Ticagrelor, a P2Y receptor antagonist, has been demonstrated to induce dyspnea, which is not associated with cardiac or pulmonary alterations, or metabolic disturbances. The attribution of ticagrelor-related dyspnea to excess adenosine has been widely proposed, yet is not supported by experimental data. In this paper, we put forth a novel hypothesis that the hyperactivity of the retrotrapezoid nucleus, a group of ventral medullary neurons involved in respiratory modulation, is the underlying cause of ticagrelor-related dyspnea. This hypothesis offers a theoretical resolution to the discrepancies and controversies present in previous theories.
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Department of Cardiology, Ankara Etlik City Hospital, Ankara, Republic of Turkey.
Ticagrelor, a P2Y receptor antagonist, has been demonstrated to induce dyspnea, which is not associated with cardiac or pulmonary alterations, or metabolic disturbances. The attribution of ticagrelor-related dyspnea to excess adenosine has been widely proposed, yet is not supported by experimental data. In this paper, we put forth a novel hypothesis that the hyperactivity of the retrotrapezoid nucleus, a group of ventral medullary neurons involved in respiratory modulation, is the underlying cause of ticagrelor-related dyspnea.
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Department of Pharmacy, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
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