Ticagrelor-Induced Bradyarrhythmias in Acute Coronary Syndrome: A Case Series of Three Patients.
Molleti Ashish A, Sankaran Ramesh R, Vinod Kumar Balakrishnan B, Arul Judah N JN
Ticagrelor is a reversible oral P2Y12 receptor inhibitor recommended in preference to clopidogrel for most patients with acute coronary syndrome. In addition to inhibiting platelets, it raises extracellular adenosine, which is thought to explain its underappreciated capacity to cause bradyarrhythmia. We report three consecutive patients with acute coronary syndrome who developed serious bradyarrhythmias after ticagrelor administration. The first, a 58-year-old woman treated with a drug-eluting stent to the left anterior descending artery, developed high-grade atrioventricular block with asystolic pauses that required a temporary pacing wire, after which ticagrelor was stopped, prasugrel was substituted, and she recovered. The second, a 48-year-old woman with an anterior myocardial infarction, had a cardiac arrest with complete heart block after ticagrelor loading, was resuscitated, paced temporarily, switched to prasugrel, and recovered. The third, a 77-year-old man with an inferoposterior and right ventricular myocardial infarction, had recurrent asystole and ventricular arrhythmia that persisted despite switching to prasugrel and required a permanent pacemaker. None of the patients were receiving an atrioventricular nodal blocking drug, and in every patient the treated coronary lesion was patent on a repeat angiogram, which made ongoing ischemia from stent failure an unlikely sole explanation. A formal Naranjo assessment rated the association as possible in each case. A ticagrelor-induced adverse effect should be considered in any patient who develops unexplained bradycardia or syncope after its administration. Early rhythm monitoring and prompt withdrawal are the key steps, and although the rhythm usually recovers, permanent pacing may be needed when conduction disease is superimposed on ischemic injury to the conduction system.