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 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.