Aspirin I.V. Loading during Elective Percutaneous Coronary Intervention

• Published in: Pharmacology Vol. 106; no. 11-12; p. 682
• Main Authors: Naguib, David, Helten, Carolin, Zako, Saif, Mourikis, Philipp, M'Pembele, René, Trojovsky, Kajetan, Ahlbrecht, Samantha, Zikeli, Dorothee, Zeus, Tobias, Kelm, Malte, Dannenberg, Lisa, Polzin, Amin
• Format: Journal Article
• Language: English
• Published: Switzerland 01.11.2021
• Subjects: Administration, Intravenous; Aged; Aged, 80 and over; Aspirin - administration & dosage; Aspirin - adverse effects; Aspirin - therapeutic use; Cardiovascular Diseases - prevention & control; Dose-Response Relationship, Drug; Female; Hemorrhage - chemically induced; Humans; Male; Middle Aged; Percutaneous Coronary Intervention - methods; Pilot Projects; Platelet Aggregation - drug effects; Platelet Aggregation Inhibitors - administration & dosage; Platelet Aggregation Inhibitors - adverse effects; Platelet Aggregation Inhibitors - therapeutic use; Prospective Studies; Thrombosis - prevention & control; Aspirin; Percutaneous coronary intervention; Acetylsalicylic acid; Elective percutaneous coronary intervention; High on-treatment platelet reactivity
• ISSN: 1423-0313
• DOI: 10.1159/000517994

Additional loading dose of acetylsalicylic acid (ASA) during percutaneous coronary interventions (PCIs) despite permanent oral ASA medication is frequently applicated. The impact on platelet reactivity and clinical events is not known. In this pilot study, we aimed to analyze high on-treatment platelet reactivity (HTPR) to aspirin in patients undergoing elective PCI. Platelet reactivity was measured using light-transmission aggregometry in 100 patients on permanent low-dose ASA medication undergoing elective PCI. Platelet reactivity measured by arachidonic acid-induced maximum of aggregation (MoA) in patients with versus without additional peri-procedural ASA loading (500 mg i.v.) was compared. HTPR was defined as MoA >20% for ASA. Major adverse cerebro- and cardiovascular events (MACCEs) and bleeding events were evaluated during hospital course. HTPR rate was similar in both groups (HTPR to ASA: loading vs. control 6% vs. 16%, odds ratio [OR] = 0.33, 95% confidence interval [CI] 0.08-1.35, p = 0.12). In-hospital MACCEs were not different between groups (MACCE: loading vs. control: 0 vs. 0 patient, OR = 1.32, 95% CI 0.03-67.95, p = 0.89). Thrombolysis in myocardial infarction minimal bleedings were numerically higher in patients without ASA loading dose. In this pharmacodynamic pilot study, additional ASA loading did not reduce HTPR to ASA. Furthermore, ASA loading did not increase in-hospital MACCE and bleeding complications.