Myopericarditis as a Manifestation of Long COVID Syndrome.

The main presentation of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is respiratory. However, there are extrapulmonary manifestations such as myocardial and pericardial injury. The term long COVID syndrome describes the persistence of symptoms in patients who have recovered from the infection. A 31-year-old man presented with mild coronavirus disease 2019 (COVID-19) symptoms for three days. Two weeks later, he developed chest pain, pericardial rub, and pericardial effusion; he underwent echocardiography showing pericarditis and an MRI which revealed inferoseptal hypokinesia and mild global myocardial hyperintensity, cardiac scintigraphy with Ga-67, and an inflammatory process in the myocardium. He was treated with methylprednisolone pulse (1g IV/day) and tapering prednisone (5 mg/day), with gradual evolution of symptoms for one year. In conclusion, this is a patient without comorbidities with clinical, laboratory, and imaging diagnosis of myopericarditis as a manifestation of long COVID syndrome.

Primary and secondary central nervous system vasculitis: clinical manifestations, laboratory findings, neuroimaging, and treatment analysis.

The objectives of this study are to compare the initial clinical, laboratory, and imaging features in primary central nervous system vasculitis (PCNSV) vs secondary central nervous system vasculitis (SCNSV) and follow up after treatment with intravenous cyclophosphamide (IV-CYC) plus glucocorticosteroids (GCS): methylprednisolone (MP). Neurological, laboratory, and neuroimaging findings were analyzed in PCNSV and SCNSV patients. Cerebral biopsy (CB) was performed in nine patients. Both groups received at onset MP plus IV-CYC for 6 months, followed by bimonthly IV-CYC plus prednisone (PND) for 12 months. All patients were followed during 36 months. Thirty patients were included (12 PCNSV and 18 SCNSV). Focal and non-focal neurological manifestations were similar in both groups, headache being the most frequent manifestation in both groups. Fatigue, myalgias, arthralgias, neuropathy, low leukocytes and platelets, elevated erythrocyte sedimentation rate, positive antinuclear antibodies (ANA), anti-double-stranded DNA (dsDNA), antineutrophil cytoplasmic antibodies (ANCA), low complement, and rheumatoid factor were more frequent in SCNSV (p < 0.05). In cerebrospinal fluid, pleocytosis and proteins were higher in PCNSV (p < 0.05). Periventricular and subcortical hyperintense lesions were observed in cranial magnetic resonance imaging in both vasculitides. Cerebral angiography and angioresonance showed narrowing of vasculature in all patients in both groups. CB showed gliosis and lymphocytic infiltration within and around the walls in four patients and granulomatous infiltration in the other patients. After treatment, the Kaplan-Meier survival curve showed a higher relapse-free survival in PCNSV (p < 0.05). Neurological manifestations and neuroimaging findings were similar in both groups of vasculitides, but general symptoms, joint, musculoskeletal, and peripheral neuropathy were preponderant in SCNSV. After treatment with IV-CYC and GCS, patients with PCNSV had a higher relapse-free survival than those with SCNSV.