Pulmonary Co-Infections Detected Premortem Underestimate Postmortem Findings in a COVID-19 Autopsy Case Series.

Bacterial and fungal co-infections are reported complications of coronavirus disease 2019 (COVID-19) in critically ill patients but may go unrecognized premortem due to diagnostic limitations. We compared the premortem with the postmortem detection of pulmonary co-infections in 55 fatal COVID-19 cases from March 2020 to March 2021. The concordance in the premortem versus the postmortem diagnoses and the pathogen identification were evaluated. Premortem pulmonary co-infections were extracted from medical charts while applying standard diagnostic definitions. Postmortem co-infection was defined by compatible lung histopathology with or without the detection of an organism in tissue by bacterial or fungal staining, or polymerase chain reaction (PCR) with broad-range bacterial and fungal primers. Pulmonary co-infection was detected premortem in significantly fewer cases (15/55, 27%) than were detected postmortem (36/55, 65%; p < 0.0001). Among cases in which co-infection was detected postmortem by histopathology, an organism was identified in 27/36 (75%) of cases. Pseudomonas, Enterobacterales, and Staphylococcus aureus were the most frequently identified bacteria both premortem and postmortem. Invasive pulmonary fungal infection was detected in five cases postmortem, but in no cases premortem. According to the univariate analyses, the patients with undiagnosed pulmonary co-infection had significantly shorter hospital (p = 0.0012) and intensive care unit (p = 0.0006) stays and significantly fewer extra-pulmonary infections (p = 0.0021). Bacterial and fungal pulmonary co-infection are under-recognized complications in critically ill patients with COVID-19.

SARS-CoV-2 infection and persistence in the human body and brain at autopsy.

Coronavirus disease 2019 (COVID-19) is known to cause multi-organ dysfunction1-3 during acute infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients experiencing prolonged symptoms, termed post-acute sequelae of SARS-CoV-2 (refs. 4,5). However, the burden of infection outside the respiratory tract and time to viral clearance are not well characterized, particularly in the brain3,6-14. Here we carried out complete autopsies on 44 patients who died with COVID-19, with extensive sampling of the central nervous system in 11 of these patients, to map and quantify the distribution, replication and cell-type specificity of SARS-CoV-2 across the human body, including the brain, from acute infection to more than seven months following symptom onset. We show that SARS-CoV-2 is widely distributed, predominantly among patients who died with severe COVID-19, and that virus replication is present in multiple respiratory and non-respiratory tissues, including the brain, early in infection. Further, we detected persistent SARS-CoV-2 RNA in multiple anatomic sites, including throughout the brain, as late as 230 days following symptom onset in one case. Despite extensive distribution of SARS-CoV-2 RNA throughout the body, we observed little evidence of inflammation or direct viral cytopathology outside the respiratory tract. Our data indicate that in some patients SARS-CoV-2 can cause systemic infection and persist in the body for months.

A Unique Case of Acute Coronary Syndrome in a Patient With COVID-19 Infection.

The coronavirus pandemic has caused significant mortality and morbidity in just over a year of its course since the first case was identified in Wuhan, China in December 2019. The varied presenting symptoms of this enveloped positive-sense single-stranded RNA virus infection and the unknown surrounding the pathophysiology of the disease process have been extensively reported in the literature. In this case report, we present a coronavirus disease 2019 (COVID-19) positive patient who presented with chest pain, diagnosed with acute coronary syndrome. Interestingly, the patient was noted to have non-ST elevation myocardial infarction with cardiac catheterization showing coronary microthrombi rather than typical acute coronary thrombotic occlusive disease.

A Rare Case of Mass-Like Hypertrophic Cardiomyopathy.

Mass-like hypertrophic cardiomyopathy (HCM) is a unique variant of HCM. HCM predominantly causes mid-ventricular, concentric hypertrophy, and asymmetric septal hypertrophy; however, focal hypertrophy mimicking a cardiac fibroma is rare. A 29-year-old female with a past medical history of recurrent orthostatic hypotension and syncope presented to the emergency department (ED) complaining of lightheadedness, dizziness, and generalized weakness associated with a syncopal episode. The patient reported a history of recurrent pre-syncope and syncope since her teenage years, as well as a family history of sudden cardiac death. Three years prior to her current presentation, the patient had an exercise stress test, 24-hour Holter monitor, and two echocardiograms that were unremarkable. Three weeks prior to presentation, the patient had a cardiac MRI that revealed focal mass hypertrophy of the basal anterior to mid anterior wall measuring up to 2.5 cm. In the ED, the patient was treated with intravenous fluid and beta-blockers; however, beta-blocker therapy had to be discontinued because the patient was experiencing presyncopal episodes and orthostatic hypotension. The patient was started on midodrine with partial improvement lightheadedness, dizziness, and presyncope. The patient was transferred to a tertiary center with the plan to do serial imaging and place an implantable cardioverter-defibrillator (ICD) if the focal mass thickness reached 3 cm and explore surgical intervention if symptoms worsened. Identifying and reporting anomalous variants of HCM is critical for optimal management of patient care and to improve outcomes.

Nonsurgical Management of a Giant Coronary Artery Aneurysm.

Coronary artery aneurysms (CAAs) are rare dilations of arterial segments. These aneurysms are mostly caused by atherosclerosis. Due to the rarity of this condition, there are no official guidelines for its management; therefore, management is mainly based on case reports. We present a patient with a giant CAA in the left anterior descending artery who was treated medically. At 12-month follow-up,  he was asymptomatic and had no complications.

Etiology and Age Distribution of Syncope in a Predominantly African-American Population.

BACKGROUND: Syncope, the sudden transient loss of consciousness due to multiple etiologies, usually has worse outcomes in African Americans compared with other races because of other comorbidities. This study aims to identify a correlation between the etiologies of syncope and age in a predominantly African-American sample population to facilitate future investigations with potentially improved specificity to address this condition. METHODS: We reviewed the medical records of 155 patients who presented with syncope concerns to the emergency department at our university hospital. After three charts were discarded due to poor data, the patients were divided into four age groups: <40 years old (25 patients), 40-60 years old (62 patients), 61-80 years old (44 patients), and >80 years old (21 patients). The etiology of syncope was reviewed in each case and categorized as either a vasovagal episode, orthostatic hypotension, pulmonary embolism, and related to cardio, neurologic, drug, or unspecified. RESULTS: For most of the patients in our study population, regardless of age, the etiology of syncope remained unspecified. Vasovagal related was the second most common etiology. The likelihood of having cardiac etiology under the age group of 40 is very low compared with those over 40 years (p = 0.026). Also, the incidence of pulmonary embolism is very low in all age groups with pulmonary embolism as a cause of syncope seen in only three patients (n = 3; 1.95%). CONCLUSIONS: Except for cardiac etiology being more likely in patients over age 40, we found no other correlation of age to syncope etiology. We also found that the etiology of syncope in African-American patients is similar to that of the general population. We recommend physicians to order a relevant workup, when clinical suspicion for syncope is present along with specific etiologies.