This issue was addressed in the following three linked articles:
The effects of P2Y12 adenosine receptors' inhibitors on central and peripheral chemoreflexes
Potential Role of Endogenous Adenosine in Ticagrelor-Induced Dyspnea.
Key points from these articles are:
Ticagrelor causes dyspnea in 15 to 20 percent of patients. It is usually mild
and usually resolves with continuedtreatment, although is occasionally intolerable to where discontinuation is necessary.
The mechanism is poorly understood
It alters adenosine kinetics but that's not the only effect and likely not the main reason it causes dyspnea. More on that below.
How does Ticagrelor alter adenosine kinetics?
Ticagrelor inhibits cellular uptake of adenosine, prolonging its half life in the circulation.
Excess adenosine can cause stimulation of vagal C fibers in the lungs but that does not seem to be an adequate explanation for the dyspnea.
Ticagrelor has another mechanism that is a more likely cause.
It increases chemoreceptor sensitivity, increasing the hypoxic and hypercapnic drives thus heightening the sense of dyspnea.
It is safe and not considered contraindicated in patients with COPD.
Despite theoretical concerns about increased adenosine levels and the potential for bronchospasm, Ticagrelor does not alter pulmonary function in patients with mild asthma or mild to moderate COPD.
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