Abstract 15677: Comprehensive Physiological Phenotyping Reveals Deconditioning Among Individuals With Long-COVID-19

Abstract

Introduction: Post-acute COVID-19 sequalae (PASC) is a poorly understood constellation of symptoms that persist or emerge following the post-viral convalescent period. We sought to comprehensively evaluate cardiac and autonomic function and deconditioning as possible contributors to PASC associated fatigue. Methods: Thirty individuals with PASC (20F:10M; 41±11yrs; 137-730 days post-infection) prospectively underwent measures of autonomic function (heart rate [HR] and muscle sympathetic nerve activity [MSNA] response to passive head-up tilt 60° [HUT]); cardiac function (echocardiogram); arrhythmia burden (24-hour Holter monitor); exercise capacity (cardiopulmonary exercise test); hemoglobin and inflammatory biomarkers (CRP, troponin, IL-6, TNFα, IL-10). Participants were stratified by ongoing fatigue and symptoms of breathlessness (SOB+ or SOB-). Individuals with pre-existing conditions associated with fatigue were excluded. Results: Sixteen individuals (53%) reported breathlessness. Other common symptoms were palpitations (n=9; 30%) and light-headedness (n=5; 17%). Exercise capacity normalised for age and gender was lower in breathless subjects (SOB+) than in non-breathless subjects (SOB-); 70±11% vs 85±15%, p =0.004. The SOB+ group tended to have a blunted MSNA response to HUT when compared to SOB- ( p =0.06), with similar prevalence of postural orthostatic tachycardia (SOB+ n=5 vs SOB- n=5). Echocardiography revealed that global longitudinal strain trended higher in the SOB+ group compared with SOB- ( p= 0.075), with similar prevalence of participants who fulfilled diastolic dysfunction criteria (SOB+ 5 vs SOB- 4). There were no significant sustained arrhythmias on 24-hour Holter monitoring. Hemoglobin, troponin and cytokines were all similar (p>0.05), but CRP was higher in the breathless group ( p =0.016). Conclusions: This is the first comprehensive phenotyping of PASC with ongoing fatigue and breathlessness. We found that these symptoms were associated with reduced exercise capacity but without any associated cardiac impairment, arrhythmias, or autonomic dysfunction. These findings suggest that deconditioning may contribute to the pathophysiology of PASC.