolic events including stroke were similar at either moderately high INR (2.0-4.5) or low INR (1.4-3.0). There was a significant reduction in minor bleeds at the low INR. There are no adequate and well-controlled studies in populations with atrial fibrillation and valvular heart disease. Similar data from clinical studies in valvular atrial fibrillation patients are not available. The trials in non-valvular atrial fibrillation support the American College of Chest Physicians’ (7th ACCP) recommendation that an INR of 2.0-3.0 be used for warfarin therapy in appropriate AF patients.4
Oral anticoagulation therapy with warfarin is recommended in patients with persistent or paroxysmal AF (PAF) (intermittent AF) at high risk of stroke (i.e., having any of the following features: prior ischemic stroke, transient ischemic attack, or systemic embolism, age >75 years, moderately or severely impaired left ventricular systolic function and/or congestive heart failure, history of hypertension, or diabetes mellitus). In patients with persistent AF or PAF, age 65 to 75 years, in the absence of other risk factors, but who are at intermediate risk of stroke, antithrombotic therapy with either oral warfarin or aspirin, 325 mg/day, is recommended. For patients with AF and mitral stenosis, anticoagulation with oral warfarin is recommended (7th ACCP). For patients with AF and prosthetic heart valves, anticoagulation with oral warfarin should be used; the target INR may be increased and aspirin added depending on valve type and position, and on patient factors.4
Post-Myocardial Infarction: The results of the WARIS II study and 7th ACCP guidelines suggest that in most healthcare settings, moderate- and low-risk patients with a myocardial infarction should be treated with aspirin alone over oral Vitamin-K antagonist (VKA) therapy plus aspirin. In healthcare settings in which meticulous INR monitoring is standard and routinely accessible, for both high- and low-risk patients after myocardial infarction (MI), long-term (up to 4 years) high-intensity oral warfarin (target INR, 3.5; range, 3.0 to 4.0) without concomitant aspirin or moderateintensity oral warfarin (target INR, 2.5; range, 2.0 to 3.0) with aspirin is recommended. For high-risk patients with MI, including those with a large anterior MI, those with significant heart failure, those with intracardiac thrombus visible on echocardiography, and those with a history of a thromboembolic event, therapy with combined moderate-intensity (INR, 2.0 to 3.0) oral warfarin plus low-dose aspirin (≤100 mg/day) for 3 months after the MI is suggested.8
Mechanical and Bioprosthetic Heart Valves: For all patients with mechanical prosthetic heart valves, warfarin is recommended. For patients with a St. Jude Medical (St. Paul, MN) bileaflet valve in the aortic position, a target INR of 2.5 (range, 2.0 to 3.0) is recommended. For patients with tilting disk valves and bileaflet mechanical valves in the mitral position, the 7th ACCP recommends a target INR of 3.0 (range, 2.5 to 3.5). For patients with caged ball or caged disk valves, a target INR of 3.0 (range, 2.5 to 3.5) in combination with aspirin, 75 to 100 mg/day is recommended. For patients with bioprosthetic valves, warfarin therapy with a target INR of 2.5 (range, 2.0 to 3.0) is recommended for valves in the mitral position and is suggested for valves in the aortic position for the first 3 months after valve insertion.3
Recurrent Systemic Embolism and Other Indications: Oral anticoagulation therapy has not been evaluated by properly designed clinical trials in patients with valvular disease associated with atrial fibrillation, patients with mitral stenosis, and patients with recurrent systemic embolism of unknown etiology. A moderate dose regimen (INR 2.0 to 3.0) is recommended for these patients.4
An INR of greater than 4.0 appears to provide no additional therapeutic benefit in most patients and is associated with a higher risk of bleeding.
REFERENCE
- COUMADIN Package Insert.
- Büller HR, Agnelli G, Hull RD, Hyers TM, Prins MH, Raskob GE. Antithrombotic therapy for venous thromboembolic disease. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:401S-428S.
- Salem DN, Stein PD, Al-Ahmad A, et al. Antithrombotic therapy in valvular heart disease–native and prosthetic. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:457S-482S.
- Singer DE, Albers GW, Dalen JE, Go AS, Halperin JL, Manning WJ. Antithrombotic therapy in atrial fibrillation. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:429S-456S.
- Kearon C, Ginsberg JS, Kovacs MJ, et al, for the Extended Low-Intensity Anticoagulation for Thrombo-Embolism Investigators. Comparison of low-intensity warfarin therapy with conventional-intensity warfarin therapy for longterm prevention of recurrent venous thromboembolism. N Engl J Med. 2003;349:631-639.
- Schulman S, Granqvist S, Holmström M, et al, and the Duration of Anticoagulation Trial Study Group. The duration of oral anticoagulant therapy after a second episode of venous thromboembolism. N Engl J Med. 1997;336:393-398.
- Ridker PM, Goldhaber SZ, Danielson E, et al, for the PREVENT Investigators. Long-term, low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med. 2003;348:1425-1434.
- Harrington RA, Becker RC, Ezekowitz M, et al. Antithrombotic therapy for coronary artery disease. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126:513S-548S.
Prothrombin time (PT)/International Normalized Ratio (INR) determinations are used to measure the patient’s response to warfarin therapy. Periodic determination of PT/INR or other suitable coagulation test is essential. Numerous factors, alone or in combination, may influence the response of the patient to anticoagulants (eg, travel, changes in diet, environment, physical state, and medication, including botanicals). Consequently, it is generally good practice to monitor the patient’s response with additional PT/INR determinations in the period immediately after discharge from the hospital, and whenever other medications, including botanicals, are initiated, discontinued, or taken irregularly.
Drugs may interact with COUMADIN® (Warfarin Sodium Tablets, USP) Crystalline through pharmacodynamic or pharmacokinetic mechanisms. Pharmacodynamic mechanisms for drug interactions with COUMADIN® are synergism (impaired hemostasis, reduced clotting factor synthesis), competitive antagonism (Vitamin K), and altered physiologic control loop for Vitamin K metabolism (hereditary resistance). Pharmacokinetic mechanisms for drug interactions with COUMADIN® are mainly enzyme induction, enzyme inhibition, and reduced plasma protein binding. It is important to note that some drugs may interact by more than one mechanism.
Because a patient may be exposed to a combination of factors, the net effect of COUMADIN® on PT/INR response may be unpredictable. Medications of unknown interaction with coumarins are best regarded with caution. When these medications are started or stopped, or taken irregularly, more frequent PT/INR monitoring is advisable.
DECREASED
PT/INR
|
INCREASED
PT/INR
|
CLASSES
OF DRUGS
|
| |
 |
5-lipoxygenase inhibitor |
|
|
Adrenal Cortical Steroid Inhibitors |
| |
|
Adrenergic Stimulants (Central) |
| |
|
Alcohol Abuse Reduction Preparations |
| |
|
Analgesics |
| |
|
Anesthetics (Inhalation) |
|
|
Antacids |
| |
|
Antiandrogen |
|
|
Antianxiety Agents |
|
|
Antiarrhythmics |
|
|
Antibiotics |
| |
|
Aminoglycosides (oral) |
| |
|
Cephalosporins (parenteral) |
| |
|
Macrolides |
| |
|
Miscellaneous |
| |
|
Penicillins (Intravenous, High Dose) |
| |
|
Quinolones (Fluoroquinolones) |
| |
|
Sulfonamides (Long Acting) |
| |
|
Tetracyclines |
| |
|
Anticoagulants |
|
|
Anticonvulsants |
|
|
Antidepressants |
|
|
Antihistamines |
| |
|
Antimalarial Agents |
|
|
Antineoplastics |
| |
|
Antiparasitic/Antimicrobials |
| |
|
Antiplatelet Drugs/Effects |
|
|
Antipsychotic Medications |
|
|
Antithyroid Drugs |
|
|
Barbiturates |
| |
|
Beta-Adrenergic Blockers |
| |
|
Cholelitholytic Agents |
| |
|
Diabetes Agents (Oral) |
|
|
Diuretics |
|
|
Enteral Nutritional Supplements |
|
|
Fungal Medications (Intravaginal, Systemic) |
|
|
Gastric Acidity and Peptic Ulcer Agents |
| |
|
Gastrointestinal |
| |
|
Prokinetic Agents |
| |
|
Ulcerative Colitis Agents |
| |
|
Gout Treatment Agents |
| |
|
Hemorrheologic Agents |
| |
|
Hepatotoxic Drugs |
| |
|
Hyperglycemic Agents |
| |
|
Hypertensive Emergency Agents |
|
|
Hypnotics |
|
|
Hypolipidemics |
|
|
Bile Acid Binding Resins |
| |
|
Fibric Acid Derivatives |
|
|
HMG-CoA Reductase Inhibitors |
|
|
Immunosuppressives |
| |
|
Leukotriene Receptor Antagonist |
| |
|
Monoamine Oxidase Inhibitors |
| |
|
Narcotics (Prolonged) |
| |
|
Nonsteroidal Anti-inflammatory Agents |
|
|
Oral Contraceptives (Estrogen Containing) |
| |
|
Psychostimulants |
| |
|
Pyrazolones |
| |
|
Salicylates |
|
|
Selective Estrogen Receptor Modulators |
| |
|
Selective Serotonin Reuptake Inhibitors |
|
|
Steroids (Adrenocortical) |
| |
|
Steroids (Anabolic, 17-Alkyl Testosterone
Derivatives) |
| |
|
Thrombolytics |
| |
|
Thyroid Drugs |
|
|
Tuberculosis Agents |
| |
|
Uricosuric Agents |
| |
|
Vaccines |
|
|
Vitamins |
DECREASED
PT/INR |
INCREASED
PT/INR |
SPECIFIC
DRUGS REPORTED |
| |
|
Acetaminophen |
|
|
Alcohol |
| |
|
Allopurinol |
|
|
Aminoglutethimide |
| |
|
Aminosalicylic Acid |
| |
|
Amiodarone HCl |
|
|
Amobarbital |
| |
|
Aspirin |
|
|
Atorvastatin |
|
|
Azathioprine |
| |
|
Azithromycin |
|
|
Butabarbital |
| |
|
Capecitabine |
|
|
Carbamazepine |
| |
|
Cefamandole |
| |
|
Cefazolin |
| |
|
Cefoperazone |
| |
|
Cefotetan |
| |
|
Cefoxitin |
| |
|
Ceftriaxone |
| |
|
Celecoxib |
| |
|
Cerivastatin |
| |
|
Chenodiol |
|
|
Chloral Hydrate |
| |
|
Chloramphenicol |
|
|
Chlordiazepoxide |
| |
|
Chlorpropamide |
|
|
Chlorthalidone |
|
|
Cholestyramine |
| |
|
Cimetidine |
| |
|
Ciprofloxacin |
| |
|
Cisapride |
| |
|
Clarithromycin |
| |
|
Clofibrate |
|
|
Clozapine |
|
|
Corticotropin |
|
|
Cortisone |
| |
|
COUMADIN® Overdosage |
|
|
COUMADIN® Underdosage |
|
|
Cyclophosphamide |
| |
|
Danazol |
| |
|
Dextran |
| |
|
Dextrothyroxine |
| |
|
Diazoxide |
| |
|
Diclofenac |
|
|
Dicloxacillin |
| |
|
Dicumarol |
| |
|
Diflunisal |
| |
|
Disulfiram |
| |
|
Doxycycline |
| |
|
Erythromycin |
|
|
Ethchlorvynol |
| |
|
Ethacrynic Acid |
| |
|
Fenofibrate |
| |
|
Fenoprofen |
| |
|
Fluconazole |
| |
|
Fluorouracil |
| |
|
Fluoxetine |
| |
|
Flutamide |
| |
|
Fluvastatin |
| |
|
Fluvoxamine |
| |
|
Gemfibrozil |
| |
|
Glucagon |
|
|
Glutethimide |
|
|
Griseofulvin |
|
|
Haloperidol |
| |
|
Halothane |
| |
|
Heparin |
| |
|
Ibuprofen |
| |
|
Ifosfamide |
| |
|
Indomethacin |
| |
|
Influenza Virus Vaccine |
| |
|
Itraconazole |
| |
|
Ketoprofen |
| |
|
Ketorolac |
| |
|
Levamisole |
| |
|
Levofloxacin |
| |
|
Levothyroxine |
| |
|
Liothyronine |
| |
|
Lovastatin |
| |
|
Mefenamic Acid |
|
|
Meprobamate |
|
|
6-Mercaptopurine |
|
|
Methimazole |
| |
|
Methyldopa |
| |
|
Methylphenidate |
| |
|
Methylsalicylate Ointment (topical) |
| |
|
Metronidazole |
| |
|
Miconazole (intravaginal, systemic) |
|
|
Moricizine Hydrochloride |
|
|
Nafcillin |
| |
|
Nalidixic Acid |
| |
|
Naproxen |
| |
|
Neomycin |
| |
|
Norfloxacin |
| |
|
Ofloxacin |
| |
|
Olsalazine |
| |
|
Omeprazole |
| |
|
Oxaprozin |
| |
|
Oxymetholone |
|
|
Paraldehyde |
| |
|
Paroxetine |
| |
|
Penicillin G (intravenous) |
|
|
Pentobarbital |
| |
|
Pentoxifylline |
|
|
Phenobarbital |
| |
|
Phenylbutazone |
|
|
Phenytoin |
| |
|
Piperacillin |
| |
|
Piroxicam |
|
|
Pravastatin |
|
|
Prednisone |
|
|
Primidone |
| |
|
Propafenone |
| |
|
Propoxyphene |
| |
|
Propranolol |
|
|
Propylthiouracil |
| |
|
Quinidine |
| |
|
Quinine |
|
|
Raloxifene |
|
|
Ranitidine |
|
|
Rifampin |
| |
|
Rofecoxib |
|
|
Secobarbital |
| |
|
Sertraline |
| |
|
Simvastatin |
|
|
Spironolactone |
| |
|
Stanozolol |
| |
|
Streptokinase |
|
|
Sucralfate |
| |
|
Sulfamethizole |
| |
|
Sulfamethoxazole |
| |
|
Sulfinpyrazone |
| |
|
Sulfisoxazole |
| |
|
Sulindac |
| |
|
Tamoxifen |
| |
|
Tetracycline |
| |
|
Thyroid |
| |
|
Ticarcillin |
| |
|
Ticlopidine |
| |
|
Tissue Plasminogen Activator (t-PA) |
| |
|
Tolbutamide |
| |
|
Tramadol |
|
|
Trazodone |
| |
|
Trimethoprim/Sulfamethoxazole |
| |
|
Urokinase |
| |
|
Valproate |
|
|
Vitamin C (high dose) |
| |
|
Vitamin E |
|
|
Vitamin K |
| |
|
Zafirlukast |
| |
|
Zileuton |
Coumarins may also affect the action of other drugs. Hypoglycemic agents (chlorpropamide and tolbutamide) and anticonvulsants (phenytoin and phenobarbital) may accumulate in the body as a result of interference with either their metabolism or excretion.
Caution should be observed when COUMADIN® (Warfarin Sodium Tablets, USP) (or warfarin) is administered concomitantly with nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin, to be certain that no change in anticoagulation dosage is required. In addition to specific drug interactions that might affect PT/INR, NSAIDs, including aspirin, can inhibit platelet aggregation, and can cause gastrointestinal bleeding, peptic ulceration and/or perforation.
It has been reported that concomitant administration of warfarin and ticlopidine may be associated with cholestatic hepatitis.
DECREASED
PT/INR |
INCREASED
PT/INR |
OTHER FACTORS THAT MAY
AFFECT PT/INR |
| |
|
Blood Dyscrasias (See Contraindications in the
full prescribing information)
|
| |
|
Cancer |
| |
|
Collagen Vascular Disease |
| |
|
Congestive Heart Failure |
| |
|
Diarrhea |
|
|
Diet High in Vitamin K |
| |
|
Dietary Deficiencies |
|
|
Edema |
| |
|
Elevated Temperature |
| |
|
Hepatic Disorders: |
| |
|
Infectious Hepatitis, Jaundice |
|
|
Hereditary Coumarin Resistance |
|
|
Hyperlipemia |
| |
|
Hyperthyroidism |
|
|
Hypothyroidism |
|
|
Nephrotic Syndrome |
| |
|
Other Medications Affecting Blood Elements
That May Modify Hemostasis |
| |
|
Poor Nutritional State |
| |
|
Prolonged Hot Weather |
| |
|
Steatorrhea |
|
|
Unreliable PT/INR Determinations |
| |
|
Vitamin K Deficiency |
Patients should be warned that all warfarin sodium, USP, products represent the same medication and should not be taken together as overdosage may result.
Patients have mistakenly taken both COUMADIN® and generic warfarin, resulting in overdosage. Increased INRs have been reported in these patients.
Caution should be exercised when botanical medicines (botanicals) are taken concomitantly with COUMADIN® (Warfarin Sodium Tablets, USP). Few adequate, well-controlled studies exist evaluating the potential for metabolic and/or pharmacologic interactions between botanicals and COUMADIN®. Due to a lack of manufacturing standardization with botanical medicinal preparations, the amount of active ingredients may vary. This could further confound the ability to assess potential interactions and effects on anticoagulation. It is good practice to monitor the patient’s response with additional PT/INR determinations when initiating or discontinuing botanicals.
Specific botanicals reported to affect therapy for COUMADIN® include the following:
- Bromelains, danshen, dong quai (Angelica sinensis), garlic, Ginkgo biloba, and ginseng are associated most often with an INCREASE in the effects of COUMADIN®.
- Coenzyme Q10 (ubidecarenone) and St. John’s wort are associated most often with a DECREASE in the effects of COUMADIN®.
Some botanicals may cause bleeding events when taken alone (eg, garlic and Ginkgo biloba) and may have anticoagulant, antiplatelet, and/or fibrinolytic properties. These effects would be expected to be additive to the anticoagulant effects of COUMADIN®. Conversely, other botanicals may have coagulant properties when taken alone or may decrease the effects of COUMADIN® (Warfarin Sodium Tablets, USP).
Some botanicals that may affect coagulation are listed below for reference; however, this list should not be considered all-inclusive. Many botanicals have several common names as well as a scientific name. The most widely recognized common botanical names are listed.
| BOTANICALS THAT CONTAIN COUMARINS WITH POTENTIAL ANTICOAGULANT EFFECTS |
| Agrimony§ |
Cassia‡ |
Parsley |
| Alfalfa |
Celery |
Passion Flower |
Angelica Sinensis
(Dong Quai) |
Chamomile
(German and Roman) |
Prickly Ash
(Northern) |
| Aniseed |
Dandelion‡ |
Quassia |
| Arnica |
Fenugreek |
Red Clover |
| Asa Foetida |
Horse Chestnut |
Sweet Clover |
| Bogbean* |
Horseradish |
Sweet Woodruff |
| Boldo |
Licorice‡ |
Tonka Beans |
| Buchu |
Meadowsweet* |
Wild Carrot |
| Capsicum† |
Nettle |
Wild Lettuce |
| MISCELLANEOUS BOTANICALS WITH ANTICOAGULANT PROPERTIES |
| Bladder Wrack (Fucus) |
Pau d’arco |
|
| BOTANICALS THAT CONTAIN SALICYLATE AND/OR HAVE ANTIPLATELET PROPERTIES |
| Agrimony§ |
Dandelion‡ |
Meadowsweet* |
| Aloe Gel |
Feverfew |
Onionƒ |
| Aspen |
Garlicƒ |
Policosanol |
| Black Cohosh |
German Sarsaparilla |
Poplar |
| Black Haw |
Ginger |
Senega |
| Bogbean* |
Ginkgo Biloba |
Tamarind |
| Cassia‡ |
Ginseng (Panax)ƒ |
Willow |
| Clove |
Licorice‡ |
Wintergreen |
*Contains coumarins and salicylate. †Contains coumarins and has fibrinolytic properties. ‡Contains coumarins and has antiplatelet properties. §Contains coumarins, has antiplatelet properties, and may have anticoagulant properties due to possible Vitamin K content. ƒHas antiplatelet and fibrinolytic properties.
Anticoagulation is contraindicated in any localized or general physical condition or personal circumstance in which the hazard of hemorrhage might be greater than the potential clinical benefits of anticoagulation. Caution should be taken when administering to the elderly and debilitated.
| BOTANICALS WITH FIBRINOLYTIC PROPERTIES |
| Bromelains |
Garlic† |
Inositol Nicotinate |
| Capsicum* |
Ginseng (Panax)† |
Onion† |
|
BOTANICALS WITH COAGULANT PROPERTIES
|
| Agrimony‡ |
Mistletoe |
Goldenseal |
| Yarrow |
|
|
*Contains coumarins and has fibrinolytic properties.
†Has antiplatelet and fibrinolytic properties.
‡Contains coumarins, has antiplatelet properties, and may have coagulant properties due to possible Vitamin K content.