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.
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.