ASPIRIN RESISTANCE IN PATIENTS WITH OSA: ARISA TRIAL

Abstract

SESSION TITLE: New Insights Into the Relationship Between OSA and Cardiovascular Disease SESSION TYPE: Original Investigations PRESENTED ON: October 18-21, 2020 PURPOSE: Obstructive sleep apnea (OSA) is one of the leading independent risk factors associated with cardiovascular events. Untreated OSA is associated with endothelial dysfunction and platelet hyperactivity through multiple metabolic, thrombotic and inflammatory pathways linked to development of cardiovascular disease. Patients with concomitant OSA and cardiovascular risks are routinely prescribed aspirin for primary and/or secondary prevention; however, it is proposed this population carries higher risk of aspirin therapy resistance. Proposed mechanisms of aspirin resistance include increased platelet turnover, gene polymorphisms (COX-1, COX-2, GPIIb/IIIa), decreased aspirin-mediated acetylation, and prothrombotic effects of leptin – all shared mechanisms with OSA. We hypothesized that compliant use continuous positive airway pressure (CPAP) therapy, which is known to improve endothelial function and decrease platelet hyperactivity may improve endothelial function and aspirin responsiveness in this population. METHODS: In Phase 1, prevalence of aspirin resistance was determined in a group of OSA patients (n=59) on daily low-dose aspirin utilizing the VerifyNow Aspirin laboratory test. Aspirin resistance was defined as aspirin reaction units (ARU) ≥ 550. In Phase 2, aspirin responsiveness, stratified by pre-CPAP endothelial function determined by two methods, the VerifyNow Aspirin laboratory test and the non-invasive EndoPAT200. The measures were obtained before and after initiation of CPAP therapy in a cohort of aspirin-naïve patients with newly diagnosed OSA (n=18). Statistical significance was set as p<0.1. Aspirin resistance was defined as aspirin reaction units (ARU) ≥ 550. Endothelial dysfunction was defined as RHI <1.67. RESULTS: In Phase 1, aspirin resistance occurred in 17% of study subjects. In Phase 2, utilization of CPAP therapy was associated with significant improvement in endothelial function (p=0.03). In subjects with endothelial dysfunction pre-CPAP (44%), initiation of CPAP therapy was associated with significant decrease in mean ARU from 563 to 520 (p=0.09). Meanwhile, in subjects with normal endothelial dysfunction, ARU decreased insignificantly, from 574 to 566 (p=0.4). Control group was not part of data analysis due to limited number of subjects. CONCLUSIONS: Although a limited study due to sample size, aspirin resistance was prevalent among our cohort of OSA patients. Initiation of CPAP therapy was associated with significant improvement in aspirin responsiveness when endothelial dysfunction was present pre-CPAP therapy. CLINICAL IMPLICATIONS: The role of endothelial dysfunction and aspirin resistance should be explored in further studies that focus on the effect of CPAP and cardiovascular outcomes. DISCLOSURES: No relevant relationships by Rakhee Agarwal, source=Web Response No relevant relationships by Jose Mendez, source=Admin input No relevant relationships by Maria Scinico, source=Web Response No relevant relationships by Oleg Sostin, source=Web Response