Central apneas and Ticagrelor related dyspnea in patients with acute coronary syndrome

Abstract

Abstract Background Patients treated with ticagrelor often develop dyspnea of unknown origin. We aim to explore the contribution of central apneas to ticagrelor-related dyspnea in patients with acute coronary syndrome (ACS). Methods We consecutively enrolled patients with ACS, preserved left ventricular ejection fraction and no history of obstructive sleep apnea, treated either with ticagrelor 90 mg bid (n=30) or prasugrel 10 mg od (n=24). One week after ACS onset, all patients underwent, beyond thorough cardiovascular and respiratory assessment, 24-hour cardiorespiratory monitoring and assessment of chemosensitivity to hypercapnia. Results Patients treated with ticagrelor reported more frequently dyspnea than patients treated with prasugrel (43% versus 4%, p=0.001), despite no difference in demographic, clinical, echocardiographic and pulmonary data. Patients with dyspnea induced by ticagrelor showed higher apnea-hypopnea and central apnea index both at daytime and at nighttime compared to patients treated with ticagrelor but without dyspnea and patients treated with prasugrel (daytime AHI: 26 [7–34] vs 6 [4–14] and 6 [0–11] events/hour; nighttime AHI: 65 [17–72] vs 22 [8–37] and vs 11 [4–23] events/hour; daytime CAI: 5 [1–15] vs 1 [0–6] and 0 [0–1) events/hour; nighttime CAI 34 [2–55] vs 3 [0–9] and 0 [0–1], all p<0.05). Likewise, they also presented with higher hypercapnic ventilatory response (2.4 [1.9–2.7] vs 1.3 [1.1–1.9] and 0.9 [0.5–2.1] L/min/mmHg, all p<0.05). Conclusions Central apneas should be considered a likely mechanism of dyspnea in ACS patients treated with ticagrelor. A drug-related sensitization of the chemoreflex may be the cause of ventilatory instability in this setting. Funding Acknowledgement Type of funding source: None