A 62-year-old white male with no significant medical history except for hypertension, presented to the emergency room of one of our community hospitals with a flu-like illness of 1 week duration and shortness of breath with hypoxia. His home medications were lisinopril 40 mg once daily and atenolol 50 mg daily. On initial presentation, his vitals were normal except for a pulse oximetry of 89% and a weight of 102 kg with body mass index (BMI) of 29.8 kg/m2. Even though he complained of low grade fever, his initial temperature was normal at 36.8°C. His cardiovascular system examination revealed a regular rhythm with normal venous pressure and heart sounds. The only positive finding in his physical examination was crackles in the back of the chest. His chest X-ray and CT scan showed multifocal bilateral infiltrates (). Initial ECG was within normal limits, with a normal PR interval of 160 ms. He was admitted to the hospital and started treatment with supplemental oxygen via a nasal canula and the antibiotics azithromycin and ceftriaxone. COVID-19 test by polymerase chain reaction (PCR) was returned positive later that day. Two days later, he developed crushing substernal chest pain with serial ECG changes suggestive of posterior myocardial infarction. Emergency coronary angiogram revealed occlusion of a large co-dominant proximal left circumflex artery (LCx), for which he promptly underwent primary percutaneous coronary intervention (PCI) with implantation of a drug-eluting stent, Xience Alpine, 3 × 15 mm (Abbott Vascular, Santa Clara, CA, USA), with excellent angiographic results (). Post-procedure, he was initiated on clopidrogel 75 mg/day in addition to aspirin 81 mg/day that was started previously. During the procedure, his respiratory distress worsened, requiring intubation and mechanical ventilation. He was transferred to our centre on the fifth day after the initial hospitalization because of worsening hypoxia and haemodynamic instability. Soon after arrival, he was placed on veno-venous extracorporeal membrane oxygenation (V-V ECMO). He was decannulated 3 days later while remaining on the ventilator. He was given a full 10-day course of hydroxychloroquine and also received the additional antibiotics piperacillin/tazobactam. Serum troponin I levels peaked at 40.47 ng/mL on day 5 of the hospitalization and then down-trended to <1 ng/mL (reference <0.03 ng/mL), though not completely reaching baseline. Other pertinent laboratory data included normal renal function, normal complete blood cell count with relative lymphopenia at 380 cells/mm3 and elevated lactate dehydrogensae (LDH) levels at 336 U/L (reference range 84–246 U/L) on admission. Interleukin-6 (IL-6) levels was at 14 pg/mL (reference range is <5 pg/mL) on day 3. C-reactive protein at 30.34 mg/dL (reference value <1), D-dimer levels of 33 976 ng/mL FEU (reference range <500) and ferritin levels at 1592 μg/L (reference range 20–300) were also elevated, on admission. On his 14th hospital day he had his first episode of asystole lasting 16 s. In the next 3 days, he had multiple sinus pauses without an escape rhythm, many lasting longer than 20 s (). These episodes occurred spontaneously without any negative chronotropic medications and without events causing an increase in intrathoracic pressure such as coughing, suctioning of the endotracheal tube, changing the patient’s position, etc. He had not been hypoxic or on any pressors or inotropes during this time. As expected, concomitant arterial pressure tracing also showed flatline, along with the episodes of asystole. At the end of each pause, the returning rhythm was atrial fibrillation that would spontaneously convert into normal sinus rhythm after several hours. His echocardiogram on the day when he had his first episode of asystole showed preserved left ventricular systolic function with an ejection fraction of 55–60% and posterior-lateral hypokinesia.\nInitially transcutaneous pacing was attempted but was not effective even at maximum outputs. The episodes continued for the next 2 days. As these episodes occurred some time after the index myocardial infarction and without provocation, the need for a permanent pacemaker was thought to be high. Because we wanted to minimize the number of procedures for the patient and reduce the risk of exposure for the healthcare staff during the implant and during the follow-up period, a decision to proceed with the implantation of a leadless pacemaker was made, without going through an interim temporary pacemaker.\nThe leadless pacemaker was inserted on the 17th hospital day after obtaining appropriate consent. Micra™ VR (Medtronic, Minneapolis MN, USA) was inserted in a standard fashion through the femoral vein (). Our pre-established COVID-19 protocol was followed, including adequate personal protective equipment and the procedure being performed in a designated, catheterization laboratory.\nOn completion of the procedure, the patient was transferred back to the COVID-19 unit, where he continued to remain on a ventilator for the next 10 days, followed by successful extubation.\nThe leadless pacemaker was interrogated wirelessly without added exposure risk to the staff on the day following the implantation and 5 days after the implant. Seven days post-implant the percentage of pacing was 3.4% and at 6 weeks post-implant it as 1.5%. A week after the implant, the patient underwent magnetic resonance imaging (MRI) of the brain due to mental status changes without any adverse effects on his pacemaker. He was successfully extubated 10 days after the leadless pacemaker implantation, and was eventually discharged on the 50th day of hospitalization to a rehabilitation facility, where he continues to recover gradually. His discharge medications included aspirin 81 mg/day, atorvastatin 80 mg/day, and metoprolol 12.5 mg twice per day.
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.