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.
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.