A 59-year-old female with no prior cardiac diagnosis presented to our hospital with 3 days of intermittent chest pain. Her cardiac risk factors included hypertension, hypercholesterolaemia, elevated body mass index, and impaired glucose tolerance. Her medical history was also significant for asthma, gastro-oesophageal reflux disease and depression. Cardiovascular examination was unremarkable with no signs of heart failure.\nHer admission electrocardiogram (ECG) showed sinus rhythm, normal axis, narrow QRS (80 ms) with no ischaemic change or conduction defects (Figure ). The patient’s serum troponin recorded a peak measurement of 0.31 µg/L (cTnI n < 0.04 µg/L). Her biochemistry and blood panels were otherwise unremarkable with normal renal and liver function. Echocardiography showed normal biventricular size and systolic function, with normal valves.\nRadial approach coronary angiography was performed and the culprit vessel was shown to be the left circumflex artery (non-dominant) with a long 80% stenosis in the mid-portion. This was treated with deployment of a Synergy 3.0 ×24 mm drug eluting stent and restoration of TIMI 3 flow (Figure ). Medical management was elected for the patient’s residual moderate diffuse left anterior descending artery disease. The right coronary artery was non-obstructed.\nAt conclusion of the procedure, an oral load of ticagrelor 180 mg was administered. Three hours after, whilst convalescing in the coronary care unit, she began complaining of dyspnoea and four pauses were observed on telemetry over a 20 min period (Figure ), the longest being 18.5 s in duration (Figure ). Correspondingly, the patient had intermittent lapses of consciousness and underwent emergency right femoral venous temporary pacing wire insertion.\nTicagrelor was considered as the probable cause for the pauses, for that reason no additional ticagrelor was given after the loading dose and clopidogrel was commenced in place. No further brady-arrhythmias were detected in the subsequent 24 h and the un-utilized temporary pacing wire was removed. The patient was also discharged with aspirin, atorvastatin, perindopril, and amlodipine. A loop recorder (Medtronic Reveal LINQ) was implanted. Beta-blocker therapy was not prescribed in view of preceding events. Notably, there had not been a prior personal or family history of syncope.\nNo cardiorespiratory symptoms were raised during regular follow-up over 12 months with no arrhythmic events recorded on loop recorder interrogation.
A 51-year-old male patient, with a history of hypertension and hyperlipidemia, presented to the emergency department with an anterior ST-elevation myocardial infarction (). A loading dose of both ticagrelor (180 mg) and aspirin (ASA, 250 mg i.v.) was administered and the patient sent to the cath-lab for primary percutaneous coronary intervention (PCI) on the left anterior descending coronary artery (Figures -). After revascularization, medical therapy included beta-blockers (carvedilol 6.25 mg b.i.d.), statins (atorvastatin 80 mg), and angiotensin II receptor antagonists (telmisartan 80 mg). Dual antiplatelet therapy was continued with ticagrelor (90 mg b.i.d.) and ASA (100 mg). At the echocardiography, performed the day after the revascularization, the ejection fraction was critically reduced (EF: 25%) with akinesia of the anteroseptal wall. Titration of carvedilol was performed during the following two days without significantly reducing the heart rate at target (90 bpm with 12.5 mg carvedilol b.i.d.). Ivabradine was then administered at 5 mg b.i.d. Few hours after the first dose, the patient presented with severe symptomatic bradycardia () and sinus arrest. Atropine and adrenaline i.v. were administered and both ivabradine and ticagrelor suspended and this latter changed with prasugrel. Any other similar event was not reported during the following days and the national competent authority was finally informed.