The Effect of Platelet Activity, Genetic Polymorphism, and Renal Function on the Development of Ticagrelor-Related Dyspnea in Patients with Acute Coronary Syndrome.

PURPOSE

The aim of this study was to determine the effect of genetic polymorphism and renal function on the occurrence of ticagrelor-related dyspnea.

PATIENTS AND METHODS

A total of 299 patients with acute with type 1, 2, or 3 myocardial infarction (with and without ST-segment elevation), who underwent coronary angiography and PTCA with stent implantation and were treated with antiplatelet drugs (ticagrelor and aspirin), were enrolled in this prospective study. For all enrolled patient's platelet aggregation (induction with high-sensitivity adenosine diphosphate, ADP HS) testing was performed using a MULTIPLATE analyzer. Venous blood was also collected for genotyping.

RESULTS

Patients experiencing ticagrelor-related dyspnea had lower ADP HS value (ADP HS ≤ 19.5 U; OR = 2.254; = 0.009), higher creatinine concentration (>90 µmol/l; OR = 3.414; = 0.019), and lower GFR value (<60 mL/min/1.73 m; OR = 2.211; = 0.035). T allele was associated with ticagrelor-related dyspnea (OR = 2.550; = 0.04).

CONCLUSION

Ticagrelor-related dyspnea was found to be related to low platelet aggregation, increased plasma creatinine concentration, decreased GFR, and T allele. Carriers of the T allele had a higher plasma creatinine concentration that could be associated with an inhibitory effect of ticagrelor on P-glycoprotein function.