Ghorbanzadeh, Atefeh

Endocardial fibroelastosis emerged as a challenging clinical phenomenon in the 1940s. It is characterized by an atypical proliferation of fibrous and elastic tissue within the heart and is primarily observed in childhood, occasionally displaying familial inheritance. While the precise cause remains elusive, various factors, including genetic, infectious, metabolic, autoimmune, oncologic, and medication-related influences, appear to play a role in its pathogenesis. The coexistence of endocardial fibroelastosis with multiple cardiac structural abnormalities manifests in symptoms of congestive heart failure and rhythm abnormalities. Despite its challenging diagnosis, various findings from ECG and imaging have proven beneficial in further evaluation of this condition. Finally, the treatment approach to endocardial fibroelastosis became complex due to addressing its concurrent cardiac abnormalities. Strategies for managing and preventing this condition are still under investigation. In this review, we intend to highlight the existing knowledge and illuminate future considerations regarding the etiology, diagnosis, and management of this disease.

AbstractPatients with thrombophilia remain concerned about venous thromboembolism (VTE) risk with COVID‐19 vaccinations. The aim of this study was to examine VTE outcomes in patients with inherited or acquired thrombophilia who were vaccinated for COVID‐19. Vaccinated patients ≥18 years between November 1, 2020 and November 1, 2021 were analyzed using electronic medical records across the Mayo Clinic enterprise. The primary outcome was imaging confirmed acute VTE occurring 90 days before and after the date of the first vaccine dose. Thrombophilia patients were identified through laboratory testing results and ICD‐10 codes. A total of 792 010 patients with at least one COVID‐19 vaccination were identified. Six thousand sixty‐seven of these patients were found to have a thrombophilia, among whom there was a total of 39 VTE events after compared to 51 VTE events before vaccination (0.64% vs. 0.84%, p = .20). In patients with Factor V Leiden or prothrombin gene mutation, VTE occurred in 27 patients before and in 29 patients after vaccination (0.61 vs. 0.65%, p = .79). In patients with antiphospholipid syndrome, VTE occurred in six patients before and four patients after vaccination (0.59% vs. 0.39%, p = .40). No difference was observed in the overall VTE rate when comparing the postvaccination 90 days to the prevaccination 90 days, adjusted hazard ratio 0.81 (95% confidence interval: 0.53–1.23). In this subgroup of COVID‐19 vaccinated patients with thrombophilia, there was no increased risk for acute VTE postvaccination compared to the prevaccination timeframe. These results are consistent with prior studies and should offer additional reassurance to patients with inherited or acquired thrombophilia.