In addition to inhibiting platelet activation, ticagrelor may influence vascular function through effects on adenosine metabolism and endothelial signaling. A translational study presented at ESH Congress 2026 evaluated the impact of ticagrelor on microvascular and endothelial function and explored potential adenosine-dependent mechanisms underlying these effects.
The study included 12 patients with CAD and healthy controls. Endothelial function in vivo was assessed using magnetic resonance imaging, while endothelial nitric oxide production was evaluated in vitro using therapeutic concentrations of ticagrelor.
Findings
- Ticagrelor-treated patients demonstrated higher ischemic response values than patients with CAD not receiving ticagrelor (IR max: 14.7±3.2% vs 6.7±4.8%), with levels comparable to healthy controls (14.9±1.9%).
- Reactive hyperemic response was higher in ticagrelor-treated patients than in untreated CAD patients (30.4±6.5% vs 18.3±8.4%) and approached values observed in healthy controls (34.2±12.2%).
- In experimental atherosclerosis models, ticagrelor increased blood adenosine concentrations following both 5 mg/kg and 15 mg/kg dosing and improved endothelial responses in a dose-dependent manner.
- Endothelial cell studies showed that ticagrelor-associated nitric oxide responses involved both A2A and A2B adenosine receptors.
The findings suggest that ticagrelor may provide vascular benefits beyond platelet inhibition, with improvements in microvascular and endothelial function observed across clinical and experimental models.
