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 76-year-old female without a past history of conduction diseases and confirmed past medical history significant for type 2 diabetes mellitus, hypertension, and coronary artery disease post PCI to right coronary artery (RCA) in 2018, treated with aspirin 100 mg, atorvastatin 20 mg, metoprolol tartrate 50 mg, isosorbide mononitrate 20 mg, and basal-bolus insulin, presented to our hospital emergency department with a 5-day history of shortness of breath that was increasing in severity and associated with central chest pain radiating to throat that started 6 h prior to admission. Her vital signs were as follows: blood pressure = 115/73 mmHg, heart rate = 106 beats per minute, temperature = 36.5 C, and oxygen saturation = 95% on room air. Her first 2 sets of troponin T were 104 ng/L and 135 ng/L (normal <14 ng/L), and her transthoracic echocardiogram showed left ventricular regional wall motion abnormalities with an ejection fraction of 38%. Her initial electrocardiogram (ECG) showed T wave inversion in anterolateral leads (V3–V6 leads) as shown in Figure . Therefore, a diagnosis of non-STEMI was made, and she was planned for in-patient coronary angiography (CAG) and hence started on aspirin 300 mg then 100 mg enteric coated (EC) daily, clopidogrel 300 mg then 75 mg daily, and enoxaparin 1 mg/Kg subcutaneous every 12 h.\nOn the second day of admission, she underwent CAG and was found to have 95% stenosis in proximal left anterior descending (LAD) artery, and a patent drug-eluting stent (DES) in the mid-RCA. A DES (3.0 × 33 mm) was placed in the proximal to mid LAD. After the PCI, she was on aspirin 100 mg EC, clopidogrel 150 mg daily, bisoprolol 5 mg, atorvastatin 40 mg, lisinopril 5 mg, spironolactone 12.5 mg daily, furosemide 40 mg intravenous twice daily, and insulin (basal glargine and bolus aspart). Two days after the PCI, it was decided to start the patient on ticagrelor 180 mg as a loading dose followed by 90 mg twice daily and to stop clopidogrel.\nOne hour after receiving ticagrelor loading dose, the patient started to develop dyspnea followed by an episode of unresponsiveness. The review of the telemetry monitoring strips showed bradycardia followed by a sinus pause of 22 s during the episode of unresponsiveness as shown in Figure . Therefore, she was transferred immediately to our cardiac intensive care unit (CICU) where she underwent transvenous pacemaker insertion, which was kept for 2 days, and ticagrelor was switched back to clopidogrel after 24 h of receiving ticagrelor loading dose, by giving a loading dose of 600 mg followed by 75 mg daily. After the removal of the pacemaker, metoprolol 12.5 mg twice daily was started, and she was observed for 2 days and remained stable without any further episodes of bradycardia or sinus pause with a heart rate ranging from 65–75 beats per minute. After which, she was discharged and then seen in the outpatient clinic within 20 days of discharge and had no complaints.