Background Patient hospitalized for coronavirus disease 2019 (COVID-19) pulmonary infection can have sequelae such as impaired exercise capacity. We aimed to determine the frequency of long-term exercise capacity limitation in survivors of severe COVID-19 pulmonary infection and the factors associated with this limitation. Methods Patients with severe COVID-19 pulmonary infection were enrolled 3 months after hospital discharge in COVulnerability, a prospective cohort. They underwent cardiopulmonary exercise testing, pulmonary function test, echocardiography, and skeletal muscle mass evaluation. Results Among 105 patients included, 35% had a reduced exercise capacity (VO2peak < 80% of predicted). Compared to patients with a normal exercise capacity, patients with reduced exercise capacity were more often men (89.2% vs. 67.6%, p = 0.015), with diabetes (45.9% vs. 17.6%, p = 0.002) and renal dysfunction (21.6% vs. 17.6%, p = 0.006), but did not differ in terms of initial acute disease severity. An altered exercise capacity was associated with an impaired respiratory function as assessed by a decrease in forced vital capacity (p < 0.0001), FEV1 (p < 0.0001), total lung capacity (p < 0.0001) and DLCO (p = 0.015). Moreover, we uncovered a decrease of muscular mass index and grip test in the reduced exercise capacity group (p = 0.001 and p = 0.047 respectively), whilst 38.9% of patients with low exercise capacity had a sarcopenia, compared to 10.9% in those with normal exercise capacity (p = 0.001). Myocardial function was normal with similar systolic and diastolic parameters between groups whilst reduced exercise capacity was associated with a slightly shorter pulmonary acceleration time, despite no pulmonary hypertension. Conclusion Three months after a severe COVID-19 pulmonary infection, more than one third of patients had an impairment of exercise capacity which was associated with a reduced pulmonary function, a reduced skeletal muscle mass and function but without any significant impairment in cardiac function.
In general, the received values were concordant to results of other studies. It concerned the MAD, aLDFA, aMPTA and angle between the mechanical limb axis and anatomic femoral axis. This is the first chronological evaluation of aMPFA and aLDTA from a relavively large series of patients. These normative data should be taken into consideration when evaluating lower limb alignment in children or applied in practice for planning and evaluation of the quality of surgical correction of complex deformities.
Rationale. Promoting endogenous pulmonary regeneration is crucial after damage to restore normal lungs and prevent the onset of chronic adult lung diseases.Objectives. To investigate whether the cell-cycle inhibitor p16 INK4a limits lung regeneration after newborn bronchopulmonary dysplasia (BPD), a condition characterized by the arrest of alveolar development, leading to adult sequelae.Methods. We exposed p16 INK4a -/-and p16 INK4a ATTAC transgenic mice to post-natal hyperoxia, followed by pneumonectomy of the p16 INK4a -/-mice. We measured p16 INK4a in blood mononuclear cells of preterm newborns and 7-to 15-year-old BPD survivors and the lungs of BPD patients. Measurements and main results. P16 INK4a levels increased in lung fibroblasts after hyperoxia-induced BPD in mice and persisted into adulthood. P16 INK4a deficiency did not protect against hyperoxia lesions in newborn pups but promoted restoration of the lung architecture by adulthood. Curative clearance of p16 INK4a positive cells once hyperoxia lung lesions were established restored normal lungs by adulthood. P16 INK4a deficiency increased neutral lipid synthesis and promoted lipofibroblast and alveolar type 2 cell (AT2) development within the stem-cell niche. Besides, lipofibroblasts support self-renewal of AT2 cells into alveolospheres. Induction with a PPARγ agonist after hyperoxia also increased lipofibroblast and AT2 numbers and restored alveolar architecture in hyperoxiaexposed mice. After pneumonectomy, p16 INK4a deficiency again led to an increase in lipofibroblast and AT2 numbers in the contralateral lung. Finally, we observed p16 INK4a mRNA over-expression in the blood and lungs of preterm newborns, which persisted in the blood of older BPD survivors.Conclusions. These data demonstrate the potential of targeting p16 INK4a and promoting lipofibroblast development to stimulate alveolar regeneration from childhood to adulthood.
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