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.

Cardiovascular diseases remains one of the leading causes of mortality worldwide, and causes more than one millions deaths annually in the United States alone. Patients with chronic kidney disease (CKD) are predisposed to different types of heart rhythm abnormalities including but not limited to atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation. Both cardiovascular diseases and chronic kidney disease (CKD) may cause various variations in the cardiovascular system, autonomic nervous system, and various electrolytes abnormalities that open the door for the occurrence of multiple cardiac arrhythmias. Various pathophysiological mechanisms have been suggested in describing the correlation of cardiac arrhythmias in CKD patients. Despite the substantial progress in the management of chronic kidney disease, cardiovascular complications still highly dominant in CKD patient. Thus, reducing mortality from cardiovascular disease and sudden cardiac death in dialysis is a global health challenge. Management of cardiac arrhythmias includes the use of antiarrhythmic drugs, in addition to the use of catheter ablation and cardiac implantable electronic devices. The present review addresses the correlation between chronic kidney disease and different cardiac arrhythmias, the different pathophysiological mechanisms explaining the high risk of arrhythmias in CKD patients, the diagnostic tools used to identify arrhythmias, and the rule of subcutaneous defibrillators in preventing sudden cardiac death in dialysis patients.

Background: Several prediction models have been proposed to assess the short outcomes and in-hospital mortality among patients with heart failure (HF). Several variables were used in common among those models. We sought to focus on other, yet important risk factors that can predict outcomes. We also sought to stratify patients based on ejection fraction, matching both groups with different risk factors. Methods:We conducted a retrospective cohort study utilizing the Healthcare Cost and Utilization Project National Inpatient Sample (HCUP-NIS) 2016 database.Results: There were totally 116,189 admissions for acute decompensated heart failure (ADHF). Of these, 50.9% were for heart failure with reduced ejection fraction (HFrEF) group (n = 59,195), and 49.1% were for heart failure with preserved ejection faction (HFpEF) group (n = 56,994). Overall, in-hospital mortality was 2.5% of admissions for ADHF (n = 2,869). When stratified by HF types, admissions for HFrEF had higher mortality rate (2.7%, n = 1,594) in comparison to admissions for HFpEF (2.2%, n = 1,275) (P < 0.001). Significantly associated variables in univariate analyses were age, race, hypertension, diabetes mellitus, chronic kidney disease (CKD), atrial fibrillation/flutter, obesity, and chronic ischemic heart disease (IHD), while gender and chronic obstructive pulmonary disease (COPD) did not achieve statistical significance (P > 0.1). Conclusions:To our knowledge, this is the first study to stratify HF patients based on ejection fraction and utilizing different predictors and in-hospital mortality. These and other data support the need for future research to utilize these predictors to create more accurate models in the future.

Background: Trisomy 18, also known as Edwards syndrome, was first described in the 1960s and is now defined as the second most common trisomy. While this genetic disease has been attributed to nondisjunction during meiosis, the exact mechanism remains unknown. Trisomy 18 is associated with a significantly increased mortality rate of about 5–10% of patients surviving until 1 year of age. We present a case of a 26-year-old female diagnosed with trisomy 18, well outliving her life expectancy, maintaining a stable state of health. Case Presentation: A 26-year-old female with non-mosaic Edwards syndrome presented to the clinic for follow up after recent hospitalization for aspiration pneumonia. The definitive diagnosis of trisomy 18 was made prenatally utilizing chromosomal analysis and G-banding and fluorescence in situ hybridization (FISH) on cells obtained via amniocentesis. Her past medical history is characterized by severe growth and intellectual limitations; recurrent history of infections, especially respiratory system infections; and a ventricular septal defect (VSD) that was never surgically repaired. She remains in good, stable health and is under close follow-up and monitoring. Conclusions: Despite the fact that Edwards syndrome carries a significantly high mortality rate due to several comorbidities, recent literature including this case report has identified patients surviving into adulthood. Advancements in early detection and parent education have likely allowed for these findings. We aim to present a case of an adult with trisomy 18, living in stable condition, with an importance on medical follow-up.

Coronary sinus thrombosis (CST) is a rare but life-threatening condition that involves clot formation within the vessel responsible for draining all of the venous blood from the myocardium itself. The coronary sinus is situated in the right atrium approximately half-way between the tricuspid value and the inferior vena cava. The coronary sinus is rarely cited in medical literature due to limited knowledge as well as rarity in clinical encounters. CST can be a rapidly progressive life-threatening emergency as the interruption of vascular drainage can result in pericardial effusions, tamponade and cardiogenic shock. A major clinical challenge in diagnosing and treating this condition is due to relative rarity as well as the non-specificity of presenting symptoms that are often associated with more commonly encountered cardiopulmonary diseases. CST is most commonly induced by endothelial damage, such as post intracardiac instrumentation with catheter guidewires, or any of the criteria outlined by Virchow's triad. Our team described the finding of a thrombus 1.8 cm in diameter in a patient with underlying hepatobiliary cancer as well as underlying bacteremia from infected ascitic fluid. Though our patient remained hemodynamically stable without cardiopulmonary complications, we hope to spark a discussion within the medical community to increase awareness as well as to highlight the need for more research on this potentially life-threatening condition.