Abstract
Background: Endothelial dysfunction has been proposed as the common pathogenic background of most manifestations of coronavirus disease 2019 (COVID-19). Among these, some authors also reported an impaired exercise response during cardiopulmonary exercise testing (CPET). We aimed to explore the potential association between endothelial dysfunction and the reduced CPET performance in COVID-19 survivors. Methods: 36 consecutive COVID-19 survivors underwent symptom-limited incremental CPET and assessment of endothelium-dependent flow-mediate dilation (FMD) according to standardized protocols. Results: A significantly higher FMD was documented in patients with a preserved, as compared to those with a reduced, exercise capacity (4.11% ± 2.08 vs. 2.54% ± 1.85, p = 0.048), confirmed in a multivariate analysis (β = 0.899, p = 0.038). In the overall study population, FMD values showed a significant Pearson’s correlation with two primary CPET parameters, namely ventilation/carbon dioxide production (VE/VCO2) slope (r = −0.371, p = 0.026) and end-tidal carbon dioxide tension (PETCO2) at peak (r = 0.439, p = 0.007). In multiple linear regressions, FMD was the only independent predictor of VE/VCO2 slope (β = −1.308, p = 0.029) and peak PETCO2 values (β = 0.779, p = 0.021). Accordingly, when stratifying our study population based on their ventilatory efficiency, patients with a ventilatory class III-IV (VE/VCO2 slope ≥ 36) exhibited significantly lower FMD values as compared to those with a ventilatory class I-II. Conclusions: The alteration of endothelial barrier properties in systemic and pulmonary circulation may represent a key pathogenic mechanism of the reduced CPET performance in COVID-19 survivors. Personalized pharmacological and rehabilitation strategies targeting endothelial function may represent an attractive therapeutic option.
Highlights
Despite the different phenotypic characteristics displayed by endothelial cells (ECs) in different organs and tissues, endothelial dysfunction shares some common features, such as reduced vasodilation, inflammation, oxidative stress and a prothrombotic state
Accumulated evidence has suggested that endothelial dysfunction may be the common pathogenic background of most manifestations of coronavirus disease 2019 (COVID-19), since ECs are a preferential target of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2]
Among a number of clinical manifestations related to SARS-CoV-2 infection, some authors reported an impaired exercise response in COVID-19 survivors during cardiopulmonary exercise testing (CPET) [5,6], which is the gold standard for assessing exercise capacity
Summary
Despite the different phenotypic characteristics displayed by endothelial cells (ECs) in different organs and tissues, endothelial dysfunction shares some common features, such as reduced vasodilation, inflammation, oxidative stress and a prothrombotic state. Accumulated evidence has suggested that endothelial dysfunction may be the common pathogenic background of most manifestations of coronavirus disease 2019 (COVID-19), since ECs are a preferential target of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [2]. This has led the European Society of Cardiology (ESC) to recommend the clinical assessment of endothelial function in the follow-up of all convalescent COVID-19 patients, aimed at monitoring the risk of long-term cardiovascular complications [3]. Personalized pharmacological and rehabilitation strategies targeting endothelial function may represent an attractive therapeutic option
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