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 47-year-old female with hypertension and hyperlipidemia was admitted to emergency department due to typical angina lasting 2 days. Her blood pressure was 150/80 mm Hg. On electrocardiogram (ECG), there was a sinus rhythm with heart rate of 67 bpm, along with ST depression of 0.5 mm on inferolateral derivations (). Echocardiography showed hypokinesis of mid-lateral wall with an ejection fraction of 48%. We detected slightly increased cardiac troponin level. Because of ACS (NSTEMI), acetylsalicylic acid (300 mg), ticagrelor (a loading dose of 180 mg and maintenance dose of 90 mg twice a day) and intravenous unfractionated heparin (10,000 IU) were given to the patient and then her coronary angiography was performed, which revealed a total occlusion of the distal ndLCx (). After the lesion was predilated with 2.0 × 15 mm sized balloon catheter, a drug eluting stent of 2.5 × 23 mm was implanted and full patency was achieved (). Thereafter, her symptoms dramatically improved. Since her heart rate was 67 beats/min, beta blocker therapy was not started. Approximately 10 h later, ECG showed first degree AVB without symptom (). Her therapy consisting of ASA, ticagrelor, ramipril and statin was continued unchanged. On the next (second) day, the patient experienced mild dizziness with complet AVB, without hemodynamic impairment (). Ticagrelor was stopped and prasugrel was initiated instead. On the third day, her ECG showed again first degree AVB without symptom (). On the fourth day, she had normal sinus rhythm without AVB and symptom (). On the fifth day, the patient was salubriously discharged from the hospital with therapy of ASA, prasugrel, rosuvastatin and ramipril. We did not observe any heart block and/or bradyarrhythmia during the 3 months of follow-up.