Comparative evaluation of the laboratory efficacy of long-term buffered and enteric-coated acetylsalicylic acid therapy in patients with stable coronary artery disease: a cross-sectional study in a real-world clinical practice

Aim. To compare the laboratory efficacy of the long-term buffered gastro-soluble (GS) and enteric-coated (EC) acetylsalicylic acid (ASA) therapy in patients with stable coronary artery disease (CAD) in a real-world clinical practice using three following methods: VerifyNow ASA, turbidimetric aggregometry, and serum thromboxane B 2 (TxB 2 ) measurement by ELISA. Material and methods. This single-center, cross-sectional, comparative study enrolled consecutive patients with stable CAD attending an outpatient clinic who had been taking ASA for ≥2 years (confirmed by interview and medical records). Patients were divided into groups according to the ASA formulation received on a long-term basis, as originally prescribed by their treating physician in routine practice. The sample was formed by sequential inclusion of patients meeting the inclusion/exclusion criteria until the planned number was reached (50 patients each in the GS and EC ASA groups). The primary endpoint for laboratory efficacy was the rate of high on-treatment platelet reactivity (HTPR), defined as ARU ≥550 by VerifyNow ASA. Secondary endpoints were the results of light transmission aggregometry (LTA) with arachidonic acid induction and serum TxB 2 levels. Results. HTPR rate was 10% in the GSF group vs 48% in the ECF group (p<0,001). Median ARU was significantly lower with the following buffered formulation: 453 (Q1-Q3: 429-484) vs 535,5 (Q1-Q3: 498-583) (p<0,001). Similar results were observed for platelet aggregation — 1,32% (Q1-Q3: 0,76-2,06%) with GS ASA vs 2,78% (Q1-Q3: 1,76-3,57%) with EC ASA (p<0,001), and for serum TxB 2 levels — 1156 (Q1-Q3: 217-2484) for GS ASA vs 3565 (Q1-Q3: 650-8700) pg/mL for EC ASA (p=0,004). Multivariate analysis identified EC ASA (OR 15,25; 95% CI 3,75-62,01; p<0,001) and a history of myocardial infarction and/or stroke (OR 6,70; 95% CI 1,50-29,95; p=0,013) as independent predictors of HTPR. Conclusion. GS ASA is significantly superior to EC ASA in terms of laboratory efficacy in patients with stable CAD, providing an almost fivefold lower rate of HTPR during long-term treatment. EC ASA and a history of myocardial infarction/stroke are independent predictors of laboratory ASA resistance.