Sustained Impairment in Cardiopulmonary Exercise Capacity Testing in Patients after COVID-19: A Single Center Experience.

Evers G; Schulze AB; Osiaevi I; Harmening K; Vollenberg R; Wiewrodt R; Pistulli R; Boentert M; Tepasse PR; Sindermann JR; Yilmaz A; Mohr M;

Canadian respiratory journal [Can Respir J] 2022 Mar 01; Vol. 2022, pp. 2466789.
Date of Electronic Publication: 2022 Mar 01 (Print Publication: 2022).

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 (O 2 ) uptake (peakV̇O 2 /kg) (mean 74.7 (±7.1) % vs. 103.6 (±14.9) %, p < 0.001). Reduced peakV̇O 2 /kg was found in 18/30 (60.0%) patients with limited EC. Patients with reduced EC widely presented an impaired maximum O 2 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 O 2 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 O 2 pulse and peakV̇O 2 /kg, which, however, did not correlate with the initial severity of COVID-19. We hypothesize that impaired microcirculation or limited peripheral O 2 utilization might be causative for prolonged deterioration of EC following acute COVID-19 infection.