Evaluation of long-term sequelae by cardiopulmonary exercise testing 12 months after hospitalization for severe COVID-19

Abstract

Background Cardiopulmonary exercise testing (CPET) is an important clinical tool that provides a global assessment of the respiratory, circulatory and metabolic responses to exercise which are not adequately reflected through the measurement of individual organ system function at rest. In the context of critical COVID-19, CPET is an ideal approach for assessing long term sequelae. Methods In this prospective single-center study, we performed CPET 12 months after symptom onset in 60 patients that had required intensive care unit treatment for a severe COVID-19 infection. Lung function at rest and chest computed tomography (CT) scan were also performed. Results Twelve months after severe COVID-19 pneumonia, dyspnea was the most frequently reported symptom although only a minority of patients had impaired respiratory function at rest. Mild ground-glass opacities, reticulations and bronchiectasis were the most common CT scan abnormalities. The majority of the patients (80%) had a peak O2 uptake (V′O2) considered within normal limits (median peak predicted O2 uptake (V′O2) of 98% [87.2–106.3]). Length of ICU stay remained an independent predictor of V′O2. More than half of the patients with a normal peak predicted V′O2 showed ventilatory inefficiency during exercise with an abnormal increase of physiological dead space ventilation (VD/Vt) (median VD/VT of 0.27 [0.21–0.32] at anaerobic threshold (AT) and 0.29 [0.25–0.34] at peak) and a widened median peak alveolar-arterial gradient for O2 (35.2 mmHg [31.2–44.8]. Peak PetCO2 was significantly lower in subjects with an abnormal increase of VD/Vt (p = 0.001). Impairments were more pronounced in patients with dyspnea. Peak VD/Vt values were positively correlated with peak D-Dimer plasma concentrations from blood samples collected during ICU stay (r2 = 0.12; p = 0.02) and to predicted diffusion capacity of the lung for carbon monoxide (DLCO) (r2 = − 0.15; p = 0.01). Conclusions Twelve months after severe COVID-19 pneumonia, most of the patients had a peak V′O2 considered within normal limits but showed ventilatory inefficiency during exercise with increased dead space ventilation that was more pronounced in patients with persistent dyspnea. Trial registration: NCT04519320 (19/08/2020).

Persisting exercise ventilatory inefficiency in subjects recovering from COVID-19. Longitudinal data analysis 34 months post-discharge

“…EV in is a well-recognized hallmark of pulmonary vascular disease and increased dead-space ventilation [ 30 ]. Despite normal V̇O 2peak levels in subjects recovered from severe COVID after one year of follow-up, dead space ventilation correlates with D-Dimer plasma concentrations during hospital stay [ 13 ].…”

“…Moreover, evidence at 12 months following severe COVID-19 infections indicates that numerous patients, despite achieving normal V̇O 2peak levels, exhibit signs of Ev in , notably linked to signs of underlying pulmonary microvascular disease and increased dead space ventilation [ 13 ]. Such vascular complications are believed to stem from endothelial dysfunction and a hypercoagulable state, both of which are acute sequelae of the systemic inflammatory response to SARS-CoV-2 infection [ 13 ].…”

“…The enduring clinical significance of EV in and the altered cardiovascular response to exercise in post-COVID patients remains an area of ongoing investigation [ 13 , 20 ]. The persistence of these conditions after 1 year following hospital discharge underscores the need for pathophysiological investigations and sustained longitudinal studies.…”

Persisting exercise ventilatory inefficiency in subjects recovering from COVID-19. Longitudinal Data Analysis 34 Months Post-Discharge Running title: Persisting Exercise Ventilatory Inefficiency in post-COVID Subjects

“…Moreover, evidence at 12 months following severe COVID-19 infections indicate that numerous patients, despite achieving normal VȮ 2peak levels, exhibit signs of Evin, notably linked to signs of underlying pulmonary microvascular disease and increased dead space ventilation [13]. Such vascular complications are believed to stem from endothelial dysfunction and a hypercoagulable state, both of which are acute sequelae of the systemic in ammatory response to SARS-CoV-2 infection [13].…”

“…The enduring clinical signi cance of EVin and the cardiovascular response to exercise in post-COVID patients remains an area of ongoing investigation [13,19]. The persistence of these conditions after 1 year following hospital discharge underscores the need for pathophysiological investigations and sustained longitudinal studies.…”