Dual Antiplatelet Therapy and ASA Allergy: What Do You Do?
How do you manage a patient with acute coronary syndrome who requires dual antiplatelet therapy but has an aspirin allergy?
Dual antiplatelet regimens are a mainstay in the management of acute coronary syndrome and typically consist of aspirin combined with a P2Y12 receptor inhibitor (eg, clopidogrel, prasugrel, ticagrelor) or a glycoprotein IIb/IIIa inhibitor (eg, abciximab, eptifibatide, tirofiban) before and during percutaneous coronary intervention (PCI). Following PCI, aspirin is combined with a P2Y12 receptor inhibitor to prevent restenosis. Aspirin sensitivity poses a significant clinical dilemma, as the safety and efficacy of oral antiplatelet combinations that exclude aspirin have not been established. Aspirin desensitization is a possible approach, but it may not always be feasible because of the urgent nature of cardiac intervention or the need for close observation in a setting equipped with resuscitative equipment.
The 2012 American College of Cardiology Foundation/American Heart Association Focused Update of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction recommends clopidogrel or ticagrelor alone in aspirin-allergic patients. These guidelines advise against combination of 2 P2Y12 receptor inhibitors as there are no data to support that approach.
The American College of Chest Physicians guidelines for primary and secondary prevention of cardiovascular disease recommend the phosphodiesterase inhibitor cilostazol, 100 mg by mouth every 12 hours, in place of aspirin 75-100 mg daily or clopidogrel 75 mg daily in patients undergoing bare metal or drug-eluting stent placement who have allergy or intolerance to either drug class. However, this recommendation was graded as weak, with a lack of outcomes data on these specific combinations.
The Society of Thoracic Surgeons guidelines for antiplatelet drugs in patients having cardiac and noncardiac operations discuss cilostazol as an antiplatelet agent but do not give any specific recommendation for or against its use. Data exist for cilostazol as part of a triple antiplatelet regimen that includes aspirin following PCI. Cilostazol is contraindicated in patients with heart failure, limiting its use in many patients with coronary heart disease.
Sensitivity to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) is attributed to either an immunologic process or a pharmacologic effect. Aspirin hypersensitivity encompasses aspirin-exacerbated respiratory tract disease (aspirin-intolerant asthma), cutaneous reactions (urticaria/angioedema), or systemic reactions (anaphylaxis). Depending on the type of reaction, desensitization can be considered, with the exception of patients with chronic idiopathic urticaria.
Before considering alternative antiplatelet regimens or attempting desensitization, the cause of the reaction should be determined with the help of a thorough patient history.
Immunologic reactions involve immunoglobulin E (IgE) production against a specific NSAID. Patients with IgE-mediated hypersensitivity tend to react only after prior exposure to a particular NSAID. Cross-reactivity is not expected in this case. If the reaction occurred with a nonaspirin NSAID and was not anaphylactic, then aspirin can typically be attempted without desensitization.
Pharmacologic reactions are induced by COX-1 inhibition and tend to cross-react within the class of NSAIDs that inhibits COX-1. These patients tend to react after the first exposure to any NSAID and would be expected to have a reaction to aspirin. Such patients could be considered for aspirin desensitization.
Gollapudi and colleagues offer a detailed algorithm to determine which patients with coronary artery disease could be considered for either aspirin challenge or aspirin desensitization. An overview of aspirin hypersensitivity and various aspirin desensitization strategies geared toward the specific types of reactions are described in the review by Lambrakis and colleagues.
The recommendations described above are varied and not based on clinical trial data. Further research is needed to identify the optimal approach for antiplatelet therapy in a patient with acute coronary syndrome who is sensitive to aspirin.
Question
How do you manage a patient with acute coronary syndrome who requires dual antiplatelet therapy but has an aspirin allergy?
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Response from Laura S. Lehman, PharmD Clinical Pharmacy Coordinator, Carroll Hospital Center, Westminster, Maryland |
Dual antiplatelet regimens are a mainstay in the management of acute coronary syndrome and typically consist of aspirin combined with a P2Y12 receptor inhibitor (eg, clopidogrel, prasugrel, ticagrelor) or a glycoprotein IIb/IIIa inhibitor (eg, abciximab, eptifibatide, tirofiban) before and during percutaneous coronary intervention (PCI). Following PCI, aspirin is combined with a P2Y12 receptor inhibitor to prevent restenosis. Aspirin sensitivity poses a significant clinical dilemma, as the safety and efficacy of oral antiplatelet combinations that exclude aspirin have not been established. Aspirin desensitization is a possible approach, but it may not always be feasible because of the urgent nature of cardiac intervention or the need for close observation in a setting equipped with resuscitative equipment.
The 2012 American College of Cardiology Foundation/American Heart Association Focused Update of the Guideline for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction recommends clopidogrel or ticagrelor alone in aspirin-allergic patients. These guidelines advise against combination of 2 P2Y12 receptor inhibitors as there are no data to support that approach.
The American College of Chest Physicians guidelines for primary and secondary prevention of cardiovascular disease recommend the phosphodiesterase inhibitor cilostazol, 100 mg by mouth every 12 hours, in place of aspirin 75-100 mg daily or clopidogrel 75 mg daily in patients undergoing bare metal or drug-eluting stent placement who have allergy or intolerance to either drug class. However, this recommendation was graded as weak, with a lack of outcomes data on these specific combinations.
The Society of Thoracic Surgeons guidelines for antiplatelet drugs in patients having cardiac and noncardiac operations discuss cilostazol as an antiplatelet agent but do not give any specific recommendation for or against its use. Data exist for cilostazol as part of a triple antiplatelet regimen that includes aspirin following PCI. Cilostazol is contraindicated in patients with heart failure, limiting its use in many patients with coronary heart disease.
Sensitivity to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs) is attributed to either an immunologic process or a pharmacologic effect. Aspirin hypersensitivity encompasses aspirin-exacerbated respiratory tract disease (aspirin-intolerant asthma), cutaneous reactions (urticaria/angioedema), or systemic reactions (anaphylaxis). Depending on the type of reaction, desensitization can be considered, with the exception of patients with chronic idiopathic urticaria.
Before considering alternative antiplatelet regimens or attempting desensitization, the cause of the reaction should be determined with the help of a thorough patient history.
Immunologic reactions involve immunoglobulin E (IgE) production against a specific NSAID. Patients with IgE-mediated hypersensitivity tend to react only after prior exposure to a particular NSAID. Cross-reactivity is not expected in this case. If the reaction occurred with a nonaspirin NSAID and was not anaphylactic, then aspirin can typically be attempted without desensitization.
Pharmacologic reactions are induced by COX-1 inhibition and tend to cross-react within the class of NSAIDs that inhibits COX-1. These patients tend to react after the first exposure to any NSAID and would be expected to have a reaction to aspirin. Such patients could be considered for aspirin desensitization.
Gollapudi and colleagues offer a detailed algorithm to determine which patients with coronary artery disease could be considered for either aspirin challenge or aspirin desensitization. An overview of aspirin hypersensitivity and various aspirin desensitization strategies geared toward the specific types of reactions are described in the review by Lambrakis and colleagues.
The recommendations described above are varied and not based on clinical trial data. Further research is needed to identify the optimal approach for antiplatelet therapy in a patient with acute coronary syndrome who is sensitive to aspirin.