Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has risen to the level of a global pandemic. Growing evidence has proven the cardiac involvement in SARS-CoV-2 infection. This study aims to evaluate the ability of cardiovascular complications determined by elevated troponin and electrocardiogram findings (e.g., corrected QT interval (QTc)) in predicting the severity of SARS-CoV-2 infection among hospitalized patients.Methods: This is a retrospective review of medical records of 800 patients, admitted to Richmond University Medical Center in Staten Island, NY, and tested positive for SARS-CoV-2 between March 1, 2020 and July 31, 2020. A total of 339 patients met the study inclusion and exclusion criteria and were included in statistical analysis.Results: Elevated serum troponin levels on admission statistically correlated with mortality in SARS-CoV-2 patients. Prolonged QTc was shown to have an independent statistically significant association with mortality among patients hospitalized with SARS-CoV-2.Conclusions: Growing concern for cardiovascular sequelae of coronavirus disease 2019 (COVID-19) has prompted many researchers to investigate the role of cardiovascular complications in mortality due to SARS-CoV-2. Obtaining a simple electrocardiogram for hospital-ized patients with COVID-19 could provide an independent prognostic tool and prompt more coordinated treatment strategies to prevent mortality among patients hospitalized with COVID-19.

Tin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 4.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Antiphospholipid syndrome (APS) is managed with warfarin for secondary prophylaxis in patients who have had a thrombotic event in the past. Warfarin has been deemed superior to novel oral anticoagulants in preventing venous and arterial thrombosis in conjunction with aspirin. The catastrophic variant of APS (CAPS) is very rarely reported, especially in those who have been on a therapeutic dose of warfarin therapy. We present a rare case of CAPS in a patient with a history of APS who had been on a therapeutic dose of warfarin along with aspirin therapy. The patient is a 70-year-old male with APS diagnosed 30 years prior when he presented with a pulmonary embolism; aspirin was added to warfarin two years ago when he had a cerebrovascular accident (CVA). He presented to the hospital with acute onset right-sided weakness and aphasia, left lower extremity pain. He had ischemic CVA, acute deep vein thrombosis (DVT), acute renal failure with a creatinine of 2.8, anemia with hemoglobin of 3.8, gastrointestinal bleed (GIB) on EGD, with INR of 3.48 cardiolipin IgM of >140g/L. He was transfused packed red blood cells, fresh frozen plasma, and provided Vit K. Subsequently, he had a cardiac arrest and was intubated and placed on a mechanical ventilator. Given simultaneous multiorgan involvement, acute arterial and venous thrombosis, the patient was diagnosed with CAPS. The patient was started on high-dose dexamethasone, intravenous immunoglobulin (IVIG), and underwent plasma exchange with significant improvement in symptoms, laboratory parameters; and was extubated with near normalization of his speech and motor deficits. He was discharged on enoxaparin and prednisone with sustained clinical improvement two months following discharge. This patient was on the recommended treatment for APS. However, he had presented with a CAPS. This is the first reported case of warfarin refractory CAPS. This case highlights that there might be a subgroup of the population in whom warfarin is not an effective form of treatment modality for an unknown cause, and in fact, it could potently expose a patient to the adverse events related to warfarin therapy as it did in our patient who had significant GIB. This case also highlights the uncommon scenario of spontaneous CAPS with no inciting event as previously reported in the literature, such as infection, recent surgeries, or trauma.

The coronavirus disease 2019 (COVID-19) pandemic is wreaking havoc across the globe. This pandemic has given rise to a mindset where physicians tend to neglect other causes of pneumonia, especially if the patient presents with signs and symptoms commonly associated with COVID-19. Herein, we report a case of a young man presenting to the emergency department with common clinical, radiological, and laboratory features of COVID-19 pneumonia such as shortness of breath, hypoxia, pulmonary embolism, elevated D-dimer, and bilateral ground glass opacities on computed tomography of the chest but was later diagnosed with Pneumocystis pneumonia that was treated with appropriate antibiotics and corticosteroids. This case highlights the importance of performing a thorough clinical history and differentiating the clinical and radiological features of COVID-19 pneumonia from pneumonia of other etiologies.

Postpartum dyspnea can be due to many causes, such as pulmonary embolism, amniotic fluid embolism, peripartum cardiomyopathy, but less frequently due to acute pulmonary edema. The incidence of acute pulmonary edema during pregnancy and in the postpartum period has been estimated to be around 0.08%. About half of the cases are attributed to tocolytic therapy. Herein, we present a case of a young woman presenting with acute hypoxia after induction of labor with oxytocin and found to have acute pulmonary edema. This case aims to illustrate and add to a growing body of literature regarding oxytocin-induced acute pulmonary edema and highlights the importance of recognizing the rare complication of oxytocin and necessary interventions to avoid complications. Oxytocin-induced pulmonary edema is a relatively uncommon condition, but physicians should have a high index of suspicion to initiate timely intervention and to avoid fetal complications.