Cardiopulmonary exercise test in patients with persistent dyspnea after COVID-19 disease

Abstract

Introduction Persistent dyspnea in patients who have suffered from COVID-19 disease has become a constant in cardiology in recent months. Healther workers have been one of the population groups mainly affected during the pandemic. Chronic involvement by COVID-19 infection, such as dyspnea, is frequent, and so far, of unknown mechanism. CardioPulmonary Exercise Test (CPET) is currently the gold standard technique in the differential diagnosis of dyspnea. Therefore, CPET could be useful in the evaluation of patients after infection by the SARS-COV2 virus; a role still unknown in this context. Objective Evaluate the parameters obtained in CPET in patients who had suffered from COVID-19 disease and who presented persistent dyspnea. Methods We conducted a single-center and prospective study that included healthcare workers who suffered from COVID-19 disease with mild-moderate intensity symptoms, without the need for hospitalization, between March-December 2020 and who presented dyspnea on exertion at least 3 months after infection, in the absence of structural heart disease. An echo was performed, and a baseline spirometry followed by a CPET. Some of the variables collected such as VO2, OUES and PulseO2 have been quantified as a percentage (%) of the predicted according to predicted equations. Results 64 healthy patients with an active baseline life (without exertional dyspnea prior to infection) were included. 7 patients were excluded for presenting previously unknown structural heart disease. Of the 57 patients (Figure 1), more than half had a functional capacity lower than predicted (50th percentile), highlighting, among the cardiovascular response variables, a peak VO2 of 79% (SD: 14.0%) of the predicted, denoting slightly depressed functional capacity. In addition, in this subgroup, a VO2 at the level of the first ventilatory threshold (VT1) of 51.1% (SD: 4.2%) is observed over the predicted value -value that is considered in the lower limits of normality-; and a PulseO2 (systolic volume reflex) and an OUES in normal ranges with respect to those predicted. In the total of the 57 patients, no alterations were observed in the ventilatory efficiency parameters with effort, nor in the baseline spirometry, nor in the breathing reserve (BR), nor in final oxygen saturation (SatO2). Conclusion CPET has made it possible to identify that more than half of the patients show a deterioration -at least slight- in functional capacity (the majority of which are women) reaffirming the value of this test. The combination of this pattern that we observed in our serie is usually seen in patients with physical deconditioning and/or obesity, and is secondary to alterations in the peripheral use of oxygen, mainly at the muscular level. Based on this, a direct or indirect potential myopathic effect of the virus cannot be ruled out as responsible for the deterioration of the functional class of patients after COVID-19 disease. Funding Acknowledgement Type of funding sources: None.

Reduced exercise capacity, chronotropic incompetence, and early systemic inflammation in cardiopulmonary phenotype Long COVID

“…Deconditioning is commonly reported, perhaps because most studies predominantly included hospitalized individuals and even non-hospitalized individuals experience deconditioning after illness. 22,[80][81][82][83][84] Although we observed findings consistent with deconditioning or obesity in a few individuals (earlier anaerobic threshold, accelerated heart rate response), our findings argue against deconditioning as the primary explanation. Identifying deconditioning as a cause is challenging because it is also an effect of reduced habitual exercise among symptomatic individuals.…”

“…Multiple case series have reported that deconditioning is the primary cause of exercise limitation in PASC. 20,[69][70][71][72] Our findings argue against deconditioning as the primary explanation as the Durstenfeld et al CPET, CMR, and Ambulatory Rhythm Findings >12 months after COVID-19 majority of individuals had normal oxygen pulse and normal VO2 to work slope which suggest normal augmentation of cardiac output. We found earlier anaerobic thresholds which can be seen in deconditioning and identified three individuals (8% of sample, 20% with reduced exercise capacity) whose pattern of findings is most consistent with deconditioning, obesity, or alterations in peripheral oxygen utilization.…”

Use of Cardiopulmonary Exercise Testing to Evaluate Long COVID-19 Symptoms in Adults

“…We identified 1 interventional study of cardiac rehabilitation 67 with baseline CPET reported in an included study. 68 27,30,33,35,36,44,47,49,52,55,56,62,66,68 only included individuals who were hospitalized for acute infection (median, 70% [range, 0-100%] hospitalized), and 15 studies (39.5%) 30,32,[39][40][41][42][43]50,51,54,55,57,59,61,64 included individuals with prevalent symptoms at CPET (median, 95% [range, 38%-100%] symptomatic).…”

“…Deconditioning was reported as the most prevalent pattern by 10 studies, 27,33,35,36,46,59,[61][62][63][64] with alterations in muscular oxygen utilization acknowledged as an alternative explanation by some.…”

Cardiopulmonary exercise testing to evaluate post-acute sequelae of COVID-19 (“Long COVID”): a systematic review and meta-analysis

“…Deconditioning was the most commonly identified pattern and the main cause of reduced exercise capacity reported by 8 studies. 39,40,42,[46][47][48][49][50][51] Although ventilatory limitations were uncommon, multiple studies reported dysfunctional breathing or hyperventilation. 50,[52][53][54][55][56][57] Muscular/peripheral oxygen extraction abnormalities were also commonly reported.…”