COVID-19 has recently been associated with the development of bradyarrhythmias, although its mechanism is still unclear. We aim to summarize the existing evidence regarding bradyarrhythmia in COVID-19 and provide future directions for research.Following the PRISMA Extension for Scoping Reviews, we searched MEDLINE and EMBASE for all peer-reviewed articles using keywords including"Bradycardia," "atrioventricular block," and "COVID-19″ from their inception to October 13, 2021. Fortythree articles, including 11 observational studies and 59 cases from case reports and series, were included in the systematic review. Although some observational studies reported increased mortality in those with bradyarrhythmia and COVID-19, the lack of comparative groups and small sample sizes hinder the ability to draw definitive conclusions. Among 59 COVID-19 patients with bradycardia from case reports and series, bradycardia most often occurred in those with severe or critical COVID-19, and complete heart block occurred in the majority of cases despite preserved LVEF (55.9%).Pacemaker insertion was required in 76.3% of the patients, most of which were permanent implants (45.8%). This systematic review summarizes the current evidence and characteristics of bradyarrhythmia in patients with COVID-19. Further studies are critical to assess the reversibility of bradyarrhythmia in COVID-19 patients and to clarify potential therapeutic targets including the need for permanent pacing.

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Introduction: Methamphetamine use is not a traditional risk factor for spontaneous coronary artery dissection (SCAD). There have been several case reports suggesting an association between methamphetamine use and SCAD. Case: We present a case of a 50-year-old female with a history of hypertension, hyperlipidemia, stroke, and active tobacco use who presented with substernal chest pain radiating to the back and abdomen with associated dyspnea and diaphoresis. The patient was also taking warfarin for a prior history of deep venous thrombosis. Her serum 5 th generation troponin level was elevated to a peak of 1135 ng/L, and a 12-lead EKG showed ST-elevations not meeting STEMI criteria (1mm in V3, 2mm in V4, and 0.5mm in V5). Coronary angiography showed a short section of SCAD type 1 involving the mid portion of the LAD with TIMI 3 flow. There was no significant atherosclerotic disease throughout any of the vessels. The patient was managed conservatively with medical therapy and had resolution of her pain. CT-angiography of the chest, abdomen and pelvis was performed to rule out dissection involving the aorta and its branches and was unrevealing. Urine toxicology screening returned positive for methamphetamine. Given a lack of other traditional risk factors aside from gender, the patient was diagnosed with SCAD secondary to methamphetamine use. Discussion: Traditional risk factors for SCAD include female sex, fibromuscular dysplasia, connective tissue disease, multiparity (our patient was parity 1), and exogenous hormone use. Methamphetamine use as well as prescription amphetamines have been associated with SCAD in several case reports. SCAD tends to occur in women with an absence of risk factors for coronary artery disease. However, even in patients with multiple risk factors for atherosclerosis and an absence of risk factors for SCAD, SCAD should not be excluded in the differential when a history of amphetamine use is elicited.

Background: Cardiac involvement is a major cause for mortality in patients with systemic sarcoidosis. Atrioventricular (AV) block caused by inflammation involving the conduction system is one of the major manifestations of cardiac involvement. The mainstay of management is immunosuppressive therapy and device implantation if high degree AV block is present. However, there is lack of evidence regarding the appropriate dose and duration of corticosteroids in the treatment of cardiac sarcoidosis. Case summary: We describe the case of a 62-year-old man who presented with symptoms of dyspnea and bradycardia and was found to be in second degree AV block type II. Computed tomography of the chest showed hilar lymphadenopathy. Echocardiography revealed reduced systolic function (LVEF of 35-40%). A FDG-PET scan showed hypermetabolic activity of the interventricular septum and pericardium consistent with sarcoidosis. Bronchoscopy with BAL and EUS biopsies revealed necrotizing granulomas consistent with pulmonary sarcoidosis. ICD/pacemaker implantation was discussed; however the patient deferred and ultimately underwent Boston Scientific ILR placement to monitor for arrhythmias. He was started on methotrexate and prednisone with improvement in heart rate from 2:1 AV block (rates 30's) to sinus rhythm with rates in the 60's. Subsequent stress testing demonstrated improvement in heart rate with exercise to 113 bpm. His AV block had decreased in frequency per Implantable loop recorder (ILR) monitoring. A month later, the patient stopped taking prednisone and methotrexate and developed a symptomatic recurrence of 2:1 AV block. He then underwent dual chamber pacemaker implantation with ILR explant. Discussion: This case highlights the importance of maintaining and educating patients about long term immunosuppressive treatment in cardiac sarcoidosis to prevent recurrence of conduction abnormalities. The initial dose for those receiving prednisone is typically 40mg daily, while for those patients receiving an additional immunosuppressive agent, the initial dose can be 20mg daily. Based on response to treatment after 1 to 3 months, immunosuppressive therapy should be continued for an additional 9 to 12 months.