Abstract
Dyspnea is a common side effect of ticagrelor, leading to drug discontinuation in roughly one in every 20 treated patients. Studies have suggested that ticagrelor inhibits the sodium-independent equilibrative nucleoside transporter-1, which may increase adenosine plasma levels and explain drug-related dyspnea. However, the identification of a pattern of periodic breathing associated to increased chemosensitivity to hypercapnia in patients with ticagrelor-related dyspnea has reinforced the hypothesis that this side effect may result from direct inhibition of P2Y receptors on neurons leading to purinergic stimulation of the chemoreflex system. Simultaneous measurements of adenosine and ticagrelor plasma levels in patients with and without dyspnea while on treatment with ticagrelor may help unraveling the mechanism of this common and clinically relevant side effect.
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