Background Long-term health sequelae of COVID-19 may be multiple but have thus far not been systematically studied. Methods All patients discharged after COVID-19 from the Radboud university medical centre, Nijmegen, The Netherlands, were consecutively invited to a multidisciplinary outpatient facility. Also, non-admitted patients with mild disease but with symptoms persisting >6 weeks could be referred by general practitioners. Patients underwent a standardized assessment including measurements of lung function, chest CT/X-ray, 6-minute walking test, body composition, and questionnaires on mental, cognitive, health status and quality of life (QoL). Results 124 patients (age 59±14 years, 60% male) were included; 27 with mild, 51 with moderate, 26 with severe and 20 with critical disease. Lung diffusion capacity was below lower limit of normal in 42% of discharged patients. Ninety-nine percent of discharged patients had reduced ground-glass opacification on repeat CT imaging, and normal chest X-rays were found in 93% of patients with mild diseases. Residual pulmonary parenchymal abnormalities were present in 91% of discharged patients, and correlated with reduced lung diffusion capacity. Twenty-two percent had low exercise capacity, 19% low fat-free mass index, and problems in mental and/or cognitive function were found in 36% of the patients. Health status was generally poor, particularly in the domains functional impairment (64%), fatigue (69%) and QoL (72%). Conclusions This comprehensive health assessment revealed severe problems in several health domains in a substantial number of ex-COVID-19 patients. Longer follow-up studies are warranted to elucidate natural trajectories and to find predictors of complicated long-term trajectories of recovery.

Skeletal muscle‐related symptoms are common in both acute coronavirus disease (Covid)‐19 and post‐acute sequelae of Covid‐19 (PASC). In this narrative review, we discuss cellular and molecular pathways that are affected and consider these in regard to skeletal muscle involvement in other conditions, such as acute respiratory distress syndrome, critical illness myopathy, and post‐viral fatigue syndrome. Patients with severe Covid‐19 and PASC suffer from skeletal muscle weakness and exercise intolerance. Histological sections present muscle fibre atrophy, metabolic alterations, and immune cell infiltration. Contributing factors to weakness and fatigue in patients with severe Covid‐19 include systemic inflammation, disuse, hypoxaemia, and malnutrition. These factors also contribute to post‐intensive care unit (ICU) syndrome and ICU‐acquired weakness and likely explain a substantial part of Covid‐19‐acquired weakness. The skeletal muscle weakness and exercise intolerance associated with PASC are more obscure. Direct severe acute respiratory syndrome coronavirus (SARS‐CoV)‐2 viral infiltration into skeletal muscle or an aberrant immune system likely contribute. Similarities between skeletal muscle alterations in PASC and chronic fatigue syndrome deserve further study. Both SARS‐CoV‐2‐specific factors and generic consequences of acute disease likely underlie the observed skeletal muscle alterations in both acute Covid‐19 and PASC.

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Objectives Our aim was to study the associations between resting lung hyperinflation, weight-bearing exercise-induced dyspnea and adipose distribution in obese and normal-weight COPD patients. Methods We performed a comparison between 80 obese COPD patients (COPDOB) with 80 age- and FEV1 matched normal-weight COPD patients (COPDNW). Dyspnea was assessed by the mMRC scale and the Borg dyspnea score before and after a 6 min walk test. Further characterization included spirometry, body plethysmography and metronome paced tachypnea (MPT) to estimate dynamic hyperinflation. Body composition was assessed with bioelectrical impedance analysis. Associations between dyspnea scores and BMI and body composition groups were studied using logistic regression models. Results COPDOB patients had attenuated increases in TLC, FRC and RV compared to COPDNW patients ( p < 0.01). The groups had comparable 6 min walking distance and ΔFRC upon MPT ( p > 0.05). Compared to COPDNW, COPDOB patients reported more often a mMRC ≥ 2 (65 vs 46%; p = 0.02; OR 3.0, 95% CI 1.4–6.2, p < 0.01) and had higher ΔBorg upon 6MWT: 2.0 (SEM 0.20) vs. 1.4 (SEM 0.16), p = 0.01; OR for ΔBorg ≥ 2: 2.4, 95% CI 1.1–5.2, p = 0.03. Additional logistic regression analyses on the associations between body composition and dyspnea indicated that increased body fat percentage, fat mass index and waist-to-hip ratio were associated with higher ORs for mMRC ≥ 2 and ΔBorg upon 6MWT ≥ 2. Conclusion Despite its beneficial effect on resting lung hyperinflation, adiposity is associated with increased weight-bearing exercise-induced dyspnea in COPD.

Muscle weakness is a prominent symptom in post-acute sequelae of COVID-19 (PASC). However, few studies have objectively and longitudinally assessed muscle strength after varying COVID-19 severity grades. This observational study aimed to explore the prevalence, determinants, and 1.5 years change of quadriceps muscle weakness in 98 patients discharged from COVID-19 hospitalization and in 50 patients with PASC following mild COVID-19. Isometric quadriceps maximal voluntary contraction (MVC) was assessed on a computerized dynamometer at three visits. Also, in a subgroup of 14 post-COVID-19 patients with quadriceps muscle weakness, muscle thickness and echo intensity were determined by muscle ultrasound of nine upper and lower extremity muscles. Muscle weakness was found in 59% of post-hospitalized patients and in 65% of those with PASC following mild COVID-19 at ~14 weeks after acute COVID-19. Whereas during ~1.5 years follow-up MVC modestly improved, muscle weakness prevalence remained unchanged. Hospital length of stay and diabetes mellitus were identified as possible predictors of muscle weakness following COVID-19 hospitalization. No predictors could be identified in those with PASC following mild COVID-19. Ultrasound outcomes revealed no large structural abnormalities. In conclusion, clinically relevant muscle weakness is common after COVID-19 and its long-term improvement is poor. Future studies with relevant control groups are warranted to confirm our data.

The incidence of chronic thromboembolic pulmonary hypertension (CTEPH) in coronavirus disease 2019 (COVID-19) survivors who were diagnosed with acute pulmonary embolism (PE) is currently unknown. Considering the high PE incidence reported in COVID-19 and its potentially unique pathophysiology, it may be hypothesised that thrombus resolution occurs to a lesser extent after COVID-19-associated PE, and that the prevalence of CTEPH is higher compared to non-COVID-19-associated PE populations. CTEPH could therefore be a treatable cause of long COVID, which captures a broad range of post-acute COVID-19 sequelae, in those with PE during acute COVID-19 [1]. In this multicentre cross-sectional study, we aimed to establish the prevalence of CTEPH and recurrent venous thromboembolism (VTE), and evaluate thrombus resolution in COVID-19-associated PE survivors.

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