It was hypothesized that chronic adenosine overload induced by ticagrelor may contribute to the vascular outcome benefit observed in PLATO, in addition to its inhibitory effect on platelet activity via P2Y12 receptor blockade. Very recently, ticagrelor has been shown to increase adenosine-induced physiological responses in human healthy subjects by shifting the dose-response curve for adenosine-induced coronary blood flow velocity (CBFV) to the left and, in non-ST-segment elevation acute coronary syndrome patients treated with percutaneous coronary intervention and receiving a maintenance dose of ticagrelor, coronary blood flow velocity augments to a greater degree compared with patients on a prasugrel maintenance dose in response to increasing adenosine concentrations. These effects are also compatible with adenosine reuptake blockage, another of the purported pleiotropic effects of ticagrelor. The enhanced ticagrelor-related adenosine bioavailabilty may have beneficial effects through three interrelated mechanisms.