A 76-year-old female without a past history of conduction diseases and confirmed past medical history significant for type 2 diabetes mellitus, hypertension, and coronary artery disease post PCI to right coronary artery (RCA) in 2018, treated with aspirin 100 mg, atorvastatin 20 mg, metoprolol tartrate 50 mg, isosorbide mononitrate 20 mg, and basal-bolus insulin, presented to our hospital emergency department with a 5-day history of shortness of breath that was increasing in severity and associated with central chest pain radiating to throat that started 6 h prior to admission. Her vital signs were as follows: blood pressure = 115/73 mmHg, heart rate = 106 beats per minute, temperature = 36.5 C, and oxygen saturation = 95% on room air. Her first 2 sets of troponin T were 104 ng/L and 135 ng/L (normal <14 ng/L), and her transthoracic echocardiogram showed left ventricular regional wall motion abnormalities with an ejection fraction of 38%. Her initial electrocardiogram (ECG) showed T wave inversion in anterolateral leads (V3–V6 leads) as shown in Figure . Therefore, a diagnosis of non-STEMI was made, and she was planned for in-patient coronary angiography (CAG) and hence started on aspirin 300 mg then 100 mg enteric coated (EC) daily, clopidogrel 300 mg then 75 mg daily, and enoxaparin 1 mg/Kg subcutaneous every 12 h.\nOn the second day of admission, she underwent CAG and was found to have 95% stenosis in proximal left anterior descending (LAD) artery, and a patent drug-eluting stent (DES) in the mid-RCA. A DES (3.0 × 33 mm) was placed in the proximal to mid LAD. After the PCI, she was on aspirin 100 mg EC, clopidogrel 150 mg daily, bisoprolol 5 mg, atorvastatin 40 mg, lisinopril 5 mg, spironolactone 12.5 mg daily, furosemide 40 mg intravenous twice daily, and insulin (basal glargine and bolus aspart). Two days after the PCI, it was decided to start the patient on ticagrelor 180 mg as a loading dose followed by 90 mg twice daily and to stop clopidogrel.\nOne hour after receiving ticagrelor loading dose, the patient started to develop dyspnea followed by an episode of unresponsiveness. The review of the telemetry monitoring strips showed bradycardia followed by a sinus pause of 22 s during the episode of unresponsiveness as shown in Figure . Therefore, she was transferred immediately to our cardiac intensive care unit (CICU) where she underwent transvenous pacemaker insertion, which was kept for 2 days, and ticagrelor was switched back to clopidogrel after 24 h of receiving ticagrelor loading dose, by giving a loading dose of 600 mg followed by 75 mg daily. After the removal of the pacemaker, metoprolol 12.5 mg twice daily was started, and she was observed for 2 days and remained stable without any further episodes of bradycardia or sinus pause with a heart rate ranging from 65–75 beats per minute. After which, she was discharged and then seen in the outpatient clinic within 20 days of discharge and had no complaints.
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.