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.
XS, a 51-year-old gentleman, came to our attention complaining of several weeks of worsening angina now occurring upon minimal exertion. Hypertension was his only cardiovascular risk factor actively treated with an angiotensin converting enzyme (ACE) inhibitor. No other relevant past medical history was noted. Physical examination was unremarkable highlighting clear heart sounds with no added murmurs and normal lung sounds. His blood pressure was 140/85 mmHg whilst his electrocardiogram (ECG), upon presentation, showed normal sinus rhythm (98 b.p.m.) with widespread ST segment depression consistent with diffuse subendocardial ischaemia (Figure ) and a first troponin sample was below the limit of significance. Given the presentation with progressively worsening angina (unstable angina) and the ECG which suggested a large area of myocardium at jeopardy the patient was loaded with aspirin 300 mg and ticagrelor 180 mg and, following a new anginal episode at rest, a decision was made to undergo urgent invasive coronary angiography. The investigation highlighted a left dominant circulation with a severe mid-left anterior descending narrowing with reduced distal coronaryflow [thrombolysis in myocardial infarction (TIMI) 1] and a severe, large, first obtuse marginal (OM1) stenosis which were both treated with drug-eluting stents implantation with excellent angiographic result, no complications and resolution of ECG anomalies (Figures ). A statin (atorvastatin 40 mg) was started as part of standard ACS therapy on top of dual antiplatelet therapy (DAPT) and ramipril, of interest no beta-blocker or other rate limiting drugs were commenced. The first 24 h a free of complications, no arrhythmic episode was registered by telemetry monitoring, a routine echocardiogram was unremarkable showing normal ejection fraction in the absence of regional wall motion abnormalities or major valvular dysfunctions, and the patient received two standard doses of ticagrelor (8 a.m. and 6 p.m.). On the second night of hospital stay, whilst lying in bed, the patient complained of the sudden feeling of lightheadness and profound sweating and called out for medical assistance. Upon medical review the patient denied any other symptoms, in particular any pain or angina, no ischaemic changes were noted on the ECG whilst telemetry monitoring review highlighted a 16 s long asystolic pause (Figure ). The episode was self-limited with return of sinus rhythm thereafter. Electrolytes were checked and found to be within normal limits. Hence, new medications were investigated looking for a possible explanation to the unexpected asystole given also the patient had no history of syncope. Ticagrelor, due to its brady-arrhythmic effect was suspected to be involved and was therefore halted shifting the patient to prasugrel following the administration of a 60 mg loading dose. A temporary pacing line (TPL) was inserted fearing possible further episodes. However, no new brady-arrhythmic episodes were noted on telemetry monitoring and the unused TPL was removed 24 h later. After 2 further days of monitoring, the patient was discharged home on Day 5 post-PCI in excellent general conditions.