Abstract
Patients recovering from COVID-19 commonly report persistence of dyspnea, exertional fatigue, and difficulties in carrying out their daily activities. However, the nature of these symptoms is still unknown. The purpose of the study was to identify limiting causes of cardiopulmonary origin for the performance of physical exercise in post-COVID-19 condition that could explain the symptomatic persistence of dyspnea or fatigue-related symptoms. Thirty-two non-hospitalized patients with post-COVID-19 condition (i.e., still presenting a chronic symptomatic phase lasting >90 days since debut of symptoms that lasted for at least 2 months and cannot be explained by an alternative diagnosis) completed a clinical examination including echocardiography, submaximal and maximal cardiorespiratory fitness tests (Ekblom-Bak and Bruce’s protocols), and a battery of validated questionnaires about fatigue and exercise intolerance. Four participants (12.5%) reported an abnormal cardiac response to exercise during the submaximal test, which aroused suspicion of the presence of chronotropic incompetence. All of them were confirmed with a positive diagnosis maximal exercise test after cardiology screening, even with a comprehensive clinical examination, resting ECG, and echocardiogram, without other findings. No statistical differences were found in any physiological variables or questionnaire values, between patients with positive and negative diagnoses. Chronotropic incompetence and other autonomic disorders may appear in patients with mild forms of COVID-19 presentation and may persist in the long term, being responsible for exercise intolerance after resolution of acute infection. Clinicians should be aware that chronotropic incompetence and other autonomic disorders may be a complication of COVID-19 and should consider appropriate diagnostic and therapeutic interventions in these patients, especially when early exercise-related fatigability is reported.
Highlights
After a year of the coronavirus disease (COVID-19) pandemic, it has become evident how SARS-CoV2 can be responsible for damage in the central nervous system (CNS) [1]and in the autonomic nervous system (ANS), both in the acute and in the chronic, persistent phase of the disease
Consisting of a range of limiting symptoms which dramatically reduce quality of life, the post-COVID-19 condition patients mostly refers to fatigue, post-exertional malaise, dyspnea, headache, and many other neurocognitive conditions described as brain fog or inability to perform daily physical tasks [5]
Thirty-two individuals fit the eligibility criteria including a diagnosis of SARS-CoV2 using real-time reverse transcriptase polymerase chain reaction (PCR) tests or antigenic rapid tests, who still presented a chronic symptomatic phase lasting >90 days since the debut of symptoms, who were not hospitalized, and who had no evidence on clinical record of pneumonia or any other organ failure related to SARS CoV-2 infection
Summary
After a year of the coronavirus disease (COVID-19) pandemic, it has become evident how SARS-CoV2 can be responsible for damage in the central nervous system (CNS) [1]and in the autonomic nervous system (ANS), both in the acute and in the chronic, persistent phase of the disease. In a large cohort of COVID-19 patients, a significant increase in mean HR followed by a decrease in mean HR was observed from the seventh day of symptoms (relative bradycardia), which was maintained until the 21st day of evolution This alteration was associated with a loss of HR variability (HRV), both suggesting the existence of a secondary autonomic malfunction in HR control [8]. Other sequelae attributable to autonomic dysfunction have been found in patients with long COVID-19, such as postural orthostatic tachycardia syndrome (POTS) [9] Both direct involvement of the sinus node in the heart and injury to the regulatory centers of the brainstem have been postulated as pathogenic mechanisms responsible for poor HR control during SARS-CoV2 infection [10]. These lesions could be mediated by cytokine storm during the acute phase, by direct structural injury related to the expression of ACE II receptors (angiotensin II receptor) present in cardiac tissue, or immunemediated by the action of specific antibodies against the brainstem and neural tissues [10]
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