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.
In May of 2016, a 55-year-old male with history of hypertension, hyperlipidemia, and coronary artery disease (CAD) status after angioplasty of left anterior descending (LAD) artery 2 years ago presented to the emergency room (ER) with substernal chest pain. His cardiac enzymes were not elevated and electrocardiogram (EKG) showed normal sinus rhythm at a rate of 62 bpm with borderline AV conduction delay and right bundle branch block (RBBB) pattern (). The patient was only taking aspirin and had discontinued his statin due to muscle ache and metoprolol because of fatigue. His chest pain was relieved with sublingual nitroglycerin in the ER. In view of his significant history of CAD and typical anginal symptoms, patient underwent cardiac catheterization. It revealed 90 percent stenosis of the left mid circumflex coronary artery which was successfully stented with a drug-eluting stent. Right coronary artery (RCA) showed 50–60% stenosis while LAD showed patent stent. The patient recovered very well. After calculating the GRACE score, the patient was discharged on aspirin and ticagrelor as per the ACC guidelines. He was also prescribed rosuvastatin and metoprolol. Two months after PCI, the patient presented to his primary cardiologist due to worsening fatigue and intermittent dizziness. His metoprolol was stopped. In November, 2016, he was brought by emergency squad to the hospital due to worsening dizziness and diaphoresis at rest. He denied any h/o chest pain, palpitations, nausea, or loss of consciousness. The patient had stopped ticagrelor 1 day prior to this admission since he ran out of it. The patient requested a second opinion on this admission. On physical examination, his blood pressure was 126/66 mmHg and heart rate was regular at 42 beats per minute. The neck was supple with no carotid bruits and cardiac auscultation revealed 2/6 ejection systolic murmur in the left sternal border. Patient's EKG revealed second-degree type II atrioventricular (AV) block which was new (). His cardiac enzymes, thyroid stimulating hormone, serum potassium, and magnesium were within normal range. The patient did not receive ticagrelor further during the admission. Cardiac catheterization revealed RCA stenosis of 60–70% but no intervention was required as this was not the cause of the new onset heart block. We considered starting patient on oral theophylline on admission had the heart block not resolved within 24 hours. His second-degree heart block resolved 2 days after discontinuation of ticagrelor and his EKG showed sinus bradycardia (heart rate = 54 bpm) with borderline AV conduction delay with RBBB pattern () which was similar to his baseline EKG. Clopidogrel was started as an alternative P2Y12 platelet receptor inhibitor and aspirin was continued. He was discharged after an event monitor was placed.