Dyspnea related to reversibly-binding P2Y12 inhibitors: A review of the pathophysiology, clinical presentation and diagnostics

- Not all dyspnea is reflected by bronchopulmonary function impairment.
- The mechanisms of drug associated dyspnea are still not fully understood.
- Mostly P2Y12 inhibitor associated dyspnea considerably improves or fully disappears within a few weeks post treatment onset
- Drugs seem to be discontinued prematurely when dyspnea occurs during drug treatment.
- Medical history and advanced pulmonary function testing are critical elements before discontinuing a potentially vital drug

Dyspnea is a common symptom physiologically associated with strenuous exercise and pathologically reflecting well-known diseases and conditions that are predominantly pulmonary, cardiovascular, and weight-related in origin. Dyspnea improves with appropriate measures that enhance physical performance and treatment of the underlying diseases. Dyspnea is less commonly triggered by other causes such as the environment (e.g., ozone), drugs, and others, some of which do not seem to affect bronchopulmonary function as evidenced by normal results of comprehensive pulmonary function testing. In cardiovascular medicine, dyspnea has recently attracted attention because it has been reported that this symptom occurs more frequently with the administration of the new oral reversibly-binding platelet P2Y12 receptor inhibitors ticagrelor [1-6], cangrelor [7-10], and elinogrel [11].This paper succinctly addresses the current understanding of the pathophysiology, clinical presentation, and diagnostics of dyspnea, associated either with bronchopulmonary function impairment, as triggered mainly by pulmonary and cardiovascular diseases, or without bronchopulmonary function impairment, as induced by endogenous or external compounds such as drugs in order to provide a context for understanding, recognizing and managing P2Y12 inhibitor-induced dyspnea.