National Institute of Health Research, Imperial College London.

There is growing evidence of histopathological changes in autopsied individuals infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); however, data on histopathological changes in autopsied patients with eradicated COVID-19 are limited. We performed an autopsy on a Caucasian female in her 80s, who died due to severe, bilateral pulmonary fibrosis after eliminated SARS-CoV-2 infection. In addition, CT scans from 2 months before infection and from 6 days prior to death were compared. Comparison of the CT scans showed bilateral development of widespread fibrosis in previously healthy lungs. Microscopic examination showed different areas with acute and organising diffuse alveolar damage and fibrosis with honeycomb-like remodelling and bronchial metaplasia. We here report a unique autopsy case with development of widespread pulmonary fibrosis in a woman in her 80s with previous COVID-19 and no history of pulmonary illnesses.

Background and purpose Among post‐COVID‐19 symptoms, fatigue is reported as one of the most common, even after mild acute infection, and as the cause of fatigue, myopathy diagnosed by electromyography has been proposed in previous reports. This study aimed to explore the histopathological changes in patients with post‐COVID‐19 fatigue. Methods Sixteen patients (mean age = 46 years) with post‐COVID‐19 complaints of fatigue, myalgia, or weakness persisting for up to 14 months were included. In all patients, quantitative electromyography and muscle biopsies analyzed with light and electron microscopy were taken. Results Muscle weakness was present in 50% and myopathic electromyography in 75%, and in all patients there were histological changes. Muscle fiber atrophy was found in 38%, and 56% showed indications of fiber regeneration. Mitochondrial changes, comprising loss of cytochrome c oxidase activity, subsarcollemmal accumulation, and/or abnormal cristae, were present in 62%. Inflammation was found in 62%, seen as T lymphocytes and/or muscle fiber human leukocyte antigen ABC expression. In 75%, capillaries were affected, involving basal lamina and cells. In two patients, uncommon amounts of basal lamina were found, not only surrounding muscle fibers but also around nerves and capillaries. Conclusions The wide variety of histological changes in this study suggests that skeletal muscles may be a major target of SARS‐CoV‐2, causing muscular post‐COVID‐19 symptoms. The mitochondrial changes, inflammation, and capillary injury in muscle biopsies can cause fatigue in part due to reduced energy supply. Because most patients had mild–moderate acute affection, the new variants that might cause less severe acute disease could still have the ability to cause long‐term myopathy.

Antihypertensive treatment based on telemonitoring of home BP was as effective as usual monitoring of office BP with regards to reduction of BP.