Abstract
Background Following COVID-19, patients often present with ongoing symptoms comparable to chronic fatigue and subjective deterioration of exercise capacity (EC), which has been recently described as postacute COVID-19 syndrome. Objective To objectify the reduced EC after COVID-19 and to evaluate for pathologic limitations. Methods Thirty patients with subjective limitation of EC performed cardiopulmonary exercise testing (CPET). If objectively limited in EC or deteriorated in oxygen pulse, we offered cardiac stress magnetic resonance imaging (MRI) and a follow-up CPET. Results Eighteen male and 12 female patients were included. Limited relative EC was detected in 11/30 (36.7%) patients. Limitation correlated with reduced body weight-indexed peak oxygen (O2) uptake (peakV̇O2/kg) (mean 74.7 (±7.1) % vs. 103.6 (±14.9) %, p < 0.001). Reduced peakV̇O2/kg was found in 18/30 (60.0%) patients with limited EC. Patients with reduced EC widely presented an impaired maximum O2 pulse (75.7% (±5.6) vs. 106.8% (±13.9), p < 0.001). Abnormal gas exchange was absent in all limited EC patients. Moreover, no patient showed signs of reduced pulmonary perfusion. Using cardiac MRI, diminished biventricular ejection fraction was ruled out in 16 patients as a possible cause for reduced O2 pulse. Despite noncontrolled training exercises, follow-up CPET did not reveal any exercise improvements. Conclusions Deterioration of EC was not associated with ventilatory or pulmonary vascular limitation. Exercise limitation was related to both reduced O2 pulse and peakV̇O2/kg, which, however, did not correlate with the initial severity of COVID-19. We hypothesize that impaired microcirculation or limited peripheral O2 utilization might be causative for prolonged deterioration of EC following acute COVID-19 infection.
Highlights
In late 2019, a novel SARS-associated coronavirus was identified as the cause of an increased incidence of pneumonia cases in Wuhan, Hubei Province of China [1]
After approval of the study conducted by the local ethics committee (Ref. 2020-585-f-S), patients with persistent, subjective deterioration in exercise capacity (EC) or with symptoms consistent with dyspnea or fatigue at follow-up visits after COVID-19 were offered prospective follow-up bicycle-exhausting cardiopulmonary exercise testing (CPET) at our outpatient clinic
With respect to the cause of EC limitation, we found an insufficient O2 pulse increment, defined as maximum O2 pulse
Summary
In late 2019, a novel SARS-associated coronavirus was identified as the cause of an increased incidence of pneumonia cases in Wuhan, Hubei Province of China [1]. Following COVID-19, patients often present with ongoing symptoms comparable to chronic fatigue and subjective deterioration of exercise capacity (EC), which has been recently described as postacute COVID-19 syndrome. Thirty patients with subjective limitation of EC performed cardiopulmonary exercise testing (CPET). If objectively limited in EC or deteriorated in oxygen pulse, we offered cardiac stress magnetic resonance imaging (MRI) and a follow-up CPET. Limitation correlated with reduced body weightindexed peak oxygen (O2) uptake (peakVO2/kg) (mean 74.7 (±7.1) % vs 103.6 (±14.9) %, p < 0.001). Reduced peakVO2/kg was found in 18/30 (60.0%) patients with limited EC. Patients with reduced EC widely presented an impaired maximum O2 pulse (75.7% (±5.6) vs 106.8% (±13.9), p < 0.001). Using cardiac MRI, diminished biventricular ejection fraction was ruled out in 16 patients as a possible cause for reduced O2 pulse. Deterioration of EC was not associated with ventilatory or pulmonary vascular limitation
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