Acute Myopericarditis with Pericardial Effusion and Cardiac Tamponade in a Patient with COVID-19.

BACKGROUND Coronavirus disease 2019 (COVID-19) is primarily a respiratory illness. However, with rising numbers of cases, multiple reports of cardiovascular manifestations have emerged. We present a case of COVID-19 infection complicated by myopericarditis and tamponade requiring drainage. CASE REPORT An 82-year-old woman with multiple comorbidities presented with five days of productive cough, fever with chills, and intermittent diarrhea. She tested positive for COVID-19. Index EKG revealed new diffuse T-wave inversions and a prolonged QT interval (>500 ms). Troponin was mildly elevated without any anginal symptoms. Hydroxychloroquine and azithromycin were not initiated due to concerns about QT prolongation. The echocardiogram revealed preserved left ventricular (LV) function, a small global pericardial effusion, and apical hypokinesis. Serial echocardiograms revealed an enlarging circumferential pericardial effusion with pacemaker wire reported as 'piercing' the right ventricular (RV) apex alongside early diastolic collapse of the right ventricle, suggesting echocardiographic tamponade. Chest CT revealed extension of the RV pacemaker lead into the pericardial fat. Interestingly, on comparison with a previous chest CT from 2019, similar lead positions were confirmed. Pericardiocentesis was performed with removal of 400 cc exudate. CONCLUSIONS Acute myopericarditis and pericardial effusion can occur in COVID-19 infection, even in the absence of severe pulmonary disease. This case highlights the importance of awareness of rare cardiac manifestations of COVID-19 in the form of acute myopericarditis and cardiac tamponade and their early diagnosis and management.

Delayed acute pancreatitis induced by nilotinib in a patient with chronic myeloid leukemia attaining sustained complete molecular response.

Advent of tyrosine kinase inhibitors (TKI) have revolutionized therapy of chronic myeloid leukemia. Imatinib was the first agent utilized in the therapy of CML. Nilotinib, a second generation TKI, results in an increase in number of patients achieving major molecular response at an earlier time point. Asymptomatic elevations in pancreatic enzyme is common and acute pancreatitis within weeks to months from start of therapy has been observed. Delayed onset pancreatitis has not been reported. We report a case of delayed onset pancreatitis in a patient with sustained complete molecular response. On account of the deep response, we were able to avoid starting alternate tyrosine kinase inhibitors that could also result in pancreatitis as a class effect.

Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior.

Haploinsufficiency of the AT-rich interactive domain 1B (ARID1B) gene causes autism spectrum disorder and intellectual disability; however, the neurobiological basis for this is unknown. Here we generated Arid1b-knockout mice and examined heterozygotes to model human patients. Arid1b-heterozygous mice showed a decreased number of cortical GABAergic interneurons and reduced proliferation of interneuron progenitors in the ganglionic eminence. Arid1b haploinsufficiency also led to an imbalance between excitatory and inhibitory synapses in the cerebral cortex. Furthermore, we found that Arid1b haploinsufficiency suppressed histone H3 lysine 9 acetylation (H3K9ac) overall and particularly reduced H3K9ac of the Pvalb promoter, resulting in decreased transcription. Arid1b-heterozygous mice exhibited abnormal cognitive and social behaviors, which were rescued by treatment with a positive allosteric GABAA receptor modulator. Our results demonstrate a critical role for Arid1b in interneuron development and behavior and provide insight into the pathogenesis of autism spectrum disorder and intellectual disability.