Novel coronavirus 2019 (COVID‐19) has been the focus of the medical community since its emergence in December 2019 and has already infected more than 100 million patients globally. Primarily described to cause a respiratory illness, COVID‐19 has been found to affect almost every organ system. Bradycardia is a newly recognized ramification of COVID‐19 that still has unknown prognostic value. Studies have shown an increase in the incidence of arrhythmias, cardiomyopathies, myocarditis, acute coronary syndromes, and coagulopathies in infected patients as well as an increased risk of mortality in patients with preexisting cardiovascular disease. While the pathogenesis of bradycardia in COVID‐19 may be multifactorial, clinicians should be aware of the mechanism by which COVID‐19 affects the cardiovascular system and the medication side effects which are used in the treatment algorithm of this deadly virus. There has yet to be a comprehensive review analyzing bradyarrhythmia and relative bradycardia in COVID‐19 infected patients. We aim to provide a literature review including the epidemiology, pathogenesis, and management of COVID‐19 induced bradyarrhythmia.

Acute kidney injury (AKI) due to an acute interstitial nephritis (AIN) is common and can lead to increased morbidity and mortality. Medications such as antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPI) and rifampin are common offending agents. Anticoagulant-associated AIN is more frequently reported with the use of warfarin; however, only few case reports have reported an association with the use of novel oral anticoagulants (NOACs). Herein, we report the case of a 59-year-old male who developed AKI after initiating dabigatran for the treatment of atrial fibrillation. Laboratory data demonstrated elevated blood urea nitrogen (BUN) of 115 mg/dL (baseline = 35 mg/dL) and serum creatinine (Cr) of 5.06 mg/dL (baseline = 1.3 mg/dL). Urinalysis revealed eosinophiluria. Renal biopsy disclosed diffuse tubulointerstitial nephritis and eosinophils and confirmed the diagnosis of AIN. At 1 week, renal function improved (BUN/Cr = 53/2.73 mg/dL) with steroid therapy and discontinuation of dabigatran. With an increasing use of NOACs, it is important to monitor renal function to diagnose AIN in a timely fashion. Early diagnosis and prompt treatment can mitigate serious renal damage induced by dabigatran.

Cardiac arrhythmias were reported in cases of West Nile Virus (WNV) encephalitis; however, the underlying pathophysiology remains incompletely understood. We present a 67-year-old male with altered mental status, later diagnosed with WNV encephalitis. Hospital course was complicated by progressive sinus bradycardia and corrected QT (QTc) prolongation. These findings persisted despite the absence of classical causes and resolved only after improvement of the underlying encephalitis. After excluding classical causes, autonomic dysfunction is one of the proposed mechanisms behind cardiac arrhythmias in WNV encephalitis. Resolution of arrhythmias is expected after the improvement of underlying encephalitis and should be taken into consideration before proceeding for pacemaker placement or other cardiac intervention. Furthermore, this case highlights the importance of continuous cardiac monitoring in WNV encephalitis patients.

Despite the numerous advancements in cardiac implantable electronic defibrillator (CIED) designs and implantation techniques, device-related infections continue to represent significant morbidity and mortality. Although Gram-positive bacteria remain the most commonly reported organisms, various other bacterial families have been reported. We describe a 61-year-old patient with a history of non-ischaemic cardiomyopathy who presented with implantable cardioverter defibrillator pocket infection due to Stenotrophomonas maltophilia and Pantoea calida that developed a few days following the device generator replacement. Early device explantation, tissue sampling and initiation of sensitivity-directed antibiotics are necessary steps for early diagnosis and management of such CIED-related infections. S. maltophilia and P. calida should be added to the expanding list of the causative organisms behind CIED-related infections. Our case and available literature demonstrated excellent sensitivity of these two organisms to sulfamethoxazole-trimethoprim treatment.