Prusinski, Christian C

AbstractPersistent chest pain (PCP) following acute COVID‐19 infection is a commonly reported symptom with an unclear etiology, making its management challenging. This scoping review aims to address the knowledge gap surrounding the characteristics of PCP following COVID‐19, its causes, and potential treatments. This is a scoping review of 64 studies, including observational (prospective, retrospective, cross‐sectional, case series, and case–control) and one quasi‐experimental study, from databases including Embase, PubMed/MEDLINE, Cochrane CENTRAL, Google Scholar, Cochrane Database of Systematic Reviews, and Scopus. Studies on patients with PCP following mild, moderate, and severe COVID‐19 infection were included. Studies with patients of any age, with chest pain that persisted following acute COVID‐19 disease, irrespective of etiology or duration were included. A total of 35 studies reported PCP symptoms following COVID‐19 (0.24%–76.6%) at an average follow‐up of 3 months or longer, 12 studies at 1–3 months and 17 studies at less than 1‐month follow‐up or not specified. PCP was common following mild—severe COVID‐19 infection, and etiology was mostly not reported. Fourteen studies proposed potential etiologies including endothelial dysfunction, cardiac ischemia, vasospasm, myocarditis, cardiac arrhythmia, pneumonia, pulmonary embolism, postural tachycardia syndrome, or noted cardiac MRI (cMRI) changes. Evaluation methods included common cardiopulmonary tests, as well as less common tests such as flow‐mediated dilatation, cMRI, single‐photon emission computed tomography myocardial perfusion imaging, and cardiopulmonary exercise testing. Only one study reported a specific treatment (sulodexide). PCP is a prevalent symptom following COVID‐19 infection, with various proposed etiologies. Further research is needed to establish a better understanding of the causes and to develop targeted treatments for PCP following COVID‐19.

AbstractBackground and purposeReal‐time quaking‐induced conversion (RT‐QuIC) assays offer a sensitive and specific means for detection of prions, although false negative results are recognized in clinical practice. We profile the clinical, laboratory, and pathologic features associated with false negative RT‐QuIC assays and extend these to frame the diagnostic approach to patients with suspected prion disease.MethodsA total of 113 patients with probable or definite prion disease were assessed at Mayo Clinic (Rochester, MN; Jacksonville, FL; Scottsdale, AZ) or Washington University School of Medicine (Saint Louis, MO) from 2013 to 2021. RT‐QuIC testing for prions was performed in cerebrospinal fluid (CSF) at the National Prion Disease Pathology Surveillance Center (Cleveland, OH).ResultsInitial RT‐QuIC testing was negative in 13 of 113 patients (sensitivity = 88.5%). RT‐QuIC negative patients were younger (median = 52.0 years vs. 66.1 years, p < 0.001). Other demographic and presenting features, and CSF cell count, protein, and glucose levels were similar in RT‐QuIC negative and positive patients. Frequency of 14‐3‐3 positivity (4/13 vs. 77/94, p < 0.001) and median CSF total tau levels were lower in RT‐QuIC negative patients (2517 vs. 4001 pg/mL, p = 0.020), and time from symptom onset to first presentation (153 vs. 47 days, p = 0.001) and symptomatic duration (710 vs. 148 days, p = 0.001) were longer.ConclusionsRT‐QuIC is a sensitive yet imperfect measure necessitating incorporation of other test results when evaluating patients with suspected prion disease. Patients with negative RT‐QuIC had lower markers of neuronal damage (CSF total tau and protein 14‐3‐3) and longer symptomatic duration of disease, suggesting that false negative RT‐QuIC testing associates with a more indolent course.