Low-dose aspirin remains the most commonly used antiplatelet agent among patients with atherosclerotic cardiovascular disease. Aspirin hypersensitivity occurs in 1% to 5% of patients and is among the most frequent causes for prohibiting the use of aspirin, posing a significant dilemma on how to manage these patients in clinical practice. Aspirin hypersensitivity is often misinterpreted and confused with aspirin intolerance, with treatment approaches being often unclear and lacking specific recommendations. Aspirin desensitization and low-dose aspirin challenge have emerged as pragmatic, effective, and safe approaches in patients with suspected or confirmed aspirin hypersensitivity who require aspirin therapy, but they are underused systematically in clinical practice. Furthermore, there is confusion over alternative antiplatelet agents to be used in these patients. The pathophysiological mechanisms and classification of aspirin hypersensitivity, as well as alternative strategies and practical algorithms to overcome the need for aspirin use in patients with atherosclerotic cardiovascular disease with suspected aspirin hypersensitivity, are discussed. 

Aspirin Hypersensitivity in Patients With Atherosclerotic Cardiovascular Disease

Aspirin has been known for a long time and currently stays as a cornerstone of antithrombotic therapy in cardiovascular disease. In patients with either acute or chronic coronary syndromes undergoing percutaneous coronary intervention aspirin is mandatory in a dual antiplatelet therapy regimen for prevention of stent thrombosis and/or new ischaemic events. Aspirin is also currently a first-option antithrombotic therapy after an aortic prosthetic valve replacement and is occasionally required in addition to oral anticoagulants after implantation of a mechanical valve. Presumed or demonstrated aspirin hypersensitivity is a main clinical problem, limiting the use of a life-saving medication. In the general population, aspirin hypersensitivity has a prevalence of 0.6%-2.5% and has a plethora of clinical presentations, ranging from aspirin-exacerbated respiratory disease to anaphylaxis. Although infrequent, when encountered in clinical practice aspirin hypersensitivity poses for cardiologists a clinical dilemma, which should never be trivialized, avoiding-as much as possible-omission of the drug. We here review the epidemiology of aspirin hypersensitivity, provide an outline of pathophysiological mechanisms and clinical presentations, and review management options, starting from a characterization of true aspirin allergy-in contrast to intolerance-to suggestion of desensitization protocols.

Aspirin hypersensitivity: a practical guide for cardiologists.

Background Acetylsalicylic acid hypersensitivity (ASAH) limits therapeutic options in patients with acute coronary syndrome (ACS), who benefit from dual antiplatelet therapy (DAPT), especially when undergoing stent implantation. Our aim was to evaluate the safety and efficacy of triflusal in patients with ACS and ASAH. Methods and results Two-center retrospective study of patients diagnosed with ACS and ASAH from January 1, 2000, to May 1, 2020. Sixty-six patients were treated with triflusal. ASAH was confirmed with tests in 15 patients (22.7%). Forty-nine patients (74.2%) presented history of other drug allergies. Fifty-nine patients (89.4%) underwent stent implantation. DAPT was prescribed for ≥12 months in 54 patients. No adverse reactions to triflusal were reported. During a median follow-up of 5.12 years [IQR 2.7-9.9], rate of cardiovascular (CV) mortality was 6.1%, nonfatal myocardial infarction 12.1%, and ischemic stroke 4.5%. No cases of definite stent thrombosis occurred. Bleeding Academic Research Consortium grade ≥2 was observed in 3 patients during follow-up. Conclusion In this series of patients presenting with ACS and ASA hypersensitivity, triflusal showed good tolerability and was associated with a low rate of CV and bleeding events.

Triflusal in Patients with Acute Coronary Syndrome and Acetylsalicylic Acid Hypersensitivity

Acetylsalicylic acid (ASA) hypersensitivity still represents one of the major deals for patients with atherosclerotic cardiovascular disease (ASHD), especially for those requiring percutaneous coronary interventions in the absence of validated alternative options. Despite symptoms after ASA administration being reported in 6-20% of cases, true ASA allergy only represents a minority of the patients, pointing to the importance of challenge tests and potential strategies for tolerance induction. ASA desensitization protocols were proposed several decades ago, with accumulating the literature on their use in patients undergoing PCI either for chronic disease or acute coronary syndromes. Nevertheless, the promising results of the studies and meta-analyses have not been validated so far by the support of large-scale randomized trials or unique indications from guidelines. Therefore, ASA desensitization is still largely unapplied, leaving the management of ASA hypersensitivity to the individualized approach of cardiologists.

ASA Allergy and Desensitization Protocols in the Management of CAD: A Review of Literature.

Aspirin hypersensitivity in patients with coronary artery disease: linking pathophysiology to clinical practice

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Aspirin hypersensitivity in patients with coronary artery disease: linking pathophysiology to clinical practice