Discussion
SARS-CoV-2 infection, bronchiectasis, dyspnea, critically ill, fibrosis, COVID-19 infection, abnormal respiratory alkalosis, pulmonary abnormalities, endothelial cell dysfunction, ground-glass opacities
ACUTE INFECTION, SYSTEMIC INFLAMMATORY RESPONSE, SARS-COV-2 INFECTION, BRONCHIECTASIS, CRITICALLY ILL, COVID-19 PNEUMONIA, FIBROSIS, COVID-19 INFECTION
This prospective study assessed cardiopulmonary exercise performance in 60 patients, 12 months after a critical COVID-19 infection during the first wave that required initial ICU management. The patients of our cohort presented well-established risk factors for severe COVID-19 such as advanced age, a predominance of male sex and a high BMI [Despite the severity of the initial clinical presentation, exercise capacity assessed by CPET were within normal limits in most of the patients 12 months after the acute infection. Impairment was predominantly related to persistent deconditioning or prior respiratory comorbidities. These results confirm previous studies assessing exercise capacity by CPET 3 to 6 months after hospital release and reporting that remaining exercise limitation after COVID-19 is primarily related to physical deconditioning rather than to physiological impairment [In our study, 12 months after the acute infection, the length of ICU stay was still an independent predictor of peak V′OAnother intriguing observation in our study was that many patients having a peak V′OIn our patients, there was no evidence of exaggerated hyperventilatory response. Indeed, we did not see abnormal respiratory alkalosis, nor anarchical evolution of tidal volume. However, ventilatory inefficiency was associated in our study with increased physiological dead space ventilation. Indeed, we observed that nearly two-thirds of the patients with a normal peak predicted V′OIn healthy individuals, VD/Vt decreases usually during exercise as Vt increases several folds and to a much greater extent than the small increase in VD [It is now apparent that SARS-CoV-2 infection induces endothelial cell dysfunction with systemic inflammatory response resulting in a prothrombotic state manifesting especially with microthrombosis [It was interesting to note, that 12 months after the severe COVID-19 pneumonia, more than 80% of the patients showed still pulmonary abnormalities on CT chest. Mild ground-glass opacities, reticulations and bronchiectasis were most common and honeycombing was only seen in 3 patients. Therefore, underlying parenchymal microscopic fibrosis may also contribute to our observations. Indeed, even if the majority of patients had a diffusion capacity at rest considered within normal limits 12 months after the acute infection, peak VD/Vt was significantly correlated to predicted DHalf of our patients, including those who had an exercise capacity within normal limits, still complained of dyspnea. A recent study evaluating the health-related quality of life and persistent symptoms in critically ill COVID-19 patients at twelve months identified a similar proportion with 58.4% of patients with persistent mild dyspnea that was weakly correlated with both DLCO and length of invasive mechanical ventilation [Some potential limitations of our study should be noted. Our study was conducted in a single center. There was also a missing baseline assessment of dyspnea and cardiopulmonary function at rest before SARS-CoV-2 infection in our patients. Even if nearly all the patients with normal exercise capacity and ventilatory inefficiency at exercise had spirometry and predicted DLCO within normal limits, it would have been interesting to compare the results with matched controls. Indeed, more than half of our study cohort were smokers or former smokers. Moreover, we were not able to measure the diffusing capacities of the lung for nitric oxide (NO) which combined to D