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

Author:

Evers Georg1ORCID,Schulze Arik Bernard1ORCID,Osiaevi Irina1ORCID,Harmening Kimon1ORCID,Vollenberg Richard2ORCID,Wiewrodt Rainer1ORCID,Pistulli Rudin3ORCID,Boentert Matthias4ORCID,Tepasse Phil-Robin2ORCID,Sindermann Juergen R.3ORCID,Yilmaz Ali3ORCID,Mohr Michael1ORCID

Affiliation:

1. Department of Medicine A,Hematology,Oncology and Pulmonary Medicine, University Hospital Münster, Münster, Germany

2. Department of Medicine B for Gastroenterology,Hepatology,Endocrinology and Clinical Infectiology, University Hospital Münster, Münster, Germany

3. Department of Cardiology I,Coronary and Peripheral Vascular Disease and Heart Failure, University Hospital Münster, Münster, Germany

4. Department of Neurology, University Hospital Münster, Münster, Germany

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.

Publisher

Hindawi Limited

Subject

Pulmonary and Respiratory Medicine

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