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 55-year-old female presented to the hospital after an episode of syncope at home. Her past medical history included Hashimoto’s thyroiditis and hypertension, and both were chronically stable on levothyroxine and an angiotensin receptor blocker. Her current condition had started about seven days prior to the presentation when the patient had developed a dry cough and nasal congestion. She had decided to get tested for SARS-CoV-2 because of her close contact with family members who were positive for SARS-CoV-2 infection. She had turned out to be positive for SARS-CoV-2 infection as well. She had also developed symptoms of progressive episodes of diarrhea. On the day of the presentation, she had been sitting on the toilet seat having a bowel movement when she had suddenly felt her arms and legs becoming weak. She had passed out on the toilet seat and her husband had helped her off the toilet. She denied any head trauma, aura, palpitations, tongue bite, or confusion after the episode of syncope. She had been immediately brought to the hospital for her unwitnessed syncopal episode.\nOn presentation, her review of systems included subjective fever, shortness of breath on exertion, decreased oral intake, diarrhea, and nausea, but she denied any vomiting, chest pain, and abdominal pain.\nThe patient tested positive for SARS-CoV-2 on nasal swab again on admission to the hospital. The EKG on admission showed normal sinus rhythm. The vital signs in the emergency department were as follows - temperature: 98.8 °F, heart rate: 60 beats/minute, blood pressure: 106/56 mmHg, respiratory rate: 20 breaths/minute, and pulse oximetry: 93% on room air. She was admitted to the telemetry floor as a part of an evaluation of a suspected syncopal episode. The laboratory results upon admission were as follows - white cell count: 5,860 cell count/uL, hemoglobin: 13.3 g/dL, platelets: 1,36,000 cells/uL, and the complete metabolic panel was unremarkable except for a potassium level of 3.3 mmol/L and blood glucose of 141 mg/dL. The cardiac enzyme (troponin T) was <0.01 ng/ml. Orthostatic vitals on admission were also normal. The inflammatory markers at the time of admission are summarized in Table . The patient's chest X-ray is shown in Figure , and her baseline EKG is presented in Figure .\nOn the third day post-admission, a rapid response was called on her due to acute hypoxia and a brief syncopal episode while she was using the bathroom in the hospital. She was immediately transferred to the bed and evaluated at the bedside. Upon assessment, the patient had regained her consciousness and was oriented to time, place, and person. Her vitals at the time were as follows - heart rate: 62 beats/minute, blood pressure: 153/73 mmHg, but her oxygen saturation had dropped to 88% on the room air, and hence she was placed on a nasal cannula with 4 liters of oxygen per minute. On the telemonitor, she was found to have two consecutive episodes of asystole lasting approximately one minute, 20 seconds, and later one minute, 30 seconds (Figure ). She was immediately placed on pacer pads and upgraded to the intensive care unit for further evaluation.\nThe patient was evaluated by the cardio-electrophysiology team for the symptomatic asystole episodes. She was further investigated for thyroid function, cardiac enzymes, and echocardiogram, which were in the normal range. She successfully underwent dual chamber pacemaker placement. For hypoxia, she received remdesivir and steroid treatment as a part of COVID-19 pneumonia treatment. In the later part of the hospital stay, she remained stable and was subsequently discharged home with an outpatient follow-up with the pulmonologist and cardiologist.