Factors Determining Ticagrelor-Induced Dyspnea in Patients with Acute Coronary Syndrome

Abstract

(1) Background: The aim of this study was to determine clinical and genetic factors predicting the development of dyspnea in patients receiving ticagrelor. (2) Methods: A total of 277 patients with acute myocardial infarction (with and without ST-segment elevation), who underwent coronary angiography and PTCA with stent implantation and treated with antiplatelet drugs (ticagrelor and aspirin), were enrolled in this study. Platelet aggregation (induction with high-sensitivity ADP, ADP HS) testing was performed using a MULTIPLATE analyzer and reagents for the determination of P2Y12 receptor activity. Venous blood samples were collected for genotyping. (3) Results: Patients experiencing ticagrelor-related dyspnea had lower ADP HS. ROC curve analysis showed that an ADP HS cut-off of ≤19.5 U was associated with the development of dyspnea. The ADP HS value of ≤19.5 U and any dose of atorvastatin lower than 80 mg (or no atorvastatin) increased the risk of dyspnea by more than 4 and 2 times, respectively (OR = 4.07, p ≤ 0.001 and OR = 2.25; p = 0.008). (4) Conclusion: A lower ADP HS value possibly indicates greater ticagrelor activity and a higher plasma concentration of this drug. Atorvastatin might have an impact on the occurrence of ticagrelor-related dyspnea by affecting ticagrelor metabolism. No impact of any genetic variant on the development of dyspnea was determined.

Keywords

• ticagrelor
• dyspnea
• antiplatelet therapy
• ticagrelor pharmacogenomics
• platelet aggregation
• ADP HS